Tag Archives: ISSN

Gain Muscle, Jack Your RMR – Sorta?

 

Key Points

  • The number of calories you burn for every pound of lean body mass is equal to a cherry tomato.
  • Teleologically, it makes no sense for RMR to increase to any appreciable extent if one does gain lean body mass.
  • Heavy resistance training is great for pretty much everyone. But don’t be hoodwinked by the promise of a jacked up RMR.

By Jose Antonio PhD FNSCA FISSN CSCS – How often have you heard the following refrain? “To increase your resting metabolic rate, you need to lift weights. Putting on muscle is the sure-fire way to have the metabolism of a blue whale.” And that way, the fat will melt off your flabby belly like a stick of metabolic-ratebutter on a hot stove. Ok, I put the blue whale part in there. Blue whales can apparently consume half a million calories in one mouthful. Whoa. Can you say Thanksgiving buffet with every bite?! So does making those bi’s, tri’s and glutes a tad bit larger result in resting metabolism that’s copious, capacious or colossal? Or is this Much Ado About Nothing? Before I provide a teleological explanation of why this notion is cockeyed, here’s some food for thought.1, 2 According to Robert R Wolfe PhD, “every 10-kg difference in lean mass translates into a difference in energy expenditure of ~100 kcal/d.” Or in units us Americans prefer, that’s about an increase of 4.5 calories for every pound gained.2 Regardless of whether that number is entirely accurate, let’s just say RMR per unit of fat free mass is about as impressive as dunking a basketball on an 8 foot hoop.

Nonetheless, here’s an investigation that examined resting metabolic rate (RMR) pre and post resistance training. They looked at the effects of 24 weeks of strength training on RMR, energy expenditure of physical activity (EEPA), and body composition. For the purposes of this article, we’ll focus on RMR. They had subjects divided by age and sex: 10 young men (20-30 years), 9 young women (20-30 years), 11 older men (65-75 years) and 10 older women (65-75 years). They performed whole body resistance training 3/week for 24 weeks. Their baseline or pre- and post-training RMR were as follows:

Pre-training

Young men – 12.2 kcal/lb FFM/d

Young women – 13.5 kcal/lb FFM/d

Older men – 12.0 kcal/lb FFM/d

Older women – 13.6 kcal/lb FFM/d

Post-training

Young men – 12.8 kcal/lb FFM/d

Young women – no change

Older men – 12.8 kcal/lb FFM/d

Older women – no change

The first thing that stands out is that in both young and older women, their metabolic rate didn’t change at all. The other thing that stands out is how truly unimpressive the number of calories burned for one pound of fat-free mass (FFM). All groups increased FFM: +4.4 lb in young men, +4.18 lb in young women, +2.2 lb in older men, +1.98 lb in older women. In general, this study suggests that you burn roughly 12-13 kcal per pound of FFM daily. The authors of the study said that changes in absolute and relative RMR in response to heavy resistance training are influenced by sex but not age; that’s good news for us old guys.1

Pratley et al. looked at RMR after 16 weeks of resistance training in 13 healthy 50-65 year olds.3 They found that RMR before and after training was 11.8 kcal/lb FFM/d and 12.3 kcal/lb FFM/d. Interestingly, Broeder et al. found no change in RMR when adjusted for FFM.4

So what gives? Clearly there is quite a bit of variability in the RMR response to gains in FFM. Some folks gain, others nada. Maybe a sex difference exists with men responding better than women. Also, changes in RMR are not solely due to changes in FFM (or skeletal muscle mass). Perhaps it is related to changes in basal sympathetic nervous system tone. Alternatively,

Mongolian-born grand sumo champion Yokozuna Asashoryu wears a ceremonial belly band as he performs a ring-entering ritual at Meiji Shrine in Tokyo January 7, 2008. Asashoryu was banned in August 2007 and fled to his homeland after he outraged fans when he was caught on video playing soccer while supposedly out of action with a back injury. REUTERS/Toru Hanai (JAPAN) - RTX5ATL

Mongolian-born grand sumo champion Yokozuna Asashoryu wears a ceremonial belly band as he performs a ring-entering ritual at Meiji Shrine in Tokyo January 7, 2008. Asashoryu was banned in August 2007 and fled to his homeland after he outraged fans when he was caught on video playing soccer while supposedly out of action with a back injury. REUTERS/Toru Hanai (JAPAN) – RTX5ATL

changes in organ mass (particularly in very large individuals such as sumo wrestlers) may also account for gains in RMR.5 Have you ever seen the distended guts of professional bodybuilders? That ain’t skeletal muscle. Nonetheless, one might argue that these small changes in RMR could account for significant changes over years and decades. And that certainly may be true. However, it is evident that trifling changes in diet can negate any increase in RMR. For instance, if you gained 5 pounds of lean body mass, that translates roughly into about 50 extra calories per day. That’s not even a mug of beer. Boo.

It makes no sense for RMR to increase significantly even with large gains in skeletal muscle. –  One of my favorite college classes as an undergrad was on Evolutionary Biology. The human animal (or heck any animal) has two primary objectives: survival and reproduction. If you can throw in a good sushi buffet, a cruise to the Bahamas, and the Cubs winning the World Series, than even better. Anyhow, getting back to evolution. Let’s take a trip back to the days when there was no running cavemen-food-nutritionwater or electricity. Man was left to fend for itself like any other wild animal. It helped having a big brain because there was no chance in hell that humans could use physical strength or speed to kill its next meal. Conversely, humans developed quite the endurance capacity to ‘out-work’ its prey and a brain to ‘out-think’ just about every creature on Earth. You’ll notice that even modern day hunter-gatherer societies are ‘endurance’ oriented. You need endurance just to stay alive. Having large muscles serves no survival benefit.

Now let’s say some wacky caveman found that lifting big rocks made his chest and arms bigger. Now pretend that for every pound he gained, that would be an extra 50-100 calories per day (urban legend says this figure is true). So a 5 lb gain, which is certainly attainable by even the most average of men, would result in an cavemanhunting-1160x683increased caloric need of 250-500 calories (according to the urban legend figure). Now where would a caveman get these calories? Would he open the fridge to get a protein shake? Go to Burger King and order a Whopper? Duh. It makes zero evolutionary sense for RMR to go up to any appreciable extent if you gain lean body mass. Or put another way. It is energetically costly to gain and maintain skeletal muscle mass. Why? Because you’d have to feed it you knucklehead. It makes evolutionary sense that it is difficult to gain muscle (which it is) and easy to gain fat (which it is). Why? So you can survive the next go round of the zombie apocalypse when an asteroid the size of Hawaii blasts Earth into a nuclear-winter oblivion. If that happens and you survive, you better pray that you have the genes for putting on fat easily. Otherwise, you and all the Victoria’s Secret models will shrivel to death in a matter of weeks.

Bottom line: Don’t believe the hype when folks say, “a great way to elevate RMR is by increasing skeletal muscle mass via resistance training.” Lifting weights does a lot of great things. In fact, heavy resistance training can help athletes of all kinds (i.e., endurance and strength-power). And yes it does increase muscle mass. But the change in RMR is like pissing in the ocean. And we all know what that’s like. Unless of course you live in Iowa.

About the Author – Jose Antonio earned his PhD at the University of Texas Southwestern Medical Center in Dallas. He completed a post-doctoral research fellowship there as well. His current research focus is on the effects of various ergogenic aids on body composition and performance. He is the CEO of the ISSN and an Associate Professor at Nova Southeastern University.13119931_10156866463875440_6050451888342188203_o

References

  1. Lemmer JT, Ivey FM, Ryan AS, et al.: Effect of strength training on resting metabolic rate and physical activity: Age and gender comparisons. Med Sci Sports Exerc 2001, 33:532-41.
  2. Wolfe RR: The underappreciated role of muscle in health and disease. Am J Clin Nutr 2006, 84:475-82.
  3. Pratley R, Nicklas B, Rubin M, et al.: Strength training increases resting metabolic rate and norepinephrine levels in healthy 50- to 65-yr-old men. J Appl Physiol (1985) 1994, 76:133-7.
  4. Broeder CE, Burrhus KA, Svanevik LS, et al.: The effects of either high-intensity resistance or endurance training on resting metabolic rate. Am J Clin Nutr 1992, 55:802-10.
  5. Midorikawa T, Kondo M, Beekley MD, et al.: High ree in sumo wrestlers attributed to large organ-tissue mass. Med Sci Sports Exerc 2007, 39:688-93.

 

What makes a scientist, a scientist?

 

As a university professor, I often get asked ‘what is a scientist?’ What do these geeks actually do? Fortunately, I teach a university-level Research Methods course. Thus, I have a mad-scientistforum for giving a somewhat elaborate response to my students. I think what’s confusing to the untrained or novel eye is that social media has witnessed a proliferation of those who claim to be ‘researchers.’ For the purpose of this article, I’ll treat ‘researchers’ and ‘scientists’ synonymously. Nevertheless, I will address the question of what exactly a scientist is. And more specifically, what a professional scientist actually does. Furthermore, I’m writing this from the standpoint of someone trained in the biological sciences because I’m not familiar with the manner in which chemists or physicists conduct ‘science.’ So to my students who have asked this question, I’ve finally put pen to paper, or more precisely, fingers to keyboard, and given you a somewhat limited answer to a rather complex question.

Key Points to Remember

  • Sitting in your Garanimals® while doing a PubMed search does not make you a scientist.
  • Being published in a peer-reviewed journal does not make you a scientist (I can see the confusion in many faces now).baby-typing-laptop-computer-keyboard-28598956
  • Professional scientists are typically involved in a series of steps that are unseen by non-scientists. In the short run, publication is the goal of professional scientists. In the long run, if you want to make a significant impact on our field, you need to conduct original investigations (i.e., generate original data).
  • Conducting original investigations is the hallmark of ‘doing science.’ If you’ve never done this, then you’re not a scientist. Review papers and meta-analyses are great for giving a ‘snapshot’ of the current state of science in a given field; however, they are not original investigations. They’re summaries of other original investigations (i.e., the work of other scientists).big-data-definition
  • It is easy to criticize a study. Students in my Research Methods class are often surprised as to the ease of finding limitations in studies published in peer-reviewed journals. However, try being the PI (principal investigator) of a study. When you walk a mile in someone else’s shoes, you’ll realize that banging your keyboard in the comfort of your underwear ain’t nothing like being the PI of a study. It’s the difference between being a movie critic and someone who makes movies.
  • You can indeed be very good at using the scientific method in your profession (e.g., personal trainer, dietitian, etc.) without being an actual scientist. I wholeheartedly implore everyone in the fitness-nutrition fields to embrace science. It would be like embracing medicine. You don’t have to be an MD to do that.

Let me outline the typical steps that a scientist performs before you, John Q. Public, can sit in your La-Z-Boy chair and leisurely read a peer-reviewed publication. I’m coming from a background of having done both extensive animal (i.e., rodents, birds, etc) and human research.1-7 The process is similar.lazboy

  1. Ideation phase – this is perhaps the most fun. Why? Because it’s free and anyone can do it. In this phase, you basically come up with an experimental idea. Interestingly, these ideas can arise at any time: while sunbathing, working out, or after consuming 6 beers. For instance, my idea of coming up with the initial high protein diet (4.4 g/kg/d) arose from a random conversation with a recreational bodybuilder who admitted to eating boatloads of protein.8 I asked myself: “what if we just got trained guys and girls to just eat a lot of protein?” Simple enough, right? Uh no. The hard part comes after this.
  2. Delineating the experimental protocol – now you put the pedal to the metal and write the IRB proposal (Institutional Review Board) and Informed Consent to submit to the university. If you work for a private clinical research organization or CRO, there are external IRBs that you can submit your proposal to. If you don’t like writing, you’ll hate this phase. At my university, it requires that you fill out a 20-page form. Yeah fun. Like stepping on a porcupine. I think pretty much every scientist dislikes this phase. Why? Because the folks who often review your IRB proposal are not experts in your particular field. Thus, the questions you receive regarding your protocol are often bizarre. But this is a hurdle every scientist must jump over before you initiate subject recruitment.irb_banner
  3. Subject recruitment – after getting IRB approval, which can take anywhere from 1 month (a rarity) to several months (for me, the average length is about 3 months), you subsequently initiate subject recruitment. This is perhaps one of the most misunderstood steps. First of all. It is difficult to recruit subjects for a study. In fact, getting the right subjects for a study is absolutely critical. For example, doing studies on untrained subjects is largely irrelevant to those who work with athletes. Why? Because untrained people respond to pretty much anything you throw at them. Yet many studies published in the sports sciences use untrained subjects. Why? Because the subject pool is enormous. When boneheads on Facebook lament the fact that a study has “only 20 highly trained cyclists (or any athletic group)” (meaning the sample size is ‘too small’ to be meaningful), it clearly underscores how little they know about research in general and subject recruitment specifically. Give me 20 highly trained athletes any day versus 60 untrained slobs.
  4. Data collection – I want to clear one thing up. If a study has 40 subjects for instance, it does not mean you pre- and post-test all 40 of them on the same days. Folks don’t understand why studies often take an inordinately long time. Once you’ve recruited subjects, data collection is typically staggered. Meaning, you get subjects in the lab (or field) when you can. Sometimes pre-testing a group of subjects can cover the span of months. Moreover, data collection requires its own unique set of skills. And like any skill, if you don’t use it, you lose it. Data collection would be akin to swimming in water. Reading about data collection would be like watching someone swim. Guess which is more difficult? The critiques I see on social media often underscore how little folks know about data collection. So unless you’ve actually jumped in the water, you will never truly know what it’s like to collect data. And the studies that are the absolute most difficult to do? Dietary intervention studies (i.e., comparing ketogenic vs. low carb vs. high carb vs. any random diet). I cringe a bit when I read social media critiques of diet studies. If folks only knew how difficult it is to ‘control’ these studies then one might get a better appreciation for these kinds of investigations. And there is a trade-off between control and real-world application. The more tightly a study is ‘controlled’ (e.g., metabolic ward diet studies), the less it resembles what free-living human beings do. The less tightly a study is controlled (i.e., getting highly trained, free-living subjects to comply with an intervention), the more applicability it may have to real life. Clearly both have their pros and cons.
  5. Data analysis – once you’ve collected all your data (the shortest time frame for collecting data-interpretation-tipsdata that I’ve done was 1 month; the longest was > 1 year), then the fun begins: interpreting the data. This is perhaps one of the more confusing steps for scientists-in-training (i.e., grad students). You can present the same data set to a dozen scientists and you may end up with a dozen different interpretations. In fact, it may be confusing to scientists themselves. Data
    interpretation requires that you have a solid background in the basic sciences (e.g., biology, chemistry, physics, math, etc). Furthermore, an extensive knowledge of the existing literature is key. Like any skill, this one requires practice, practice and more practice.
  6. Presentation at a science conference – prior to submitting a study (in the form of a manuscript) for publication in a peer-reviewed science journal, scientists will often present their data at a science conference. For instance, the International Society of Sports Nutrition conference has some of the latest research presented in the form of poster presentations and/or tutorials. If you fear public speaking more than sharks, then perhaps science ain’t the best career for you.
  7. Publication – writing a paper for publication is the ‘last’ step in the process. Though in jissnactuality, each study you do will likely lead to a different experimental question which in turn leads to another investigation. The mark of an excellent scientist isn’t just the ‘answers’ they arrive at, but the questions they generate. I actually enjoy writing. It’s like the icing on the cake. Writing for scientific journals is its own unique skill. There are some individuals
    who are amazing writers. Two of the very best I’ve read are Peter Lemon PhD and John Ivy PhD. Meanwhile, others are about as eloquent as a chimpanzee banging on a Mac Pro laptop. Inasmuch as English is now the language of science, English-writing skills are wso_monkey_team_absolutely critical for anyone who wishes to be a published scientist.
  8. Repeat steps 1-7

If you don’t do the steps outlined above, then you’re not a professional scientist. Anything less than the above dilutes the meaning of the word ‘scientist.’ The fact of the matter is that conducting original investigations is quite difficult. The notion that scientists can “control” all extraneous variables is very much a Sisyphean task.

But what if I’m published in a peer-reviewed science journal? Does that mean I’m a professional scientist? The simple answer to that is ‘no.’ They’ve basically skipped steps #1-7. Keep in mind that for many published papers, students and lab techs are often listed as co-authors. Does that mean they are now ‘scientists?’ Uh no. It’s like calling yourself a medical mybrainisfulldoctor because you wear a white lab coat, hang a stethoscope around your neck and watch re-runs of Grey’s Anatomy. The most important individuals listed on a scientific paper are the first and last (senior) author. The last author is typically the PI and runs the lab. The first author is often the person who does most of the data collection. Sometimes the PI is also the primary data collector. Not everyone follows this ‘rule’ so to speak. But most do. Either way, research is always a team effort. You need students, lab techs as well as your science colleagues.

You can still use the scientific method even if you’re not a scientist. You don’t have to be a scientist to be able to deftly use the scientific method in your daily life. In fact, you can be one helluva ‘thinker’ (in the scientific sense) and not be a scientist. For instance, personal trainers who use and embrace science and the scientific method are better trainers because of it. Why? Because rather than just being a parrot telling their clients what to do (because that’s what they were told when they were younger), they understand the ‘why’ of their advice. And if they don’t understand the ‘why’ of their advice, they’ll fully admit to not knowing. And that’s fine. The more you learn in this field, the more realize there’s a lot of stuff that you don’t know. The scientific method is the single most powerful way of thinking. Embrace it. Anecdotes are nice. But data trumps anecdotes.

BIO – I live in South Florida with my wife and twin daughters. I teach at Nova Southeastern University. I run the ISSN. I paddle in the ocean. I eat a lot. I have a daily beer or wine and last but not least, I worship the sun.miami-paddle-race

References

  1. Vierck J, O’Reilly B, Hossner K, et al.: Satellite cell regulation following myotrauma caused by resistance exercise. Cell Biol Int 2000, 24:263-72.
  2. Antonio J and Gonyea WJ: Skeletal muscle fiber hyperplasia. Med Sci Sports Exerc 1993, 25:1333-45.
  3. Bertocci LA, Fleckenstein JL, and Antonio J: Human muscle fatigue after glycogen depletion: A 31p magnetic resonance study. J Appl Physiol (1985) 1992, 73:75-81.
  4. Antonio J, Wilson JD, and George FW: Effects of castration and androgen treatment on androgen-receptor levels in rat skeletal muscles. J Appl Physiol (1985) 1999, 87:2016-9.
  5. Antonio J and Gonyea WJ: Progressive stretch overload of skeletal muscle results in hypertrophy before hyperplasia. J Appl Physiol (1985) 1993, 75:1263-71.
  6. Antonio J and Gonyea WJ: Role of muscle fiber hypertrophy and hyperplasia in intermittently stretched avian muscle. J Appl Physiol (1985) 1993, 74:1893-8.
  7. Antonio J and Gonyea WJ: Muscle fiber splitting in stretch-enlarged avian muscle. Med Sci Sports Exerc 1994, 26:973-7.
  8. Antonio J, Peacock CA, Ellerbroek A, et al.: The effects of consuming a high protein diet (4.4 g/kg/d) on body composition in resistance-trained individuals. J Int Soc Sports Nutr 2014, 11:19.

 

Implementing low carbohydrate availability training- Part 2

Kedric Kwanby Kedric Kwan CISSN. There is definitely a discrepancy between mitochondrial adaptation and performance. After reading the literature, there are a few factors that needs to be accounted for during the implementation to optimise both the mitochondrial adaptation and performance outcome. The first factor is to ensure that the second bout of exercise is commenced with low muscle glycogen levels.Cycling_20-2

Not doing so might not facilitate the desired adaptation which can translate to performance. This could be seen in an acute study done by Cochran and colleagues (2010) who had 10 active males participated in a trial where they were split into two groups, both groups performed 5 x 4 minutes bout of cycling at 90-95% heart rate reserve followed by a 3 hour recovery where both groups consumed the drinks provided. One group ingested a high carbohydrate drink (HI-HI) and the other ingested a placebo drink (HI-LOW). After the 3 hour recovery, the same exercise protocol was repeated. The HI-LOW group showed greater increased of p38 MAPK compared to the HI-HI group. However the increase of PGC-1α and cytochrome c oxidase (COX IV) mRNA which plays a role in the synthesis of ATP increased with no difference between groups. This is due to the fact that both groups started the second bout of exercise with similar muscle glycogen content.

In addition, to further emphasize the importance of muscle glycogen content, two different studies measured the activity level of AMPK. Using a cycling model one study showed that AMPK levels were not different in both groups despite one group consuming CHO during exercise (Lee Young et al., 2006). This was in contrast to the result by Akestrom et al (2006) which showed a higher increase in the group that consumed a placebo drink. This could be caused by the different exercise mode used in the experiments due to a cycling model used rowingby Lee Young and colleagues whereas Akestrom and colleagues used a single knee extensor model. The nature of the single knee extensor model is highly concentrated and possibly targeted the carbohydrate glucose supplementation which spared muscle glycogen which explains the difference in findings between the two studies. Another interesting study found that carbohydrate ingestion during endurance exercise resulted in similar increases in CS levels with the placebo group. An incremental maximal cycling test also showed similar improvements in both groups (Nybo et al., 2009). This was also only conducted after an overnight fast with no glycogen depletion prior which further indicates the role of glycogen on these adaptations.

The last study that really cements the role of muscle glycogen is done by Lane and colleagues (2015) This study was done to examine the effects of sleeping with low carbohydrate availability on acute training responses and this showed greater upregulation of signalling proteins involved in fat oxidation but fail to show an increase of upregulation of markers of mitochondrial biogenesis. The participants recruited in this study were highly trained and it is well documented that trained individuals have a higher capacity to store glycogen compared to untrained. Despite muscle glycogen content was reduced by 50% but because of the high level of starting muscle glycogen, participants started the second exercise bout with reduced muscle glycogen but the levels were not low enough to illicit changes in mitochondrial adaptation that was hypothesized to occur. This shows that the actual content of muscle glycogen seems to play a larger role than the relative amount of runningmuscle glycogen. What is the sweet spot for muscle glycogen content to illicit a response is still unclear and hopefully future research will shed some light on it.

The more trained you are, the greater cellular disruption you would need to cause an adaptation, hence there seems to be an inverse relationship between training status and muscle glycogen level. The more well trained you are, lower muscle glycogen levels might be needed to create additional adaptation. If you’re relatively untrained, performing exercise after a long bout of fasting might be able to cause some form of improvement.

Another factor that to take into account during implementation is the intensity or stimulus from the training bout. As mentioned above, p38 MAPK is one of the regulators of the master regulator of mitochondrial biogenesis, PGC-1 α. Research have shown that p38 MAPK is sensitive to the stress that is being imposed during training and it is also regulated by the reactive oxygen species (ROS) induced during exercise. In fact, oxidative stress seems to be higher after a short bout of high intensity exercise compared to a submaximal steady state exercise (Olcina et al., 2008) further showing the role of intensity in regulating this protein. The hypothesis that higher exercise intensity would cause higher oxidative stress leading to higher levels of p38MAPK seems valid. Hence, a constant intensity might not be able to illicit significant adaptation for the trained athlete.

The other upstream protein, AMPK seems to response to exercise stimulus and intensity as well. Nielsen and workers (2002) showed that at the end of a 20 minute exercise bout at 80% VO2max AMPK levels were reduce.d This is possibly due to the fact that AMPK response to a change to the initial bout of intensity and reduces thereafter. Another study showed that AMPK activation was lowered after 3 weeks of moderate intensity at the same workload. This could be caused by the initial adaptation to the initial stimulus and that intensity wasn’t sufficient to further induce additional adaptation in later stages (McConell et al., 2005).13119931_10156866463875440_6050451888342188203_o

Most training bouts used in the studies used fixed bout of exercise, an example from one study used a high intensity training model consisting of 8 x 5 minutes of all-out effort alternating with 1 minute of recovery for 3 weeks (Hulston et al., 2010). It is possible that because the exercise bouts did not increase, a “tolerance” was built up to it. Hence a reduced stimulus of exercise intensity took place further into the training intervention. Moreover, how much time of the 5 minute all-out effort was actually maximal effort because I doubt that anyone could sustain an all-out effort for 5 minutes. Shorter bouts of all-out efforts such as the one used in Sprint Interval Training (SIT) might be able to elicit a stronger stimulus. In fact, Granata et al (2015) showed that SIT actually increased PGC-1 α and p53 much higher than regular high intensity training or sub-lactate threshold training even though total work done was lower in the SIT group. However, this study was not done in a limited carbohydrate availability state but the importance of intensity should be noted from this study. Given that the activation of these two upstream regulators responses to the exercise stimulus and intensity, it make sense that some form of progressive overload is needed to induce some form of additional improvement that could translate into performance.

In a discussion with Professor John Hawley (you should know who he is, if you don’t, you haven’t been reading up enough) he said that currently measurement tools might not be sensitive enough to show a statistical significance on performance when training with a reduced carbohydrate availability, so if tools aren’t sensitive enough, the only possible way I could think of is to create additional performance large enough to be detected. While the verdict on performance isn’t actually out yet, future studies that is conducted with much better methods might actually create more performance changes using a “train low” method strategically.

For the general lay person wanting to implement some form of reduced carbohydrate availability training, you could probably start by doing some form of fasted exercise or simply performing two bouts of exercise with no carbohydrate in between sessions. While the exact amount of muscle glycogen depletion would not be accurate, I believe most readers here aren’t elite endurance athlete hence there might still be small additional benefits to us.

A very interesting study I would like to conduct which would benefit meathead powerlifters like myself would be to actually examine if performing resistance training with reduced glycogen availability could improve endurance performance compared to actually performing resistance training in a carbohydrate fed state. If this hypothesis works, simply restricting carbohydrate consumption prior to lighter lifting sessions might actually improve our aerobic capacity without the need of too much additional cardio.

And yes, despite being a powerlifter, I still see the importance of the aerobic system so if it’s possible to kill two birds with one stone solely through lifting, I would be highly interested to do a study as such.

Take home message: As far as the evidence would suggest, training with low glycogen/carbohydrate availability and periodizing it to a well thought of training schedule can bring about additional benefits. No study have shown a decrement in performance which would be a relief to most wanting to experiment with it.gym-treadmill-use

This field of research is relatively new and there would definitely be more studies coming out in the near future. I hope I’ve given some insight on the mechanism behind how low glycogen/carbohydrate availability training works and the physiology and biochemistry lessons didn’t bore you out of your minds!

Fun Reading for My Fellow Geeks

Akerstrom, T., Birk, J., Klein, D., Erikstrup, C., Plomgaard, P., Pedersen, B. and Wojtaszewski, J. (2006). Oral glucose ingestion attenuates exercise-induced activation of 5’-AMP-activated protein kinase in human skeletal muscle. Biochemical and Biophysical Research Communications, 342(3), pp.949-955.

Cochran, A., Little, J., Tarnopolsky, M. and Gibala, M. (2010). Carbohydrate feeding during recovery alters the skeletal muscle metabolic response to repeated sessions of high-intensity interval exercise in humans. Journal of Applied Physiology, 108(3), pp.628-636.

Granata, C., Oliveira, R., Little, J., Renner, K. and Bishop, D. (2015). Training intensity modulates changes in PGC-1α  and p53 protein content and mitochondrial respiration, but not markers of mitochondrial content in human skeletal muscle. The FASEB Journal, 30(2), pp.959-970.

 

Hulston, C., Venables, M., Mann, C., Martin, C., Philip, A., Baar, K. and Jeukendrup, A. (2010). Training with Low Muscle Glycogen Enhances Fat Metabolism in Well-Trained Cyclists. Medicine & Science in Sports & Exercise, 42(11), pp.2046-2055.

 

Lane, S., Camera, D., Lassiter, D., Areta, J., Bird, S., Yeo, W., Jeacocke, N., Krook, A., Zierath, J., Burke, L. and Hawley, J. (2015). Effects of sleeping with reduced carbohydrate availability on acute training responses. Journal of Applied Physiology, 119(6), pp.643-655.

 

Lee-Young, R. (2006). Carbohydrate ingestion does not alter skeletal muscle AMPK signaling during exercise in humans. AJP: Endocrinology and Metabolism, 291(3), pp.E566-E573.

McConell, G., Lee-Young, R., Chen, Z., Stepto, N., Huynh, N., Stephens, T., Canny, B. and Kemp, B. (2005). Short-term exercise training in humans reduces AMPK signalling during prolonged exercise independent of muscle glycogen. The Journal of Physiology, 568(2), pp.665-676.

 

Nielsen, J., Mustard, K., Graham, D., Yu, H., MacDonald, C., Pilegaard, H., Goodyear, L., Hardie, D., Richter, E. and Wojtaszewski, J. (2002). 5′-AMP-activated protein kinase activity and subunit expression in exercise-trained human skeletal muscle. Journal of Applied Physiology, 94(2), pp.631-641.

 

Nybo, L., Pedersen, K., Christensen, B., Aagaard, P., Brandt, N. and Kiens, B. (2009). Impact of carbohydrate supplementation during endurance training on glycogen storage and performance. Acta Physiologica, 197(2), pp.117-127.

Olcina, G., Munoz, D., Timón, R., Maynar, M., Robles, M., Caballero, M. and Maynar, J. (2008). Oxidative Stress And Antioxidant Response In Trained Men After Different Exercise Intensities. Medicine & Science in Sports & Exercise, 40(Supplement), pp.S384-S385.

 

 

 

 

 

 

 

Key micronutrients for building muscle

Livia Ly

By Livia Ly MS RD LDN. You are a weight trainer and you eat adequate amounts of carbs, protein and fat. You also take supplements, sleep well, rest enough, train hard, and change your training periodically. But still, it seems like you’ve hit a plateau trying to build more muscle. There could be multiple reasons for this, but one that I’m particularly interested in is a deficiency of micronutrients. There is no point in having a high calorie / protein diet if your body is lacking key nutrients that are crucial for specific reactions to form extra muscle cells. Some of these nutrients are needed for amino acid metabolism, others are indirectly related because they increase insulin sensitivity, which promotes muscle building through a pathway called the mTOR Signaling Pathway. Ok, enough of the geeky stuff, let’s take a look at a list of vitamins and minerals to take into consideration and check for possible deficiencies, so you can have meal plans created by your dietitian that are right for you.supplements (1)

  1. B-complex vitamins: physiologically speaking, vitamins B2, B6, and folate are all associated with the amino acid metabolism and transamination.

Rich food sources of B vitamins: beans, dark green leafy vegetables, all meats, cruciferous vegetables, tempeh, yogurt, crimini mushrooms, sweet potato, bell peppers, beets, parsley, sea vegetables, banana, sunflower seeds.

  1. Chromium: it has been suggested that chromium not only increases insulin sensitivity but also protects against muscle atrophy by preventing muscle degradationB.

Rich food sources of chromium: brewer’s yeast, beef, wheat and barley, mussel, shrimp and oyster, Brazil nut, dried dates, pear, tomato, mushroom, broccoli.

  1. Vitamin D: it is also recommended to adjust deficiency of vitamin D, considering its crucial role in the skeletal muscle, as vitamin D deficiency may promote insulin resistanceC,D.

Rich food sources of vitamin D: salmon, sardines, cow’s milk, tuna, eggs, and shiitake mushrooms.

  1. Magnesium: as the fourth most abundant element in the body and involved in hundreds of enzymatic reactions, magnesium also play a role in protein synthesisA.

Rich food sources of magnesium: magnesium is part of chlorophyll, thus plants contain high amounts of it. Dark green leafy vegetables, seeds, and beans are great sources.

  1. Zinc: the relationship between this mineral and protein synthesis is similar to that of chromium. Zinc may participate on the insulin signaling and proliferation of muscle cellsE.

Rich food sources of zinc: red meat, spinach, asparagus, shiitake and crimini mushrooms, seeds, and beans.

  1. Iodine: makes thyroid hormones and these hormones promote protein synthesis. So, iodine is directly related to muscle building as well.

Rich food sources of iodine: sea vegetables, scallops, cod, yogurt, and shrimp.

There you have it. A balanced, nutritious, adequate and complete diet plan is crucial for your goal of muscle building. If possible, talk to your doctor and ask him or her to check your health by measuring your vitamin D, or checking your thyroid health, for example.

References

A) de Baaij JH, Hoenderop JG, Bindels RJ. Magnesium in man: implications for health and disease. Physiol Rev. 2015;95(1):1-46.

B) Dong F et al. Chromium supplement inhibits skeletal muscle atrophy in hindlimb-suspended mice. J Nutr Biochem. 2009;20(12):992-9.

C) Garcia LA et al. 1,25(OH)(2)vitamin D(3) enhances myogenic differentiation by modulating the expression of key angiogenic growth factors and angiogenic inhibitors in C(2)C(12) skeletal muscle cells. J Steroid Biochem Mol Biol. 2013;133:1-11.

D) Girgis CM et al. Effects of vitamin D in skeletal muscle: falls, strength, athletic performance and insulin sensitivity. Clin Endocrinol (Oxf). 2014;80(2):169-81.

E) Ohashi K et al. Zinc promotes proliferation and activation of myogenic cells via the PI3K/Akt and ERK signaling cascade. Exp Cell Res. 2015;333(2):228-37.

BIO – Check out my site at http://www.nutri.ly/

Livia Ly

 

 

 

The King of All Ergogenic Aids

 

by Sérgio Fontinhas. What’s the best ergogenic aid? Is it creatine? Caffeine? Vitamin D?

If you answered ‘water,’ then you’re clearly a Mensa member.women-water-12

The human body is approximately 60% to 70% water (with a range of 45-75%) (1). It can be is less with increasing body fat because fat is known as “anhydrous” with about 10% water, however fat-free mass can be 70-80% water (1). An average 70-kg person has approximately 42 L of total body water, with a range of 31–51 L (1). Improper hydration will result in either dehydration or overhydration (hyponatremia). Daily water balance depends on the net difference between water gain and water loss.

Individuals are routinely at a risk of mild dehydration day to day (2). Public surveys (10,11) and experimental trials (12,13) indicate that the general public, and most importantly special populations such as children and older adults, are at a risk of voluntary dehydration (14,15). Even experienced athletes can underestimate their hydration status and may drink insufficient amounts of water resulting in sustained dehydration (16).

Sustained dehydration is associated with poor health (3,4) and increases the likelihood of kidney stones and urinary tract infection by a significant degree (3,5). Additionally, prolonged vasoconstriction due to chronic dehydration increase the risk of hypertension and stroke (6).

An emergent body of evidence also suggests water consumption (and the food we eat) affect mental and physical performance (7). Water is essential to the maintenance of normal physical and cognitive function (8), and there are some recommended intake guidelines of 2000 ml of fluids for females and 2500 ml for males per day (9). More specifically it is recommended 3.7 L for 70 kg males and 2.7 L for 57 kg females (29).

Water is the medium of circulatory function, biochemical reactions, metabolism, substrate transport across cellular membranes, temperature regulation, and numerous other physiological processes (28). The loss or increase in fluids and electrolytes (potassium, sodium, calcium, magnesium…) affects cellular performance, and can cause cell death, and even death of the entire organism.

Assessing hydration status – Individuals should monitor their own hydration levels using markers such as urine color (27). Although dilution methods to determine total body water via plasma osmolality measurement are the most accurate, valid, and sensitive ways, they are not practical for most situations (30,122), but total body mass and urine color when used in conjunction is a good way to assess hydration status (30,122).

First-morning urine should look like pale yellow (27), indicating the normal and expected presence of some waste products from metabolism overnight. This color corresponds to a state of euhydration (34,35). I shouldn´t look at water, or anything dark.

Thirst is initially perceived when a body weight deficit of 1–2% exists (36,37), fluid consumption should be adequate to avert the perception of thirst. Thirst signals any imbalances of the osmolality of fluids and tissues (the electrolyte concentration), and the total amount of water in our body (volume).

Dehydration – Dehydration is characterized by weight loss, confusion, dry skin that is hot to the touch, and possibly an elevated core body temperature. In a hot climate, dehydration can be dangerous and result in thermal injury. Other causes of dehydration can be excess diarrhea, vomiting due to GI dysfunction, kidney disease, and diuretic medications.

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Thirst may be a poor measure of hydration because of the lag between the physiological dehydration and the thirst signal. Special populations require more attention, elderly are less sensitive to the thirst mechanism the deterioration of osmoreceptor sensitivity in older adults (30,38,39,40,121); and children are inexperienced in interpreting the thirst response (41,42). Older adults are also at higher risk for reduced kidney filtration function, which results in less efficient water conservation (when dehydrated), further exacerbating difficulties in recognizing a dehydrated state (43).

Physiology of dehydration / physiological response

When the body is in a state of dehydration, many substrates and neurotransmitters are influenced by circulating vasopressin (antidiuretic hormone) and angiotensin II (44,45).  Dehydration can increase levels of cortisol (46). Interestingly, even a decrease in cell volume caused by hypohydration promotes insulin resistance (47,48,49).

Conditions dehydrating insulin target tissues such as hyperosmolarity or amino acid deprivation are associated with insulin resistance; blockage of the cell volume response to insulin may be the common denominator in dehydration-induced insulin resistance (47).

As a consequence of dehydration, the blood–brain barrier permeability is altered by serotonergic and dopaminergic systems, potentially causing central nervous system dysfunction if dehydration is prolonged (50).  Chronic dehydration influence inhibitory and excitatory activities of the brain by increasing aminobutyric acid and glutamate levels (51), by stimulating γ-aminobutyric acid and N-methyl-D-aspartate receptors, to synthesize and release antidiuretic hormone (56).

Even mild dehydration produces significant changes at the neural level: total brain volume shrinkage and over-recruitment of specific brain areas during cognitively demanding tasks (52).

Hypohydration and exercise

Hypohydration during exercise strongly rises the catabolic hormonal response to resistance exercise, and increase circulating concentrations of metabolic substrates. Hydration status during exercise changes the endocrine and metabolic adaptive responses to resistance exercise and also changes the postexercise internal environment. Specifically, there’s increase in cortisol, epinephrine, and norepinephrine (46).

Hypohydration stimulates the catabolic hormones by increasing core temperature (69,70) and increases cardiovascular demand due to decreased plasma volume (71,72,73). A 3% to 4% loss of body weight (water) reduces strength by about 2% and power by about 3% (35).

As noted before, a decrease in cell volume caused by hypohydration promotes insulin resistance (47,48,49). Resistance exercise might exacerbate the effects of hypohydration on insulin resistance, because muscle damage is also related with insulin resistance (74,75,76,77). There’s decreased GLUT-4 protein content (78,79), and impaired insulin signal transduction at the level of IRS-1, PI 3-kinase, and Akt-kinase (75). Downhill treadmill running and resistance exercise result in transient insulin resistance (80,81,82), and the reductions in glucose uptake in muscle damage models may be of the order of 20–30% (78,80).Muscle damage and insulin resistance

 

 

 

 

 

 

 

 

(74).

Hyponatremia – Extreme exercise conditions (equal or above three hours continuously), such as the marathon or triathlon, without the intake of electrolytes increase the risk dehydration or hyponatremia (83). Symptomatic hyponatremia is typically observed with greater than 6 hours of prolonged exercise. Acute water toxicity happens due to rapid consumption of large quantities of water that greatly exceeded the kidney’s maximal excretion rate (from 0.7 to 1.0 L/hour) (1).

Severe exercise-associated hyponatremia (EAH) starts as significant mental status changes resulting from cerebral edema, at times associated with noncardiogenic pulmonary edema (84,85). The osmotic imbalance results in fluid movement into the brain, causes swelling, which then leads to disorientation, confusion, general weakness, grand mal seizures, coma, and possibly death (35,124,125,126).

Exercise-associated hyponatremia (EAH) typically occurs during or up to 24 hours after prolonged physical activity, and is defined by a serum or plasma sodium concentration below the normal reference range of 135 mEq/L (86,87).

Usually only less than 1% of marathons athletes present signs of EAH (88,89), however it was as high as 23% in an Ironman Triathlon (90) and 38% in runners participating in a marathon and ultramarathon in Asia (91). There’s also now a trend for symptomatic EAH for shorter distance events, such as a half marathon (92) and sprint triathlon taking approximately 90 minutes to complete (93). There’s also no statistical significance for the incidence of symptomatic between genders (55), though women may be at greater risk than men (55).

We have seen that the major risk factor for developing EAH is excessive water intake beyond the capacity for renal water excretion (1,100,101) largely as a result of persistent secretion of arginine vasopressin (102,103). Elevations in brain natriuretic peptide (NT-BNP) may lead to excessive losses of urine sodium and raise the risk of hyponatremia (104).

Another concern is the inability to mobilize body sodium bound in bone. Sodium can be released from internal stores such as bone (105,106,107), 25% of body sodium is bound in bone (osmotically inactive) and is potentially recruitable. Inability to recruit sodium from that pool may increase the risk of hyponatremia.

Individuals under normal conditions are able to excrete between 500 and 1000 mL/h of water (108), plus the non-renal losses of water as sweat, so athletes should be able to consume as much as 1000 to 1500 ml/h before developing water retention and dilutional hyponatremia, therefore it seems likely that excessive water intake (>1500 mL/h) is the main cause.

The combination of excessive water intake and inappropriate AVP secretion will clearly lead to hyponatremia.exercise associated hyponatremia pathogenesis

 

 

 

 

(86)

Arginine vasopressin (AVP) must be suppressed appropriately with water loading, otherwise the ability to produce dilute urine is markedly impaired (109).

Water can also be absorbed from the gastrointestinal tract at the end of a race causing an acute drop in serum sodium concentration (110), with clinical signs of EAHE after 30 minutes. During exercise, breakdown of glycogen into lactate increases cellular osmolality and rises serum sodium, but some minutes after exercise this is reversed and serum sodium levels drop (111,112).

The risk also rises if the degree of fluid loss through sweat is sufficient to produce significant volume depletion (stimulating AVP release and impairing urine excretion of water), coupled with ingestion of hypotonic fluids (86).

Although not conclusive, nonsteroidal anti-inflammatory drugs (NSAIDs) have been implicated as a risk factor in the development of EAH by potentiating the water retention effects of AVP at the kidney (86).

At least two strategies can be used to present EAH: avoid overdrinking (real time sensation of thirst) and limiting the availability of fluids during events. Supplementation with sodium may delay of even prevent the decline in blood sodium concentration (113,114) however drinking beyond thirst (overdrinking) will not prevent hyponatremia (115), the amount of fluid ingested is more important than the amount of sodium ingested for blood sodium concentrations (116).

EAH has a complex pathogenesis and multifactorial etiology:exercise associated hyponatremia field management (1)

 

 (86)

 

 

 

 

An athlete should consume approximately 500 to 600 mL (17 to 20 fl oz) of water 2 to 3 hours before exercise (117). By hydrating several hours prior to the exercise, there is sufficient time for urine output to return toward normal before starting the event (30).

For normal athletic events in moderate temperatures (and altitudes), it should be enough to hydrate slowly over several hours. If the body needs water urgently it can absorb some water right through the walls of the stomach. A 1% to 2% decrease in your body weight (due to water loss) will affect performance.

The threshold for reduced performance appears to be 2% body water loss of total body mass (118,119). Dehydration equivalent to 1.5% to 2% of total body mass may decrease performance up to 15% (120). We’ve seen before that 3% to 4% losses impairs muscular strength by 2% and muscular power by 3% (35), and also reduces high-intensity endurance performance (e.g., distance running) by approximately 10% (123).

Energy drinks

Energy drinks typically contain water, carbohydrates, vitamins, minerals, with the aim of increasing energy, alertness, metabolism, and/or performance (e.g., caffeine, taurine, amino acids, glucoronolactone…) (127).

Caffeine is the most common ingredient, and is absorbed in 30 – 60 minutes (128). Caffeine original_238495_hro087gobfL4M69kTZcwERglvstimulates the cardiovascular system and increases epinephrine output (129,130); enhance vigilance during bouts of exhaustive exercise, and periods of sustained sleep deprivation. Energy drinks with approximately 2 mg·kgBM-1caffeine consumed 10 to 60 minutes prior to anaerobic/resistance exercise may improve upper- and lower- body total lifting volume, and improve cycling and running performance (127).

Carbohydrate feeding during exercise can improve endurance capacity and performance (131,132), through maintenance of blood glucose levels, high levels of carbohydrate oxidation (1 g of carbohydrate per minute), while sparing liver and skeletal muscle glycogen (133).

Energy drinks also have a small amount of vitamins (e.g., Vitamin B6, Vitamin B12, pantothenic acid, Vitamin C) and electrolytes (e.g., sodium, potassium, phosphorus, etc.).

Energy drinks can improve mood, reaction time, and/or markers of alertness, most likely due to the ergogenic value of caffeine and/or carbohydrate.

Caffeine can elevate metabolic rate and the rate of lipolysis. 200-500 mg of caffeine (typical of thermogenic supplements) can increase acute energy expenditure (1-24 hours) (127), chronic energy expenditure (28 days) (134), and elevate plasma free-fatty acid, glycerol levels and catecholamine secretion (127, 134). The caffeine in energy drinks ranges from 80-200 mg, and it’s not conclusive whether daily use of ED would affect long-term energy balance and body composition (127).

Individuals with metabolic syndrome and or diabetes mellitus should avoid consumption of high glycemic drinks and/or foods. More importantly, individuals with known cardiovascular disease should avoid any use of energy drinks due to the cardio stimulant effects (124).

More references here than there are chopsticks in a Chinese restaurant

1. Institute of medicine. Water. In: Dietary Reference Intakes for Water, Sodium, Chloride, Potassium and Sulfate, Washington, D.C: National Academy Press, pp. 73–185, 2005.

 

2. Greenleaf JE & Sargent F (1965). Voluntary dehydration in man. J Appl Physiol 20, 719–724

 

3. Popkin B, D’Anci K & Rosenberg I (2010). Water, hydration and health. Nutr Rev 68, 439–458.

 

4. Wilson MM & Morley JE (2003) Impaired cognitive function and mental performance in mild dehydration. Eur J Clin Nutr 57, S24–S29.

 

5. Jequier E & Constant F (2010). Water as an essential nutrient: the physiological basis of hydration. Eur J Clin Nutr 64, 115–123.

 

6. Thornton SN (2010). Thirst and hydration: physiology and consequences of dysfunction. Physiol Behav 100, 15–21.

 

7. Gomez-Pinilla F (2008). Brain foods: the effects of nutrients on brain function. Nat Rev Neurosci 9, 568–578.

 

8. EFSA (2011) Scientific opinion on the substantiation of health claims related to water and maintenance of normal physical and cognitive functions (ID 1102, 1294, 1331), maintenance of normal thermoregulation (ID 1208) and “basic requirement of all living things” (ID 1207) pursuant to Article 13(1) of Regulation

(EC) No. 1924/2006. EFSA J 9, 2075.

 

9. EFSA (2010). Scientific opinion on dietary reference values for water: EFSA panel on dietetic products, nutrition, and allergies (NDA). EFSA J 8, 1459.

 

10. Gandy J (2012). First findings of the United Kingdom fluid intake study. Nutr Today 47, S14–S16.

 

11. Gibson S, Gunn P & Maughan RJ (2012). Hydration, water intake and beverage consumption habits among adults. Nutr Bull 37, 182–192.

 

12. Bar-David Y, Urkin J, Bar-David Z, et al. (2009). Voluntary dehydration among elementary school children residing in a hot arid environment. J Hum Nutr Diet 22, 455–460.

 

13. Fadda R, Rapinett G, Grathwohl D, et al. (2012). Effects of drinking supplementary water at school on cognitive performance in children. Appetite 59, 730–737.

 

14. Greenleaf JE (1992). Problem: thirst, drinking behavior, and involuntary dehydration. Med Sci Sports Exerc 24, 645–656.

 

15. Greenleaf JE & Sargent F (1965). Voluntary dehydration in man. J Appl Physiol 20, 719–724.

 

16. Passe D, Horn M, Stofan J, et al. (2007). Voluntary dehydration in runners despite favorable conditions for fluid intake. Int J Sport Nutr Exerc Metab 17, 284–295.

 

27. Lawrence E. Armstrong (2005). Hydration assessment techniques. NutrRev 63, S40–S54.

 

28. Lawrence E. Armstrong. Assessing Hydration Status: The Elusive Gold Standard. J Am Coll Nutr. 2007 Oct;26(5 Suppl):575S-584S.

 

29. Institute of Medicine and Food and Nutrition Board. In: “Dietary Reference Intakes for Water, Potassium, Sodium, Chloride and Sulfate.” Washington, DC: National Academies Press. pp 73–185, 2004.

 

30. Sawka MN, Burke LM, Eichner ER, Maughan RJ, Montain SJ, Stachenfeld NS. American College of Sports Medicine position stand. Exercise and fluid replacement. American College of Sports Medicine. Med Sci Sports Exerc. 2007 Feb;39(2):377-90.

 

34. Armstrong LE, Soto JA, Hacker FT Jr, Casa DJ, Kavouras SA, Maresh CM: Urinary indices during dehydration, exercise, and rehydration. Int J. Sport Nutr 8:345–355, 1998.

 

35. Armstrong LE, Maresh CM, Castellani JW, Bergeron MF, Kenefick RW, LaGasse KE, Riebe D: Urinary Indices of Hydration Status. Int J Sport Nutr 4:265–279, 1994.

 

36. Greenleaf JE, Morimoto T: Mechanisms controlling fluid ingestion: thirst and drinking. In Buskirk ER, Puhl SM (eds): “Body Fluid Balance: Exercise and Sport.” Boca Raton, FL: CRC Press,1996.

 

37. Hubbard RW, Szlyk PC, Armstrong LE: Influence of thirst and fluid palatability on fluid ingestion during exercise. In Gisolfi CV, Lamb DR (eds): “Perspectives in Exercise Sciences and Sports Medicine. Fluid Homeostasis During Exercise.” Indianapolis: Benchmark Press Inc, 1990.

 

38. Begum MN & Johnson CS (2010) A review of the literature on dehydration in institutionalized elderly. e-Spen Eur e-J Clin Nutr Metab 5, e47–e53.

 

39. Mentes J (2006). Oral hydration in older adults: greater awareness is needed in preventing, recognizing, and treating dehydration. Am J Nurs 106, 40–49.

 

40. Rolls BJ & Phillips PA (2009). Aging and disturbances of thirst and fluid balance. Nutr Rev 48, 137–144.

 

41. D’Anci K, Constant F & Rosenberg I (2006). Hydration and cognitive function in children. Nutr Rev 64, 457–464.

 

42. Kenney WL & Chiu P (2001). Influence of age on thirst and fluid intake. Med Sci Sports Exerc 33, 1524–1532

 

43. Mentes J (2006). Oral hydration in older adults: greater awareness is needed in preventing, recognizing, and treating dehydration. Am J Nurs 106, 40–49.

 

44. Wilson MM & Morley JE (2003) Impaired cognitive function and mental performance in mild dehydration. Eur J Clin Nutr 57, S24–S29.

 

45. Bourque CW (2008) Central mechanisms of osmosensation and systemic osmoregulation. Nat Rev Neurosci 9, 519–531.

 

46. Daniel A. Judelson , Carl M. Maresh , Linda M. Yamamoto , Mark J. Farrell , Lawrence E. Armstrong , William J. Kraemer , Jeff S. Volek , Barry A. Spiering , Douglas J. Casa , Jeffrey M. Anderson. Effect of hydration state on resistance exercise-induced endocrine markers of anabolism, catabolism, and metabolism. Journal of Applied Physiology Published 1 September 2008Vol. 105no. 3, 816-824

 

47. Schliess F, Ha¨ussinger D. Cell hydration and insulin signaling. Cell Physiol Biochem 10: 403–408, 2000.

 

48. Schliess F, Ha¨ussinger D. Cell volume and insulin signaling. Int Rev Cytol 225: 187–228, 2003.

 

49. Schliess F, von Dahl S, Ha¨ussinger D. Insulin resistance induced by loop diuretics and hyperosmolarity in perfused rat liver. Biol Chem 382:1063–1069, 2001.

 

50. Maughan R, Shirreffs S & Watson P (2007) Exercise, heat, hydration and the brain. J Am Coll Nutr 26, 604S–612S.

 

51. Di S & Tasker J (2004) Dehydration-induced synaptic plasticity in magnocellular neurons of the hypothalamus supraoptic nucleus. Endocrinology 145, 5141–5149.

 

52. Kempton MJ, Ettinger U, Foster R, et al. (2011) Dehydration affects brain structure and function in healthy adolescents.Hum Brain Mapp 32, 71–79.

 

55. Almond, Christopher; Shin, Andrew (2005). Hyponatremia among runners in the Boston Marathon. N Engl J Med 352 (15): 1550

 

56. Babar, S. (October 2013). “SIADH Associated With Ciprofloxacin.”. The Annals of Pharmacotherapy 47 (10): 1359–1363.

 

69. Mitchell JB, Dugas JP, McFarlin BK, Nelson MJ. Effect of exercise, heat stress, and hydration on immune cell number and function. Med Sci Sports Exerc 34: 1941–1950, 2002.

 

70. Powers SK, Howley ET, Cox R. A differential catecholamine response during prolonged exercise and passive heating. Med Sci Sports Exerc 14: 435–439, 1982.

 

71. Roy BD, Green HJ, Burnett M. Prolonged exercise following diuretic induced hypohydration effects on fluid and electrolyte hormones. Horm Metab Res 33: 540–547, 2001.

 

72. Roy BD, Green HJ, Burnett ME. Prolonged exercise following diuretic induced hypohydration: effects on cardiovascular and thermal strain. Can J Physiol Pharmacol 78: 541–547, 2000.

 

74. Tee JC, Bosch AN, Lambert MI. Metabolic consequences of exercise induced muscle damage. Sports Med 37: 827–836, 2007.

 

75. Del Aguila LF, Krishnan RK, Ulbrecht JS, Farrell PA, Correll PH, Lang CH, Zierath JR, Kirwan JP. Muscle damage impairs insulin stimulation of IRS-1, PI 3-kinase, and Akt-kinase in human skeletal muscle. Am J Physiol Endocrinol Metab 279: E206–E212, 2000

 

76. Kirwan JP, Del Aguila LF. Insulin signalling, exercise and cellular integrity. Biochem Soc Trans 31: 1281–1285, 2003.

 

77. Kirwan JP, Hickner RC, Yarasheski KE, Kohrt WM, Wiethop BV, Holloszy JO. Eccentric exercise induces transient insulin resistance in healthy individuals. J Appl Physiol 72: 2197–2202, 1992.

 

78. Asp S, Daugaard JR, Kristiansen S, Kiens B, and Richter EA. Eccentric exercise decreases maximal insulin action in humans:muscle and systemic effects. J Physiol (Lond) 494: 891–898, 1996.

 

79. Asp S, Kristiansen S, and Richter EA. Eccentric muscle damage transiently decreases rat skeletal muscle GLUT-4 protein. J Appl Physiol 79: 1338–1345, 1995.

 

80. Kirwan JP, Hickner RC, Yarasheski KE, Kohrt WM, Wiethop BV, and Holloszy JO. Eccentric exercise induces transient insulin resistance

 

81. Kirwan JP, Bourey RE, Kohrt WM, Staten MA, and Holloszy JO. Effects of treadmill exercise to exhaustion on the insulin response to hyperglycemia in untrained men. J Appl Physiol 70: 246–250, 1991.

 

82. Krishnan RK, Hernandez JM, Williamson DL, O’Gorman DJ, Evans WJ, and Kirwan JP. Age-related differences in the pancreatic b-cell response to hyperglycemia after eccentric exercise. Am J Physiol Endocrinol Metab 275: E463–E470, 1998.

 

83. J,Estevez E,Baquero E,Mora-Rodriguez R (2008). “Anaerobic performance when rehydrating with water or commercially available sports drinks during prolonged exercise in the heat”. Applied Physiology, Nutrition and Metabolism 33 (2): 290–298.

 

84. Rosner MH. Exercise-associated hyponatremia. Semin Nephrol . 2009;29:271–281.

 

85. Rosner MH, Bennett B, Hew-Butler T, Hoffman MD. Exercise induced hyponatremia. In: Simon EE, ed. Hyponatremia: Evaluation and Treatment . New York, NY: Springer; 2013

 

86.  Bennett, BL; Hew-Butler, T; Hoffman, MD; Rogers, IR; Rosner, MH (Sep 2013). “Wilderness Medical Society practice guidelines for treatment of exercise-associated hyponatremia.”. Wilderness & environmental medicine 24 (3): 228–40.

 

87. Hew-Butler T, Ayus JC, Kipps C, et al. Statement of the Second International Exercise-Associated Hyponatremia Consensus Development Conference, New Zealand, 2007. Clin J Sport Med. 2008;18:111–121.

 

88. Hew TD, Chorley JN, Cianca JC, Divine JG. The incidence, risk factors, and clinical manifestations of hyponatremia in marathon runners. Clin J Sport Med . 2003;13:41–47.

 

89. Davis DP, Videen JS, Marino A, et al. Exercise-associated hyponatremia in marathon runners: a two-year experience.J Emerg Med. 2001;21:47–57.

 

90. Speedy DB, Noakes TD, Rogers IR, et al. Hyponatremia in ultra-distance triathletes. Med Sci Sports Exerc. 1999;31:809–815.

 

91. Lee JK, Nio AQ, Ang WH, et al. First reported cases of exercise-associated hyponatremia in Asia. Int J Sports Med . 2011;32:297–302.

 

92. Glace B, Murphy C. Severe hyponatremia develops in a runner following a half-marathon. JAAPA . 2008;21:27–29

 

93. Shapiro SA, Ejaz AA, Osborne MD, Taylor WC. Moderate exercise-induced hyponatremia.Clin J Sport Med . 2006;16:72–73

 

100. Speedy DB, Noakes TD, Boswell T, Thompson JM, Rehrer N, Boswell DR. Response to a fluid load in athletes with a history of exercise induced hyponatremia. Med Sci Sports Exerc. 2001;33:1434 –1442.

 

101. Noakes TD, Wilson G, Gray DA, Lambert MI, Dennis SC. Peak rates of diuresis in healthy humans during oral fluid overload. S Afr Med J. 2001;91:852– 857.

 

102. Rosner MH, Kirven J. Exercise-associated hyponatremia. Clin J Am Soc Nephrol. 2007;2:151–161.

 

103. Rosner MH. Exercise-associated hyponatremia. Semin Nephrol. 2009;29:271–281.

 

104. Hew-Butler T, Jordaan E, Stuempfle KJ, et al. Osmotic and nonosmotic regulation of arginine vasopressin during prolonged endurance exercise. J Clin Endocrinol Metab. 2008;93:2072–2078.

 

105. Noakes TD, Sharwood K, Speedy D, et al. Three independent biological mechanisms cause exercise-associated hyponatremia: evidence from 2,135 weighed competitive athletic performances. Proc Natl Acad Sci U S A. 2005; 102:18550 –18555.

 

106. Edelman IS, James AH, Brooks L, Moore FD. Body sodium and potassium. IV. The normal total exchangeable sodium; its measurement and magnitude. Metabolism. 1954;3:530 –538.

 

107. Edelman IS, James AH, Baden H, Moore FD. Electrolyte composition of bone and the penetration of radio sodium and deuterium oxide into dog and human bone. J Clin Invest. 1954;33:122–131.

 

108. Rose BD, Post TW. Clinical Physiology of Acid-Base and Electrolyte Disorders. 5th ed. New York, NY: McGraw Hill; 2001.

 

109. Siegel AJ, Verbalis JG, Clement S, et al. Hyponatremia in marathon runners due to inappropriate arginine vasopressin secretion. Am J Med. 2007;120:461.e11-e17.

 

110. Ayus JC, Varon J, Arieff AI. Hyponatremia, cerebral edema, and noncardiogenic pulmonary edema in marathon runners. Ann Intern Med. 2000;132:711–714.

 

111. Halperin ML, Kamel KS, Sterns R. Hyponatremia in marathon runners. N Engl J Med. 2005;353:427– 428.

 

112. Lindinger MI, Heigenhauser GJ, McKelvie RS, Jones NL. Blood ion regulation during repeated maximal exercise and recovery in humans. Am J Physiol. 1992;262(1 Pt 2):R126–R136.

 

113. Barr SI, Costill DL, Fink WJ. Fluid replacement during prolonged exercise: effects of water, saline, or no fluid. Med Sci Sports Exerc. 1991;23:811– 817.

 

114. Vrijens DM, Rehrer NJ. Sodium-free fluid ingestion decreases plasma sodium during exercise in the heat. J Appl Physiol. 1999;86:1847–1851.

 

115. Hew-Butler TD, Sharwood K, Collins M, Speedy D, Noakes T. Sodium supplementation is not required to maintain serum sodium concentrations during an Ironman triathlon. Br J Sports Med. 2006;40:255–259.

 

116. Weschler LB. Exercise-associated hyponatraemia: a mathematical review. Sports Med. 2005;35:899 –922

 

117. Casa, Douglas J., Armstrong, Lawrence E., Hillman, Susan K., Montain, Scott J. (2000). National Athletic Trainers’ Association Position Statement: Fluid replacement for athletes. Journal of Athletic Training, 35(2), 212-224.

 

118. Baker LB, Dougherty KA, Chow M, et al. Progressive dehydration causes a progressive decline in basketball skill performance. Med Sci Sports Exerc. 2007;39:1114–1123.

 

119. Hoffman JR, Stavsky H, Falk B. The effect of water restriction on anaerobic power and vertical jumping height in basketball players. Int J Sports Med. 1995;16:214–218.

 

120. Edwards AM, Mann ME, Marfell-Jones MJ, et al. Influence of moderate dehydration on soccer performance: physiological responses to 45 min of outdoor match-play and the immediate subsequent performance of sport-specific and mental concentration tests. Br J Sports Med. 2007;41:385–391.

 

121. Binkley HM, Beckett J, Casa DJ, et al. National Athletic Trainers’ Association position statement: exertional heat illnesses. J Athl Train. 2002;37:329–343.

 

122. Sawka M, Burke LM, Eicher ER, et al. Exercise and fluid replacement. Med Sci Sports Exerc. 39:377–390.

 

123. Judelson DA, Maresh CM, Anderson JM, et al. Hydration and muscular performance. Does fluid balance affect strength, power and high-intensity endurance? Sports Med. (New Zealand). 2007;37:907–921.

 

124. Convertino V, Armstrong LE, Coyle EF, et al. ACSM position stand: exercise and fluid replacement. Med Sci Sports Exerc. 1996;28:i–ix.

 

125. Coyle EF. Fluid and fuel intake during exercise. J Sports Sci. 2004;22:39–55.

 

126. Maughn R, Burke LM, Coyle EF, eds. Food, Nutrition and Sports Performance II. The International Olympic Committee Consensus on Sports Nutrition. London: Routledge, 2004.

 

127. Bill Campbell, Colin Wilborn, Paul La Bounty, Lem Taylor, Mike T Nelson, Mike Greenwood, Tim N Ziegenfuss, Hector L Lopez, Jay R Hoffman, Jeffrey R Stout, Stephen Schmitz, Rick Collins, Doug S Kalman, Jose Antonio and Richard B Kreider. International Society of Sports Nutrition position stand: energy drinks. Journal of the International Society of Sports Nutrition 2013, 10:1

 

128. Goldstein ER, Ziegenfuss T, Kalman D, Kreider R, Campbell B, Wilborn C, Taylor L, Willoughby D, Stout J, Graves BS, et al: International society of sports nutrition position stand: caffeine and performance. J Int Soc Sports Nutr 2010, 7:5.

 

129. Graham TE, Hibbert E, Sathasivam P: Metabolic and exercise endurance effects of coffee and caffeine ingestion. J Appl Physiol 1998, 85:883–889.

 

130. McLellan TM, Bell DG: The impact of prior coffee consumption on the subsequent ergogenic effect of anhydrous caffeine. Int J Sport Nutr Exerc Metab 2004, 14:698–708.

 

131. Jeukendrup A, Brouns F, Wagenmakers AJ, Saris WH: Carbohydrate-electrolyte feedings improve 1 h time trial cycling performance. Int J Sports Med 1997, 18:125–129.

 

132. Jeukendrup AE: Carbohydrate intake during exercise and performance. Nutrition 2004, 20:669–677.

 

133. Coyle EF, Coggan AR, Hemmert MK, Ivy JL: Muscle glycogen utilization during prolonged strenuous exercise when fed carbohydrate. J Appl Physiol 1986, 61:165–172.

 

134. Roberts MD, Dalbo VJ, Hassell SE, Stout JR, Kerksick CM: Efficacy and safety of a popular thermogenic drink after 28 days of ingestion. J Int Soc Sports Nutr 2008, 5:19.

 

 

 

 

 

Hierarchy of Evidence is Wrong

 

By Jose Antonio PhD FNSCA FISSN.

A pithy summary

  • The typical ‘Hierarchy of Evidence’ is wrong.
  • The gold standard in science will always be the randomized controlled trial or RCT (i.e. the original investigation).
  • If you truly want to change a field, you have to conduct the RCT.
  • Reviews and meta-analyses exist only because scientists have conducted prior RCTs.
  • Reviews and meta-analyses do not provide new (i.e. original data) information.
  • If you’re lazy, read reviews and meta-analyses.
  • If you’re ambitious, make sure you read RCTs.
  • If you profess to be a scientist, then there better be RCTs in your CV.
  • If you’re a Monday morning quarterback, I can’t help you there.
  • If your mommy didn’t hug you enough as a young lad, so sad.

Medical Heirarchy of EvidenceI’ve seen this pic about as often as I’ve seen fitness models posing with their butts sticking out. Funny how social media works. One person puts up this pic and before you know, you’ve got your loyal band of merry followers parroting the same ole same ole. The speed in which these pics are posted is inversely proportional to amount of thought given to the veracity of the pic. This evidence hierarchy pyramid is at best misleading and at its worst, just downright wrong. Bear with me, I’ll explain why. First some background. Variations of this pyramid exist with Cochrane Reviews sometimes at the top (i.e., it’s still a Review no matter what adjective you place in front of it). Either way, what is typically grouped at the top of the evidence pyramid are Reviews and Meta-Analyses. Ostensibly that represents the crème de la crème of science. Below that we find Randomized Controlled Trials or RCTs, Cohort/Case Control studies, Case Studies/Reports, Animal Studies, In Vitro data etc.

In the category of Sports Science, this pyramid makes no sense. Why? Because the way to make changes in a field isn’t by writing umpteen review articles and/or meta-analyses. How do you make changes in a field?

If you answered, “you have to generate original data” then go to the head of the class. Original data.  That’s right. You have to do the RCT. Or do a cohort/case control study. Though if you’re studying human performance, a cohort study is about as useful as chopsticks in a hot dog eating contest. Even though case studies get the shaft much of time, these too are important. Particularly if case studies involve what you’ve done with hundreds of athletes. Strength coaches who have worked at the collegiate or professional level with perhaps thousands of athletes must be doing something right. Nonetheless, the gold standard is the RCT.

Review papers and meta-analyses are nice and all; I’ve even written a bunch. Heck, I recommend to my students that to get an initial bird’s eye view of a topic, reading review papers and meta-analyses is a great way to start. But the key word is ‘start.’ If all you relied on were reviews, that would be like watching the finish line of the Boston Marathon. You’d have no clue as to what transpired during the first mile, mile 13, or Heartbreak Hill (mile 21). You’d have no clue as to how these runners trained for the marathon. All you’d know is how they finished. That’s a typical review. You get the finish line.

Meta-analyses are even more problematic. You’re basically ‘combining’ studies that may be as disparate as hot dogs and cotton candy. The hope is that you can narrow down a bunch of RCTs into a single number and conclusion. That would be like describing the United States by doing a meta-analysis of the 50 states. It would go something like this:

The USA is 78% white, 13% black and 17% Hispanic with a small minority of Asians, Pacific Islanders etc. The median income is $53,000, the percentage of college grads about 29% and number of those living below poverty about 15%. Get my drift? I won’t list every possible way to usa_map_onlydescribe the USA but let’s just say you can’t ‘meta-analyze it’ in a fashion that makes any sense. Clearly, there are MANY ways to ‘explain’ the USA. There are statistics galore you can use to describe the USA to someone who has never been there. But in the end, it’s a bit like grabbing water. Does anyone actually think living in Oklahoma is anything like Northern California? Is Texas anything like Massachusetts? Is the Sunshine State anything like Iowa? Not only is the racial make-up entirely different between these states, but geography, political leanings, and average income differ. Heck, you could probably divide the USA into 6 different countries. In the state of Florida alone, the Miami area is virtually a different country compared to north Florida. It makes you wonder if you’re in the same state. But I do love South Florida. :-)

So next time you think a meta-analysis is the best arbiter of science, try describing the United States using a meta-analysis. Good luck. (Note: I am a co-author on a caffeine meta-analysis as well as several review papers; so I’m not ‘bashing’ these types of publications for the sake it. I’m trying to get you to think beyond the obvious).Hierarchy wrong jpeg

Getting back to RCTs. If you want to truly change a field, you need to do the RCT. RCTs are the bread and butter of science. Without RCTs, there are no reviews or meta-analyses. The field of sports science in particular needs more RCTs. Reviews and meta-analyses exist at the behest of RCTs. So why on Earth would anyone think RCTs are less important than reviews/meta-analyses?

Androgens – Roid Rage Nonsense

Back in the 1970s and 80s, the American College of Sports Medicine (ACSM) published their Position Stands on Anabolic-Androgenic Steroids. [1] Their original Position in 1977 basically stated that anabolic steroids don’t work and are dangerous. Their revised position in 1987 Bhasinstated they might work but are still dangerous. The funny part about the 1987 revision was they changed their conclusions based on no new data. Yes you read that correctly. Nothing changed in terms of original data. That left my head scratching. Moving on. When I examined the literature way back when (and I read EVERY original paper on this subject), I had a sneaking suspicion that the ACSM was flat-out wrong on both counts. In 1996, I co-authored a review paper stating that “the use of moderate doses of androgens results in side effects that are largely benign and reversible. It is our contention that the incidence of serious health problems associated with the use of androgens by athletes has been overstated.”[2] My review was nice and all, but it really won’t change anyone’s mind. It won’t change a field. So what did change the prevailing view of androgens? If you answered an RCT, you get an “A.

Dr. Bhasin published the classic paper on androgens in the New England Journal of Medicine.[3] His research team found that “supraphysiologic doses of testosterone, especially when combined with strength training, increase fat-free mass and muscle size and strength in normal men.” So anabolic steroids work and the side effects were…oh wait…they didn’t find any. And they found no changes in mood or behavior. Yep. The myth of ‘roid rage busted. This RCT was the tipping point in the study of androgens.

Creatine – The Tipping Point

Dr. Roger Harris published the seminal paper on creatine.[4] That original investigation and the subsequent economic boom that resulted from the sales of creatine Essentials of Creatine cover 165 x 220 pixels (2)monohydrate has done more to change the sports nutrition industry (business and science) than any single supplement. Creatine gave respect to the supplement industry that otherwise was known more for selling protein powder that tasted like dirty socks soaked in sour milk. The study of creatine has generated 100s of RCTs and has probably been the topic of study for many a Masters and PhD student.

Caffeine – thank Dr. David Costill for this one

The 1978 study published in MSSE gave Dr. Costill more notoriety caffeinated_cities_smallthan his entire body of work (which was a LOT!). He showed that caffeinated coffee improved cycling performance compared to the placebo. Coffee and caffeine lovers rejoiced. Again, it was an RCT that changed the field of caffeine/exercise. There are literally hundreds of studies on caffeine and exercise. You can thank Dr. Costill for that.

The Big Picture

Having written many reviews, they do have their value. Often times reviews, and in particular the ISSN Position Stands, can give you a snapshot of the current science as we know it. Most of us don’t have time to sift through the umpteen studies on a particular subject. Hence, reviews (and meta-analyses) have an important role. Like I said before; it’s a good place to start. In fact, a great review or meta-analysis might generate the questions that will spur scientist(s) into conducting the appropriate RCT. Perhaps the RCT/Cohort/Case Study and the Review/Meta-Analysis categories are like two wheels of a bicycle. Both wheels are important. However, you can’t have the latter without the former.

Thus, don’t delude yourself into thinking that reviews/meta-analyses represent the most important pieces of evidence. They are not. They exist only because hundreds of scientists have done the hard work of performing RCTs. Heck, anyone can write a review. Just sit in your underwear, PubMed search whatever topic you like, and write. Believe me. I done my fair share of underwear-sitting and writing. I kinda like it actually. :-)Shoulders of giants

Performing an original investigation is the bread and butter of science. Original data gives a field credibility. Imagine if you were to magically delete EVERY study ever done in the world of sports nutrition and strength and conditioning. What would you have left? A bunch of angry trolls fighting online. “One set is better than three sets.” “No 10 sets is better than 3 sets.” “Squeezing my butt is best for the glutes.” “No way Jose. Squats are the best butt exercise.” “Low carb is best.” “No high carb is best.” The endless drivel would be enough to shut down Facebook. And the list goes on and on. How should these disputes be resolved. If you answered ‘science’ than go to the head of the class. Science, particularly original investigations (i.e., RCTs), are the only way to objectively resolve disputes. So unless you’ve actually conducted a study, you’ll honestly have no idea what it’s like. Doing research is a brutal teacher.

I love it when an original investigation is posted on social media. The keyboard warriors, Monday-morning-quarterbacks and University of Google “PhDs” come out in full force with their critiques of the study. “Why is the sample size so small?” “Why’d you use male subjects only and not female?” “This study is invalid because it is sponsored by a private company.” Folks who critique scientific studies (i.e., those whose experience with science is reading Discover operation_gamemagazine and playing “Operation”) are often criticized for their lack of scientific expertise. Hence, they often resort to the intellectually lazy argument of “that’s an ad hominem attack.” Judge the message, not the messenger. Sure in the world of frickin’ Utopia, we have endless hours in the day to vet everything said by everyone. But alas, I don’t live in that world. In the interest of being pragmatic (and so as to not infringe on my beach time), judgements have to be made on the messenger. And guess what. I’ll take the advice of my internal medicine doctor over some dipshit who memorizes the WebMD website. Oops. Is that an ad hominem attack? Ask me if I care. Yes it does matter WHO gives advice. Just because you have fingers, a laptop and can type search words in Google, Wikipedia or any other third party site does not make you an expert. (For an interesting piece on ‘expertise,’ read this: http://thefederalist.com/2014/01/17/the-death-of-expertise/ ).

att-stadium-071715-usnews-getty-ftr_152ey43t9604v147i8ltrani6lTrying to explain the intricacies of conducting a study would be like dry-land swimming. Sure. I can explain the stroke. I can show you videos of swimming. I’ll even let you look at the water. But unless you jump in the water, you really will have zero idea as to the process of swimming (i.e., research). Unfortunately the ratio of scientist to Monday-morning-quarterback ain’t good. It’s something like for every one genuine scientist, there are probably enough Monday-morning-QBs to fill AT & T Stadium in Dallas Texas.

Summary

I’ve published in the categories of RCTs, Reviews, Meta-Analyses, Case Studies and Animal Research. They are all important though in different ways. Keyboard warriors and Monday morning quarterbacks notwithstanding, if you want to really change a field and I mean really change it, you have to do original research. You can blog until your blue in the face and it won’t change a damn thing. It would be like putting lipstick on pig and entering it in beauty contest. Cheers.

References

1.         ACSM Position Stand on Anabolic Steroids: http://journals.lww.com/acsm-msse/Citation/1987/10000/Position_Stand_on_The_Use_of_Anabolic_Androgenic.23.aspx

2.         Street C, Antonio J, Cudlipp D: Androgen use by athletes: a reevaluation of the health risks. Can J Appl Physiol 1996, 21:421-440.

3.         Bhasin S, Storer TW, Berman N, Callegari C, Clevenger B, Phillips J, Bunnell TJ, Tricker R, Shirazi A, Casaburi R: The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. N Engl J Med 1996, 335:1-7.

4.         Harris RC, Soderlund K, Hultman E: Elevation of creatine in resting and exercised muscle of normal subjects by creatine supplementation. Clin Sci (Lond) 1992, 83:367-374.

 

In Defense of Cortisol

by Jaime Tartar PhD –  “If the glove don’t fit, you must acquit.” – Johnnie Cochran – Wacky Attorney

Why Do I Need to Write This? – If Johnnie Cochran was a scientist, he’d certainly acquit cortisol. But before I get ahead of myself, here’s a little background. Just so there’s no confusion, I’m not an expert in exercise science. The extent of my background here is that I jog regularly(ish) and lift weights often enough to psychologically validate my gym membership fees.  I’m a Behavioral Neuroscientist which basically means that I like to know how the brain and body influence each other (it’s a good gig if you can get it especially in South Florida). Because much of my background and training has been focused on the neurobiology of stress, I find myself getting eye-twitchy and moaning inwardly quite often.  It seems that there are some areas of science where anecdotal ideas and misinformation pervade and no one (in my humble, yet biased, opinion) has been more of a victim to this than my good buddy, cortisol. Facebook anyone? :-) This poor little bugger (aka cortisol) has gotten so beat up and kicked around that he could serve as the protagonist of a Victor Hugo novel. Understanding why cortisol is not “bad” is pretty straightforward. In order to help fix the tarnished reputation of cortisol I would like to consider and correct a few key ideas. Necessarily, this begins with a quick and painless overview of the network in which cortisol acts; actually there are some cool points here that can offer winning facts to pepper into a random conversation.

SUPER QUICK Overview of Cortisol Release with Stress – So here we go; stress responses actually involve two major systems: the hypothalamic–pituitary–adrenal (HPA) axis and the sympathetic nervous system (SNS). The final product from the SNS in response to stress is HPA_Axis_Diagram_(Brian_M_Sweis_2012)epinephrine (“adrenaline” if you’re nasty or European). This isn’t his story, though, so we are going to justifiably ignore him and just focus on the HPA system and cortisol for the current tale of woe and strife. While the response to stress through the HPA axis is intricate and complex, a review of the major players will suffice to shed light on why cortisol is an O.K. dude. The first step in the HPA stress response is that perceived or physical stress will induce the release of corticotrophin releasing hormone (CRH) from the hypothalamus in the brain. This guy then tells the pituitary gland to release pituitary adrenocorticotropic hormone (ACTH) into the bloodstream, who then stimulates the release of cortisol from the adrenal cortex (Hellhammer, Wust et al. 2009). The released cortisol does exactly what it is supposed to do to help deal with a stress. In response to stress, cortisol will mobilize energy for muscles, increase energy metabolism, increase cardiovascular tone, turn off nonessential activities, acutely increase immune function, and alter brain functions such as learning and perception processing (Aguilera 2011).  However cortisol’s time in the limelight after stress is short-lived.  It peaks about 30 minutes after the stressor and then further release is shut off through negative feedback regulation at all levels of the HPA axis and in an area of the brain called the hippocampus- he puts the breaks on the whole system at the level of the hypothalamus (from whence it all began).  Cortisol levels are extremely tightly regulated and follow a predicable daily/circadian pattern of release (with the peak in the morning and the trough, or nadir, occurring at night).  Although there is cortisol release with stress, the release is adaptive and helps to respond to increased energy demands – this is also why cortisol levels are high in the morning (known as the cortisol awakening response). This circadian-rhythm-cortisolsurge in a.m. cortisol helps to meet the energy demands needed to get moving and start a new day.  In general, based on the negative feedback mechanisms that are in place for cortisol, we can rest assured that, in the absence of clinical disease or chronic stress (these ideas are reviewed at the end), cortisol is doing exactly what it needs to do to keep the body healthy and capable of dealing with a stress.  Remember that cortisol reigns only briefly after stress and its actions here are beneficial in helping the body manage a perceived or physical challenge.  Based on these ideas we can now clear up the three largest misconceptions of cortisol.

Cortisol is not a stress meter – Cortisol levels do not simply rise and fall as the body is stressed.  This is subtle, and where some information is misconstrued, because, as reviewed above, cortisol will go up when the body is stressed; however, that is not the same thing as being a direct measure of stress.  Cortisol levels do not correspond directly to the type and intensity of stress and there are many individual differences in cortisol release in response to stress.  Also, cortisol levels do not go down in the absence of stress.  Please re-read that phrase. We reviewed above a typical circadian cortisol pattern. This exists because ACTH is released continuously in pulses throughout the day; the pulses speed up or slow down because they are entrained to circadian processing in the hypothalamus (Veldhuis and Johnson 1991). Negative feedback regulation of the HPA axis ensures that cortisol levels don’t get too high for too long, and when they do, they are shut cortisoldown with rapid and decisive action.  So we can appreciate that there is not signal for “Hey we are not stressed so let’s decrease cortisol!”  That’s bonkers and makes no sense since cortisol is an essential hormone in the body. This leads to the second point.

Cortisol is not “bad for you” – it helps keep you alive! – Truly! Natural selection has ensured that in response to a stressor or challenge to homeostasis, cortisol does exactly what it is supposed to do. We all get to be alive today because our ancestors could mount an appropriate stress response. Furthermore, once cortisol is increased in response to stress or a change in homeostasis (e.g. through physical exertion), the changes are short-term. Chronically low cortisol levels can lead to decreased energy, muscle weakness, and low blood sugar. Critically, also, is that cortisol helps to reign in the immune system and helps prevent chronic inflammation and autoimmunity. For example, hyporesponsive HPA activity is seen in autoimmune disorders such as rheumatoid arthritis and chronic fatigue syndrome (Demitrack, Dale et al. 1991, Chikanza, Petrou et al. 1992)

Cortisol isn’t making you fat – Many people associate increased cortisol with weight gain. This viewpoint is prevalent in the fitness world.  It’s true that elevated and sustained levels of cortisol levels can increase fat storage; especially in the abdomen and face. However, the key here is sustained elevations. For example we tend to see this body type in those with Cushing’s disease. These are individuals with pathologically high levels of cortisol. Weight gain with exercise is not likely to happen because of cortisol.  This is a misconception probably partially fat-cartoonbased off of misinterpretation of science.  For example, one study demonstrated a correlation between cotrisol and weight gain (Epel, Moyer et al. 1999); this does not mean increased cortisol caused increased weight gain (this is why the mantra of every Introduction to Statistics class is “correlation does not imply causation”).  Also, based on what we’ve reviewed about short-term cortisol actions, it would not make sense that cortisol “makes you fat” since the major role of cortisol during an intense exercise session is to mobilize energy resources to meet the immediate demands of the body. This primarily involves increased gluconeogenesis (converting glycogen to glucose), higher triglyceride levels, and increased blood flow to the heart and muscles (Majzoub 2006).  Stress can cause weight gain; but this is through increased eating behavior not increased cortisol. Cortisol is an easy target, though, because pathologically or sustained levels of cortisol can cause increased fat storage. So the faulty thinking goes like this: exercise increases cortisol and cortisol causes weight gain. This is where that idiotic idea of too much cardio making you fat comes from. This is simply not accurate and a logical fallacy BUT it is an easy way to sell people a bunch of useless cortisol-fighting pills. Do you remember CortiSham? Ooops, I mean CortiSlim. The stuff worked about as well as giving a killer whale a bite of an apple and saying ‘hey Orca, I bet that filled you up.’ Increased eating that happens with chronic stress is complex and not directly due to cortisol levels. It is likely a product of individual differences in physiology, cognitive mechanisms, and a surplus of high calorie choices (Gibson 2006, Torres and Nowson 2007).

So what the hell cortisol –  why the bad rep? – Most of the deleterious effects associated with cortisol come about as a result of chronic stress. While the HPA axis is well adapted to respond to threats, it is a reflexive physical response from the body and does not discriminate between real and perceived stress. A threat is a threat and it is was historically not adaptive for the brain to consider if something was really a threat before mounting a stress response. However, this can sometimes present problems to us “modern humans” since most of the things that stress us are not life threatening and are coming at us on a somewhat regular (chronic) basis.  Humans living in industrialized nations are not likely starving, threatened by predators or, or battling for mating rights. Though if you went to a local pub you might wonder. However, we’re very good at experiencing chronic perceived emotional (sometimes imagined) chronic stress. In the absence of a disease process (e.g. Cushing’s disease) to cause hypercortisolemia, cortisol levels can become chronically Rodney Dangerfield no respectelevated when the HPA axis is dyregulated.  While even amidst ongoing chronic stress (the daily life hassles we all experience), the HPA axis does a remarkable job of regulating cortisol.  This is pretty amazing given that we do things like respond to an asshole in traffic the way we would a predator 10,000 years ago. And we got plenty of those in South Florida. Believe me. We might mount a stress response to assholes every day, while the predator only occurred once in a while. So, good on you HPA axis- you are doing a damn fine job!  But (and this is where the mass hysteria arises) HPA axis dyregulation can come about from chronic stress through several ways.  The big one here is unremitting and uncontrollable stress. So in order to really dysregulate the HPA axis, you really need to get in there and be sure that the stress is ongoing and that there is no habituation to the stress. In other words, if someone gets punched in the face regularly and predictably it stops becoming a stressor. So for those of you interested in “death by stress,” recognize that unpredictability and uncontrollability is essential to this.  So pushing yourself in exercise won’t likely lead to a breakdown of the HPA axis since you have control and the act is predictable.  To really do someone in, you might consider having that person run on a treadmill against his or her will and have the treadmill turn on and off at random times. Sounds like a CrossFit workout.  LOL. Okay moving on. With that said, there are still some individuals that have an inability to adjust to regular, ongoing stress.  These are what we call “high responders.” They mount a stress response very easily and seem to be in perpetual hypervigilance (I say “they” but I fall directly in this camp – knowledge is not always power?)  There is evidence to suggest that these differences in stress sensitivity can be altered through stress in the womb (which changes the HPA axis “set point”) or through innate differences in physiological arousal- but this is an area that is greatly scientifically underexplored. Lastly, chronic stress can cause problems through rumination, or reactivation after stress has ended. If someone gets bitched out at work, that sucks, but since HPA activity is sensitive to psychological and physical insults, dwelling on the event and perpetually “reliving” it can cause a stress activation over and over, long after the actual event has passed.  The problem with writing this is that I fear ruminators read it and ruminate on how they ruminate too much! So I suppose the take home message here is that chronic physical or psychological stress can produce chronically high levels of cortisol under very special circumstances. Exposure to chronic or severe stress (perceived or realized) can produce dysregulation of the HPA axis, which is characterized by enduring pathological hyper- or hyposecretion of cortisol.

End on a positive! – Importantly for athletes, chronic stress in the form of endurance or exercise-induced increases in cortisol are not likely pathological or related to negative health consequences (Gerber, Brand et al. 2012). In fact, athletic training is associated with a decreased HPA response to an exercise challenge; it’s all about the habituation (Mastorakos, Pavlatou et al. 2005). Critically, also, is the overwhelming evidence that, despite HPA axis activation, regular exercise can also offer increased emotional well-being and protects against depression and other mood disorders (Galper, Trivedi et al. 2006, Lucas, Mekary et al. 2011, Hogan, Mata et al. 2013).

The bottom line is that exercise does increase cortisol, but these increases are not harmful and work to increase real energy demands on the body. Increased cortisol from exercise is not making anyone fat; that would be like blaming your fork for making you fat. Or chopsticks if you live in China. Instead blame increased eating with increased exercise.  Go ahead and work out knowing, with great confidence, that cortisol is not your enemy. Donuts maybe, but not cortisol.

BIO – Jamie Tartar PhD earned her doctorate in the area of behavioral neuroscience from the University of Florida. She did her post-doctoral studies at Harvard Medical School’s Department of Psychiatry (2004-2006) and worked with the United States Army Reserves: Medical Service Corps (1998-2004). She is currently a professor at Nova Southeastern University in the Jamie TDepartment of Neuroscience. She loves brain stuff. One of her fellow Nova colleagues, Jose Antonio PhD, suggested this article topic because as he points out, there are too many self-appointed experts who think cortisol is the enemy. But as a smart dude once said: “Wisdom is a weapon, knowledge is the armour, and ignorance is the enemy.” Cortisol ain’t the enemy. Cotton candy maybe, ice cream perhaps, but cortisol? Nah.

Science References For All You Nerds

Aguilera, G. (2011). “HPA axis responsiveness to stress: implications for healthy aging.” Exp Gerontol 46(2-3): 90-95.

Chikanza, I. C., P. Petrou, G. Kingsley, G. Chrousos and G. S. Panayi (1992). “Defective hypothalamic response to immune and inflammatory stimuli in patients with rheumatoid arthritis.” Arthritis & Rheumatism 35(11): 1281-1288.

Demitrack, M. A., J. K. Dale, S. E. Straus, L. Laue, S. J. Listwak, M. J. Kruesi, G. P. Chrousos and P. W. Gold (1991). “Evidence for impaired activation of the hypothalamic-pituitary-adrenal axis in patients with chronic fatigue syndrome.” The Journal of Clinical Endocrinology & Metabolism 73(6): 1224-1234.

Epel, E. E., A. E. Moyer, C. D. Martin, S. Macary, N. Cummings, J. Rodin and M. Rebuffe‐Scrive (1999). “Stress‐Induced Cortisol, Mood, and Fat Distribution in Men.” Obesity Research 7(1): 9-15.

Galper, D. I., M. H. Trivedi, C. E. Barlow, A. L. Dunn and J. B. Kampert (2006). “Inverse association between physical inactivity and mental health in men and women.” Medicine and Science in Sports and Exercise 38(1): 173.

Gerber, M., S. Brand, M. Lindwall, C. Elliot, N. Kalak, C. Herrmann, U. Pühse and I. H. Jonsdottir (2012). “Concerns regarding hair cortisol as a biomarker of chronic stress in exercise and sport science.” Journal of sports science & medicine 11(4): 571.

Gibson, E. L. (2006). “Emotional influences on food choice: sensory, physiological and psychological pathways.” Physiology & behavior 89(1): 53-61.

Hellhammer, D. H., S. Wust and B. M. Kudielka (2009). “Salivary cortisol as a biomarker in stress research.” Psychoneuroendocrinology 34(2): 163-171.

Hogan, C. L., J. Mata and L. L. Carstensen (2013). “Exercise holds immediate benefits for affect and cognition in younger and older adults.” Psychology and aging 28(2): 587.

Lucas, M., R. Mekary, A. Pan, F. Mirzaei, É. J. O’Reilly, W. C. Willett, K. Koenen, O. I. Okereke and A. Ascherio (2011). “Relation between clinical depression risk and physical activity and time spent watching television in older women: a 10-year prospective follow-up study.” American journal of epidemiology 174(9): 1017-1027.

Majzoub, J. A. (2006). “Corticotropin-releasing hormone physiology.” European Journal of Endocrinology 155(suppl 1): S71-S76.

Mastorakos, G., M. Pavlatou, E. Diamanti-Kandarakis and G. P. Chrousos (2005). “Exercise and the stress system.” Hormones (Athens) 4(2): 73-89.

Torres, S. J. and C. A. Nowson (2007). “Relationship between stress, eating behavior, and obesity.” Nutrition 23(11): 887-894.

Veldhuis, J. D. and M. L. Johnson (1991). “Deconvolution analysis of hormone data.” Methods in enzymology 210: 539-575.

 

Train Not Just The Booty But The Brain

 

by Deepika Chowdhury – Nutrition! I want to repeat that nutrition is the most important factor towards a great looking body. Because we are fitness enthusiasts, we need to know the ins and outs of sports nutrition.

Do you feel helpless when you want to make changes in your diet to lose fat or gain muscle DC3but don’t know where to start? Do you feel confused reading tons of articles and each saying different things? Do you feel skeptical about starting a celebrity diet plan and spending tons of money on it?! Tired of the myriad of advice given to you by your friends and so-called experts?

Yep. There’s a ‘guru’ on every corner and on every social media page. Keyboard warriors dominate the internet space. Folks who have about as much experience with scientific research as fish do in climbing trees.

Imagine, if you knew what is the best choice of food items in your diet plan for your set goals? Imagine if you could decide yourself what, how much and when to eat. You could tweak your diet plan if it didn’t give expected results. Imagine you could confidently write your own diet plan and follow it with excitement and curiosity. Think of the happiness when you walk into a supplement shop and knew exactly what you need and should spend on.

Then you don’t just do it for yourself but also become able enough to help and guide others. Because what you know is being implemented on yourself and you can see the results. How to best achieve strength goals and aesthetic goals based on all your sports nutrition knowledge is certainly within your grasp. Won’t that make you feel beyond happy, confident and powerful? If you answered ‘yes,’ then go to the head of the class!

So what am I trying to say? EDUCATE YOURSELF. Train the brain!Deepika1

I have completed basic courses in the fitness category and read reputable sports nutrition journals. I prefer to read research papers more and more these days. Sports nutrition information changes faster than the blink of an eye. So you need to stay abreast of the latest cool information.

Now I am preparing to be part of THE BEST academic organization in the field of sports nutrition – The International Society of Sports Nutrition (ISSN). This is that one place where all the sports nutrition brains (and bodies I might add) congregate. This includes scientists, practitioners, entrepreneurs and students like me. I can’t wait to attend their conference next year in Clearwater Beach Florida for three days of mind-blowing exchange of knowledge. I am calling myself a student because I am studying for certification through ISSN.

Why did I choose the ISSN? The major reason is that it’s designed by the actual scientists who conduct original research in the field. So it’s like having first class source of knowledge!! They provide access to their website and journal where tons of research papers are available for study. The course is also not time bound. After reading the study material you can choose to take the exam whenever you wish. Now that fits my schedule without stress!ISSN ORIGINAL LOGO_dkBlue

I will be extremely happy if you become my STUDY PARTNER and study with me through ISSN!! That way we can discuss our subject queries. Also it’s more fun to have a study partner. Email me if you wish to join me for the study.

NOTE TO ATHLETES: Nothing of what I have written suggests that you will not require a good coach for your goals. You can attain knowledge from your coach; but remember that the best coaches are ones who know what to do as well why it should be done. In order to know the ‘why,’ you need to know the science. That’s where the ISSN comes in. Nothing and no one can replace a good coach.

So let’s not just train the booty; you have to train your brain as well. 

Come join me June 9-11, 2016 at the ISSN Conference in Clearwater Beach FL!

About the AuthorSONY DSC

DEEPIKA CHOWDHURY

  • India’s first Figure athlete who competed in March 2014 at NPC (National Physique Committee) show Battle on the Beach in Daytona Beach, Florida, USA. She won her first competition in her class and open class both.
  • She went for her second competition in Oct 2014 for a show called Fort Lauderdale cup in Florida and won this competition as well in her class and open class both.
  • She won her third title in New Jersey on 7 April as Overall Figure Championship at Stevestone Metropolitan Championship 2015.
  • She has come back after winning fourth competition at Bev Francis Atlantic States Championship 2015 on 06th of June in New York City, USA.
  • She is certified in personal training and sports nutrition.
  • She is also a powerlifter and made the highest total in her meet at Mangalore in Bangalore State powerlifting competition as a guest lifter.
  • She is BSN (International supplement brand) athlete and also their first athlete from India. She represents Jerai Fitness brand in India as Team Jerai athlete. She is fitness ambassador for Fiber Fitness gym in Pune.
  • She was a column writer for magazine called AbraxusNU and has written on fitness mainly targeting female fitness issues. She is a blogger and her fitness blogs can be read at deepikapune.wordpress.com
  • She is a fitness model and has been cover girl for Krunch India magazine and has been featured in Vogue India and AbraxusNu.
  • She has been featured by newspapers like Indian Express, DNA and Sakal Times. And News channels like India Today.
  • She is science post graduate and professionally works at National Institute of Virology; government research institute and handles molecular biology laboratory of her department.

 

You’re Lovin’ It!

 

By Jose Antonio PhD FNSCA FISSN. 

Bite-Sized McNuggets For You To Chew On:

  • Studies on fast food and exercise are about as common as finding a walrus in your bathtub playing the trombone.
  • If anyone has told you that “they knew this already” or “what’s new with this?,” they’re either full of baloney or Nostradamus’ second-coming.
  • This is the first study that has specifically looked at McDonalds food items versus traditional carbohydrate-heavy sports supplements.
  • Trained cyclists did a glycogen-depletion ride for 90 minutes.
  • To recover, they consumed ~230 g of carbs, 27 grams of protein, and 35 grams of fat. That’s ~920 kcals of carbs, 108 kcals of protein, and 315 kcals of fat.
  • Subjects then performed a 20 km (12.4 mile) time trial with no differences between the fast food and supplement groups.
  • There was also no difference in glycogen restoration between the groups.
  • Fast food is just as good as carbohydrate-heavy sports supplements in promoting glycogen restoration and subsequent exercise performance.
  • This study doesn’t mean you should visit the Golden Arches every day.

As a kid growing up in the 70s, it was an absolute treat when my parents crammed all of us into our Vista Cruiser Station Wagon.  With no seat belts Oldsmobile-Vista-Cruiser-07and a car full of screaming kids, we headed off to McDonalds for their delicious fries and burgers. Next to watching my favorite show ‘Gilligan’s Island’ (with I Dream of Jeannie a close second) going to McDonalds was the best. It was better than eating cotton candy or playing ROCK ‘EM SOCK ‘EM ROBOTS. And oh, I like Ginger more than Mary Ann. However, in the eyes of communists and clean-eating evangelists, McDonalds represents evil incarnate. Not sure why since nobody has ever been forced to eat the stuff. Heck I’m sure North Koreans would love to have a local McDs instead of starving to death. Let’s fast-forward to a study that was just was published in the

The 'Professor' says to Mary Ann and Ginger, "to determine which of you I like the most, I must conduct a very rigorous scientific trial.  And repeat it over and over and over..." No wonder he was the 'Professor!'

The ‘Professor’ says to Mary Ann and Ginger: “To determine which of you I like the most, I must conduct a very rigorous scientific trial. And repeat it over and over and over…” No wonder he was the ‘Professor!’

International Journal of Sport Nutrition and Exercise Metabolism. It’s causing quite a bit of angst among the eat clean/squat ‘till you drop/cardio is for sissies crowd. “You mean fast food can actually help you recover?” But but…that can’t be? That’s like saying I can have my cake and eat it too. Now this isn’t an excuse to pig out on burgers and fries at the expense of more nutrient-dense foods. You know what I really love about this study? They measured the one thing that really matters in sports. Performance. Not whether your mood state was better; not whether protein synthesis increased acutely; and not whether some random hormone went up, down or sideways. Performance. In Meghan Trainor’s world it may be all about the bass. But in the sports science world, it’s all about performance. They did a head to head comparison of isocaloric sport supplements (SS) versus fast food (FF) on glycogen recovery and exercise performance. They used 11 well trained men using a randomized cross-over design. The cross-over design is great because it allows each subject to basically serve as his own control. These were young guys (28 years) with 10% body fat that were familiar with moderate aerobic exercise. So no fat boys allowed. You’ll see why.

Check out what they ate!

Check out what they ate!

Each trial included a 90-minute glycogen depletion ride followed by a 4-hour recovery period. Absolute amounts of macronutrients (1.54 g/kg carbohydrate, 0.24 g/kg fat and 0.18 g/kg of protein) as either SS or FF were provided at 0 and 2 hours. See the pic of Table 2.1 and 2.2 from the study. Subsequently, muscle biopsies were collected from the vastus lateralis muscle at 0 and 4 hours post exercise. A 20k time-trial (TT) was completed following the final muscle biopsy.

And the results were what? First of all, they found no differences in the blood glucose and insulin responses. Also, rates of glycogen recovery were not different across the diets (6.9 and 7.9 mmol per kg wet weight per hour for the SS and FF, respectively). But most importantly, there was no difference in time trial performance (34.1 and 34.3 min for SS and FF, respectively).[1]

You've got a better chance of finding a gold nugget under your pillow than getting Pauline to eat a Big Mac.

You’ve got a better chance of finding a gold nugget under your pillow than getting Pauline to eat a Big Mac.

Does this mean fast food is good? In the context of acute recovery following a kick-ass steady-state ride on a bike, it doesn’t seem to matter what the source of your macronutrients are. In fact, an examination of the sports supplements used in this study show that most of them are basically comprised of sugar. Is that really much different than eating a stack of pancakes? Keep in mind that glycogen compensation will occur whether you’re licking Aunt Jemima’s pancake syrup off your plate or eating sweet potatoes. With prolonged endurance exercise, you have a bit more leeway in terms of introducing simple sugars to your diet (post-workout or otherwise). Why? Because you burn more calories than there are Chins in a Chinese phonebook.

cocacola

Do you remember those big, thick heavy coke bottles? You could kill a Grizzly bear with those bottles because they were so thick and solid.

Coca Cola: This current study reminds me of a prior one published many moons ago. Again using competitive cyclists, they found the following cool results: 1) 6 mg/kg caffeine enhanced time-trial performance 2) replacing a sports drink with Coca-Cola during the latter stages of exercise was equally effective in enhancing endurance performance.[2] So is Coca-Cola the evil twin of McDonald’s burger and fries? Hardly. In the context of prolonged endurance exercise, coke frickin’ helps. And it helps just as well if not more so than the traditional sports drink. Does that mean you should drink Coca-Cola every day? If you answered “No,” go to the head of the class.

Practical advice: This study has little relevance for most athletes. Not many of you are willing to perform steady-state cardio for 90 minutes and follow it with a race (time trial). Even in team sports in which you run a lot (but get to rest), the conditions are quite different. In American football, you only play half the time and have halftime to recover despite the fact that games will last for 3 plus hours. Thus the circumstances that you find with endurance sports (i.e. triathlon, half- to full marathon, etc) are as unique as blue eyes in a brown-eyed world. What this study does demonstrate is that if you consume enough carbs, fat and protein after a very long bike ride, it may not matter what the ‘food’ source is. For those who compete in extreme events such as The Race Across America (3,000 mile bike race from coast coast), the Ironman World Championship in Hawaii (2.4 mile open ocean swim, 112 mile bike, and 26.2 mile run) or the Badwater Ultramarathon (135 mile running race in Death Valley), it’s clear that getting calories is the single most important nutritional consideration. So if you need to eat a stack of pancakes, with a pound of peanut butter, slathered with Mrs. Mrs ButterworthsButterworth’s pancake syrup (my fav!), then by all means go hog wild. But if your idea of a hard workout is doing 3-5 sets of 10-15 reps of the back squat, leg press, push press, leg extension, leg curls and calf raises, then you probably don’t need all those calories. Heck, a 20-40 gram protein shake post-workout will do you fine.

Final Thoughts: The beauty of science is that it doesn’t care how you feel. If new data comes along that refutes commonly held beliefs, then it’s time you change your beliefs. Otherwise, you may as well just make some random stuff up and just say “I’m right because I say so.” So whether you like it or not, the data from this study shows that fast food can indeed play a role in recovery and performance during ScienceAndBeliefs01prolonged endurance exercise. However, don’t conflate health and performance.

To wit:

  1. Nobody is recommending that fast food be an integral part of your daily food/beverage intake.
  2. In the context of acute exercise, it may indeed help. So why choose supplements? Convenience.
  3. I mean do you really want to stick burgers and fries down your pants and eat them later?
  4. Or would it make more sense to eat that sugar-filled energy bar that’s in a wrapper and won’t give you the runs while you run?
  5. This study doesn’t apply to those whose primary goal is to look puuurrrrty.
paddling with the Pups

I took Yoda paddling on the Florida Intercoastal. Ok not really. That’s my puppy (“Pooks”).

BIO – I teach young skulls full of mush at Nova Southeastern University in sunny South Florida. I love sugar, caffeine and other stuff. If loving sugar and caffeine is wrong, then I don’t want to be right.

I Dare You to Read These Studies on McDs and Coke

1.         Cramer MJ, Dumke CL, Hailes WS, Cuddy JS, Ruby BC: Post-exercise Glycogen Recovery and Exercise Performance is Not Significantly Different Between Fast Food and Sport Supplements. Int J Sport Nutr Exerc Metab 2015.

2.         Cox GR, Desbrow B, Montgomery PG, Anderson ME, Bruce CR, Macrides TA, Martin DT, Moquin A, Roberts A, Hawley JA, Burke LM: Effect of different protocols of caffeine intake on metabolism and endurance performance. J Appl Physiol (1985) 2002, 93:990-999.

 

Cardio Makes You Fat and Apples Will Rise

 

By Jose Antonio PhD FNSCA FISSN 

Key Points To Memorize for the ‘Cardio Makes You Fat’ Crowdsm_cardio-fat-banner

  • Longitudinal training studies of fat kids shows that aerobic training results in a loss of body fat.
  • Longitudinal training studies of fat adults shows that aerobic training results in a loss of body fat.
  • Those who do the most cardio over a 15- to 20-year period exhibit the lowest levels of body fat.
  • Athletes that are engaged in highly aerobic exercise have single digit body fat percentages.
  • Triathletes with a higher training volume have a lower % fat than those with a lower training volume.
  • Cardio does not make you fat.
  • Eating too much makes you fat.
  • Sitting on your ass all day makes you fat.
  • Your brain is comprised mainly of fat.  (This has nothing to do with the article but it is a fun fact).

After seeing another headline of “Does Cardio Make You Fat?” with the answer that ‘of course it does,’ I felt an urge to get off my couch, hit the pause button on “The Blacklist,” (awesome show BTW), and remind people that there is something called “science” that can actually answer that question. “I’m not sure why cardio has become the carb of the exercise world” says Rutgers professor Shawn Arent PhD.  And Dr. Arent hates cardio like rats hate cats, cats hate dogs, and dogs hate Michael Vick.

Pauline loves lifting heavy things, doing cardio and drinking coffee. She'll kick your ass too.  Ok maybe not.

Pauline loves lifting heavy things, doing cardio and eating Swedish meatballs. Ok. I made the meatball part up.

What the heck happened to folks actually reading the scientific literature? You know. Those studies in which scientists actually measure body fat. Instead folks fall hook, line and sinker for this pettifogging bullshit of how cardio affects your appetite, cortisol etc. If the claim is that ‘cardio makes you fat,’ the ONLY measure that matters is whether it makes you fat. Guess what? You need to measure body fat. It reminds me of these acute feeding studies that use whey, casein, amino acids etc. that try to extrapolate how much muscle you’d gain in the long run by looking at acute changes in muscle protein synthesis. I have a better idea. Why don’t you actually measure muscle or lean body mass after a treatment period that matters (ex. 8-12 weeks)? Getting back to my original point, imagine how boring the world would be without carbs or cardio?  You couldn’t eat donuts, take walks on the beach, or do both at the same time.

When did doing cardio suddenly become bad for fat loss?  The boneheads who write these articles should at least make a feeble attempt to read the literature. A simple search on Pubmed cross-referencing ‘aerobic’ with ‘body composition’ shows 517 publications.  There are umpteen other searches of key words you can perform. I’m certain there’s at least one study that’s looked at whether cardio turns you from a lean mean kale-eating machine to a fat slob who dreads the day that buffets are outlawed by Congress.

So what gives? Why has the ‘cardio makes you fat camp’ become so entrenched among a few vocal gurus in the fitness industry? Answer: I haven’t an f’in clue.

Anyhow, let’s harken back to when Ronald Reagan was the President of the USA; that’s the 1980s for those who flunked US History.  Twelve weeks of doing aerobic dance training (3 days per week for 45 min) resulted in “…significant increases in lean body mass and body density, together with decreases in percentage body fat and the sum of four skinfold thicknesses…”[1] Holy smokes did you read that?  They lost weight and fat doing aerobic dance no less. Hmmm.

Bill-Clinton-Jogging-for-Weight-Loss

President Clinton should have done more cardio and less McDonalds.

Let’s fast forward to when Bill Clinton was America’s Commander-in-Chief. In this particular study, 60 Japanese women (~51 years of age) participated in a 3-month weight-loss program consisting of two groups: aerobic dance group and jogging and/or cycling group. Guess what, whether you dance, jogged or cycled, you lost body weight and body fat.  The study’s authors stated “low impact aerobic dance is as useful as jogging or cycling in improving body composition and aerobic power for mildly obese middle-aged women.”  Whoa Nellie.  Isn’t cardio supposed to make you fat?[2]

What happens to fat kids who are put on an aerobic exercise program? Inquiring minds want to know. Scientists put 28 obese children (16 boys, 12 girls; aged 12-14 years) into an exercise group or control group. The exercise group participated in 16-week aerobic exercise program (four 60-min sessions per week at 70-85% of HRmax), in addition to the school’s physical education. So did the fat kids get fatter? Uh no. The kids who did aerobic exercise not only demonstrated a smaller waistline (time to buy new belts), but they also showed a significant drop in fat mass.[3]

Now let’s get a bunch of fat adults and see what happens? In this study, science nerds determined the effect of aerobic exercise, without energy restriction, on weight loss in sedentary overweight and obese men and women. The key words being ‘without energy restriction.’ Thus if cardio truly makes you a porky pig, then it would happen in this study.

Participants were randomized into a 400 calorie/session, a 600 calorie/session or to a non-exercise control. Exercise was supervised, 5 days/week, for 10 months.  Now if we use the sterling logic of the ‘cardio makes you fat’ crowd, then one would predict that the 600-calorie/session group would be the fattest at the end of the study, correct?  Well, good thing we have science to answer this question and not some voodoo-witch doctor-fitness guru bullshit.  What happened? “Significant changes in percent body fat over 10 months were observed in both the 400 (-2.9%) and 600 (-4.4%) kcal/session groups. Percent fat was unchanged in the control group (-0.6%). The reductions in body weight observed in both exercise groups were a result of decreased fat mass and preservation or increase in fat-free mass.”[4] Wait did I read that right? The group that did more aerobic exercise actually lost body weight and fat?  What’s going on here?  Why aren’t these cardio kings and queens getting fat?  Because exercising (no matter what type) doesn’t make you fat. And if you believe otherwise, then you may as well get into the business of unicorn breeding.guys-unicorns-mating_design

Are you bored yet? Does science have a way of beating the crap out of dogma? Anyone who claims that ‘cardio makes you fat’ has more hot air than the Hindenburg.

Here are a few more bite-sized bullets for you to remember:

  • A 10-week aerobic exercise program results in a small decrease in energy intake and an associated decrease in percentage of body fat in obese adolescents.[5]
  • Twelve weeks of regular aerobic exercise led to significant reductions in body weight, body fat percentage, and body mass index in the obese.[6]
  • Aerobic exercise training can reduce % body fat and enhance vascular compliance in obese male adolescents.[7]
  • “Aerobic training is the optimal mode of exercise for reducing fat mass and body mass, while a program including resistance training is needed for increasing lean mass in middle-aged, overweight/obese individuals.”[8]
  • In obese adolescent boys, both aerobic and weight-training exercises for a 3-month period resulted in a loss of total and visceral fat.[9]

What happens to athletes who train for years? This is where the story gets interesting. It should be as clear as the majestic blue water of the Caribbean that in untrained, fat, and/or average individuals, doing consistent aerobic exercise leads to a drop in body fat. The fact that I’m typing that sentence shows how silly the fitness industry has become. Perhaps in my next article, I’ll attempt to convince you that water is wet. But apparently some need convincing. Anyhow, there are several very cool studies on athletes. Do they get fat with all that aerobic exercise?

Check out my friend Arlene Semeco (left) with Dara Torres.  All that cardio (swimming) sure is making them fat, huh?

Check out my friend Arlene Semeco (left) with Dara Torres. All that swimming sure is making them fat, huh?

Steve Fleck PhD did a descriptive study back in 1983 showing the physical characteristics of elite American athletes.[10] (See Table 1) If cardio truly made you fat, then for chrissakes why are marathon runners so lean? I know I know. Genetics. Are they lean because they run?  Or do they run because they are lean? Or both? You might look at swimmers and say ‘hey, their body fat percentage tends to be higher than other elite athletes.’ And you’re correct. It has to do in part with thermoregulation (water is colder than ambient air temp), the buoyancy of fat (it floats), etc.  But to say ‘swimming makes you fat’ would make about as much sense as telling an Irishman to lay off the pint, feckin eh.’ You’ll notice that sports that are very anaerobic as well as highly aerobic in nature have athletes that demonstrate single digit body fat levels. Sports in which your body weight is supported tend to have higher body fat levels. So if your tutorial on science was from internet experts and the ‘science for dummies’ book, then you might conclude that having your body weight supported makes you fat. Watch. Some dipshit will post that as an internet meme.

Table 1. Body Composition of the Elite American Athletes[10]

Sport % Fat Male % Fat Female
Average College 15 25
Canoe/Kayak 13.0 22.2
Swimming 12.4 19.5
Boxing 6.9 n/a
Wrestling 7.9 n/a
Sprinters (100, 200, 400 m) 6.5 13.7
Marathon (26.2 miles) 6.4 n/a

A 1997 study from former QB Tim Tebow’s alma mater did a 20-year follow-up of track and field athletes.[11]  Six of these athletes ran the 800m, 17 did the 1500m distance or longer, and two were race walkers.  Athletes were divided into the follow three groups: high (remained elite), moderate (still performed frequent moderate to rigorous endurance training) and last but not least, low (greatly reduced training). So using the ‘cardio makes you fat’ logic, would not those who trained the most (i.e. high) exhibit the highest levels of fat?  See the answer in Table 2.

Table 2. 20-Year Follow Up of Track and Field Athletes

Athletic Level Baseline % Fat 20-years Later – % Fat
Low 15.7 21.8
Moderate 13.2 17.7
High 10.2 15.3

As you can see (and if you can’t, you need eyeglasses), those who train the most, have the lowest amount of fat.  This applies even as they age.  If anything, it should be clear that getting old results in higher body fat levels.  Yes.  In the battle of aging versus you doing everything right (i.e. exercise regularly and eating well), aging ALWAYS wins.

Distance Runners versus Bobsledders – In a classic comparison of endurance versus power athletes, Marti and Howald investigated the alterations in their physical characteristics over a 15-year period from 1973 to 1988.[12]  First let’s do a direct comparison of runners and bobsledders. (Table 3)Bob sledders

Table 3. 15-Year Follow-Up of Runners and Bobsledders

Group

% Fat in 1973 % Fat in 1988

Runners

8.0 12.5

Bobsledders

20.1 22.1

You’ll notice that runners are leaner than bobsledders at all time points. Wait a sec. I thought cardio makes you fat? Interestingly, bobsledders are quintessential power athletes. Shouldn’t they be leaner than distance runners? Now let’s just look at the distance runners and divide them into highly active (ran >90 km/wk), active (30-65 km/wk) and former runners (less than 30 km/wk).  (Table 4)

Table 4. 15-Year Follow-Up of Distance Runners Grouped By Distance Run/Week

Group

% Fat in 1973 % Fat in 1988
Highly Active 9.0 5.1
Active 6.5 8.6
Former 10.3 21.2
suzy_favor_hamilton4-getty_1356117573_540x540

Suzy Favor could run! We wrote a book about training and nutrition for distance running many moons ago. Check it out. It’s called “Fast Track.”

Well whaddya know.  Distance running (in general) keeps you pretty lean. Those who kept running (and did the most mileage per week) were the leanest. Those who did the least amount of that dreaded cardio, got fatter.[12]  In fact, triathletes that perform more aerobic training actually have lower % body fat levels than those who do less.[13] Why that is surprising to anyone baffles me. It’s like being surprised that kangaroos jump, eagles fly and Venezuela runs out of toilet paper.

Cardio and Muscle Mass – On the flip side, too much cardio may promote a loss of lean body mass.  But that’s NOT the same as saying ‘cardio makes you fat.’ Sometimes I feel like folks who post dopey stuff on social media need a class in ‘how to ask the right question.’  One particular study showed that in young women, doing aerobic exercise for 12 weeks promoted a loss of body weight, % body fat and BMI. But it also resulted in a loss of lean body mass.[14] On the other hand, aerobic exercise attenuated the loss of muscle mass during calorie restriction in adults with fat bellies.  Folks that dieted only lost fat and lean body mass.[15] So if you want to argue that aerobic training might result in a loss of muscle mass, you’ll have scientific support.  But it certainly isn’t universal.  Some might lose lean body mass, others not so.  Heck, some might actually gain lean body mass if they are initially very untrained.

Side Bar – Fasted versus Fed CardioIn an elegant study by Shoenfeld et al., they investigated changes in fat mass and fat-free mass following four weeks of volume-equated fasted versus fed aerobic exercise in young women on a lower calorie diet. Training consisted of 1 hour of steady-state aerobic exercise performed 3 days per week. Holy smokes!  Dr. Brad is going to make these girls fat.  How did he ever get this through the IRB and Human Subjects Review? What did they discover? Both groups showed a significant loss of weight and fat mass from baseline; however, there were no significant between-group differences. All that cardio made them fat said no scientist ever.

The moral of the story:

Pooks running

My pet dachshund “Pooks” hates cardio; she loves to sprint. But not as much as she loves to eat ground beef.

  • First of all, anyone who tells you that exercise x, y, and z (you fill in the blank) makes you fat, has about as much science training as my pet Dachshund.
  • We have a plethora longitudinal training studies as well as cross-sectional data which clearly show that performing cardio helps you lose body fat.
  • The preponderance of scientific evidence clearly demonstrates that aerobic or ‘cardio’ training results in a loss of fat.
  • If you prefer anecdotes as your ‘evidence,’ then I’d suggest you get your training/nutrition advice from Jenny McCarthy or the Food Babe.
  • If your goal is to lose body fat and look purrrty, why on god’s earth would you eliminate one form of exercise (i.e. aerobic exercise or ‘cardio’) entirely?
  • If your goal is to compete in an endurance event, then clearly you must do cardio.
  • If you’re a strength-power athlete (e.g. discus, shot put, Olympic weight lifter, powerlifter, high jump etc), you shouldn’t do any cardio.
  • If you like doing cardio, do it.
  • If you hate doing cardio, don’t do it.
  • But don’t be a fool and repeat the ‘cardio makes you fat’ mantra.
  • Getting fat is affected more by your kitchen habits than what you do in the gym/outdoors.
  • Goals determine strategies. Know your goal.

Take home message: Apples won’t rise, Pigs won’t fly, and Aerobic exercise won’t make you fat.applenewton1

Read This All You Cardio Haters

1.            Williams, L.D. and A.R. Morton, Changes in selected cardiorespiratory responses to exercise and in body composition following a 12-week aerobic dance programme. J Sports Sci, 1986. 4(3): p. 189-99.

2.            Shimamoto, H., et al., Low impact aerobic dance as a useful exercise mode for reducing body mass in mildly obese middle-aged women. Appl Human Sci, 1998. 17(3): p. 109-14.

3.            Regaieg, S., et al., The effects of an exercise training program on body composition and aerobic capacity parameters in Tunisian obese children. Indian J Endocrinol Metab, 2013. 17(6): p. 1040-5.

4.            Donnelly, J.E., et al., Aerobic exercise alone results in clinically significant weight loss for men and women: midwest exercise trial 2. Obesity (Silver Spring), 2013. 21(3): p. E219-28.

5.            Thivel, D., et al., Is energy intake altered by a 10-week aerobic exercise intervention in obese adolescents? Physiol Behav, 2014. 135: p. 130-4.

6.            Lee, S.S., et al., The Effects of 12 Weeks Regular Aerobic Exercise on Brain-derived Neurotrophic Factor and Inflammatory Factors in Juvenile Obesity and Type 2 Diabetes Mellitus. J Phys Ther Sci, 2014. 26(8): p. 1199-204.

7.            Song, J.K., et al., Effects of 12 weeks of aerobic exercise on body composition and vascular compliance in obese boys. J Sports Med Phys Fitness, 2012. 52(5): p. 522-9.

8.            Willis, L.H., et al., Effects of aerobic and/or resistance training on body mass and fat mass in overweight or obese adults. J Appl Physiol (1985), 2012. 113(12): p. 1831-7.

9.            Lee, S., et al., Effects of aerobic versus resistance exercise without caloric restriction on abdominal fat, intrahepatic lipid, and insulin sensitivity in obese adolescent boys: a randomized, controlled trial. Diabetes, 2012. 61(11): p. 2787-95.

10.          Fleck, S.J., Body composition of elite American athletes. Am J Sports Med, 1983. 11(6): p. 398-403.

11.          Pollock, M.L., et al., Twenty-year follow-up of aerobic power and body composition of older track athletes. J Appl Physiol (1985), 1997. 82(5): p. 1508-16.

12.          Marti, B. and H. Howald, Long-term effects of physical training on aerobic capacity: controlled study of former elite athletes. J Appl Physiol (1985), 1990. 69(4): p. 1451-9.

13.          Knechtle, B., et al., A comparison of anthropometric and training characteristics of Ironman triathletes and Triple Iron ultra-triathletes. J Sports Sci, 2011. 29(13): p. 1373-80.

14.          Kostrzewa-Nowak, D., et al., Effect of 12-week-long aerobic training programme on body composition, aerobic capacity, complete blood count and blood lipid profile among young women. Biochem Med (Zagreb), 2015. 25(1): p. 103-13.

15.          Yoshimura, E., et al., Aerobic exercise attenuates the loss of skeletal muscle during energy restriction in adults with visceral adiposity. Obes Facts, 2014. 7(1): p. 26-35.

BIO – Jose Antonio PhD wishes he could run but he’s slower than a sloth on Xanax. He wishes he could swim but he looks like a drunk bulldog flappin’ in the water. Instead he Paddling race SUP Clermont March 2015paddles. The beach, sunshine, and a good sweat – you can’t beat that. :-)  If you want to buy me a beer or donate money to support my sushi habit, meet me in Austin Texas June 11-13, 2015 at the ISSN Conference and Expo.

Life Ultimately Judges You From The Neck Up

 

By Jose Antonio PhD FNSCA FISSN – The ISSN

You know what’s elementary?  The science behind creatine supplementation. I’ve always found it puzzling that folks who are otherwise educated have convinced themselves hanks and soccer ballcreatine supplementation is ineffectual and perhaps harmful or dangerous.  Creatine causes cramps, is bad for your kidneys, blah blah blah.  It reminds me of that inordinately vapid movie by Tom Hanks, “Cast Away.”  You know the one where he’s stuck on a deserted island after a crash landing.  He spends his time talking to himself and his soccer ball.  Now I can understand why he would be unaware of the benefits of creatine.  Have you been stuck on a deserted island?

Hence, if you have the attention span of a billy goat, at the very least read these 8 key points:billy goat

  1. Creatine is the single best dietary supplement in the history of mankind.
  2. There’s more supportive data on creatine than ‘whole grains.’
  3. Even if you don’t care about the effects on body composition, take creatine because it’ll help your brain.
  4. Creatine supplementation can alleviate traumatic brain injury.
  5. Creatine supplementation can help your memory.
  6. Kids as young as 1 years of age have been given creatine with no side effects.
  7. Pretty people rule the world from 18-30 years of age.  After 30 years, you’re better off focusing on your IQ than your abs.
  8. Exercise hard.  Exercise frequently.

Life ultimately judges you from the neck up. Except for the delightful Kate Upton.  As I always tell my kids:  “The worst thing you can be in life is a dumbass.”  I recently watched with Kate Uptonprofound amusement as my teenage daughter found a ‘wrinkle’ on her face.  Made me wonder if she needs glasses.  Wait 40 years.  She’ll find out what real wrinkles look like.  Anyhow, the shelf life of your brain will far exceed your body.  Sure the pretty people rule the world from 18-29 years of age.  But after that, it’s all about the abacus in your cranium.  There are supplements worth taking that’ll put the oomph back in your IQ.  Yep, that’s right.  Smart is the new sexy.  Try these to start.  Might help, might not.  But once you try these, there’s one supplement that Donald Trumps them all.

  • Omega-3 fatty acids – Indeed the omega 3 fats, especially EPA (eicosapentanoic acid) and DHA (docosahexanoic acid) are an awesome brain food that can improve cognitive performance.[1]
  • Huperzine A – this herb has been shown to lessen the loss the memory with age.  I need that stuff![2]
  • Alpha-GPC –  L-alpha-glycerylphosphorylcholine (alpha-GPC) can improve learning and memory capacity.[3]
  • Gingko – Of course this supplement always comes up.  Sure, there is some suggestive data showing it might help.[4]

Now those four supplements are nice and all.  But if you really want to be a mathlete and make mental mincemeat of your friends and foe alike, creatine may be what the doctor ordered.   You’ll find that magical supplement probably sitting next to your protein powder.  Oh shit, that sounds like something Dr. Oz would say.  Rewind.  The science on creatine is astounding.  Put it this way.  Compared to green coffee bean extract, creatine would be like driving a Ferrari.  Green coffee bean extract would be like riding a Big Wheel. mathlete

As a professor, I hear some of the silliest things regarding creatine.  Not to pick on the fairer sex, but come on, creatine supplementation won’t make you look like the bearded men of Duck Dynasty.  Heck, there are college guys who train harder than one-legged man in an ass-kickin’ contest, consume gobs and gobs of creatine, protein, beta-alanine, betaine, pizza, and beer.  And yet, they still look like the letter ‘i.’ There are plenty of college women who lament “I don’t want to get big and bulky; that’s why I don’t take creatine.”  And one of my favorites:  “Is creatine a steroid?”  Whiskey-Tango-Foxtrot.  Did you fall asleep in chemistry class?  There’s about as much chance of creatine being a steroid as a donkey winning the Nobel Prize for Medicine.  Though chances of winning the Nobel Peace Prize are 1:1. Either way, even if you don’t give a rat’s ass about gaining muscle mass, the BETTER reason to supplement with creatine is because of its profound effects on the brain.  Yeah.  That fat-filled organ sitting on top of your neck.

SIDE BAR – Creatine, Energy, and Neurological Diseases

“Creatine is a critical component in maintaining cellular energy homeostasis, and its administration has been reported to be neuroprotective in a wide number of both acute and chronic experimental models of neurological disease. In the context of this chapter, we will review the experimental evidence for creatine supplementation as a neurotherapeutic strategy in patients with neurological disorders, including Huntington’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and Alzheimer’s disease, as well as in ischemic stroke, brain and spinal cord trauma, and epilepsy.”[5]

Listen Up Vegans

It makes sense that creatine is as important for your brain as it is for your muscles. 

Pauline is a big fan of creatine; therefore, you should be a big fan of Pauline.

Pauline is a big fan of creatine; therefore, you should be a big fan of Pauline.

Creatine, when combined with phosphate forms phosphocreatine (PCr).  Why is this important?  PCr acts as a reserve of high-energy phosphate (i.e. fuel). Creatine supplementation influences brain functioning as shown by various studies that have taken snapshots of brain function.  In a rarity, scientists examined young women (most studies are on men) who were vegetarians and meat-eaters.  These women consumed 20 grams of creatine (or a placebo) for 5 days.  In vegetarians but not in the meat-eaters, creatine supplementation resulted in better memory.[6]  More proof.  A study of 45 vegetarians found that creatine supplementation enhanced memory and intelligence, both tasks that require speed of processing.[7] Remember that creatine is naturally found in fish and meat.  So all you tree-huggin’, Birkenstock-wearin’, soy protein-lovin’ vegans should supplement with creatine.  Even if you take creatine ethyl ester, which BTW is an inferior form of creatine [i.e. creatine monohydrate is better], it can help cognitive performance too.[8]  Creatine supplementation helps old folks remember stuff.[9]  So next time you’re with grandpa, make sure you slip some creatine in his Metamucil.[9]

Good Night, Sleep Tight

I think one of the more fascinating roles of creatine is how it affects a sleep-deprived brain.  Sleep deprivation is something we all can relate to.  Whether it’s staying up late studying for exams (not me thank god), watching Monday Night Football milliondollarsaloonvig(on the East Coast), or hanging out at your favorite Gentlemen’s Club (or so I’ve heard from my fellow ISSN’ers), sleep often is in short supply.  So when you wake up the next day feeling like a Mack truck just played ping pong with your head, then you ought to reach for the creatine (after you reach for the java).  In fact, just taking 20 grams of creatine daily for 7 days is enough to lesson your sleep-deprived stupor.  Accordingly, scientists discovered that following 24 hours of sleep deprivation, creatine supplementation had a positive effect on mood state and tasks that place a heavy stress on the prefrontal cortex.[10]  The pre-frontal cortex is the part of the brain that is involved in abstract thinking and intricate analysis.  That’s a pretty important part of the brain.  Especially when deciding whether you should watch Game of Thrones or study for your Exercise Physiology midterm.  One reason why creatine may help your noggin is related to an increased oxygen utilization in the brain.[11]

Save the Brain

If you compete in a sport that may result in potential head trauma (i.e. football, boxing, MMA, soccer [yes even ‘futbol’]), then for Pete’s sake, open up the tub of white powder and take it.  Check this out.  In a study of 39 children and adolescents (ages 1 to 18 years) with TBI or Brain_4d5df2_1104245traumatic brain injury, scientists discovered that creatine supplementation protected the brain.  Yes sir indeed. If you’re incredulous, here’s a direct quote from the study. “The administration of Cr to children and adolescents with TBI improved results in several parameters, including duration of post traumatic amnesia (PTA), duration of intubation, intensive care unit stay. Significant improvement was recorded in the categories of headache (p<0.001), dizziness (p=0.005) and fatigue (p<0.001), aspects in all patients. No side effects were seen due to Cr administration.”[12]  Let’s hope you read the fine print.  They gave creatine to kids as young as 1 years of age with no side effects.  And yet soccer moms and dads around the world are afraid that if their teenage son takes it, it might cause harm.

After I told Mike that folks are scared of creatine, he busted out laughing say "that sssit ith funny.."

After I told Mike that folks are scared of creatine, he busted out laughing say “that sssit ith funny..”

Other intriguing studies have found that “creatine supplementation has the potential to improve neurofunction following neonatal brain damage” [13], can “rescue animals following brain damage,” [14] and may “reduce oxidative stress and afford neuroprotection” in an in vitro model.[15]

So there you have it.  Creatine does the brain good.  It’s really elementary.  

BIO – Jose Antonio PhD is the CEO of the ISSN, www.theissn.org.  He has been regularly supplementing with creatine for a score and 4 years.  If he didn’t take creatine, he’d have the memory of an aardvark.

Some Cool Creatine Studies

1.         Rachetti AL, Arida RM, Patti CL, Zanin KA, Fernades-Santos L, Frussa-Filho R, Gomes da Silva S, Scorza FA, Cysneiros RM: Fish oil supplementation and physical exercise program: distinct effects on different memory tasks. Behav Brain Res 2013, 237:283-289.

2.         Ye JW, Shang YZ, Wang ZM, Tang XC: Huperzine A ameliorates the impaired memory of aged rat in the Morris water maze performance. Acta Pharmacol Sin 2000, 21:65-69.

3.         Drago F, Mauceri F, Nardo L, Valerio C, Lauria N, Rampello L, Guidi G: Behavioral effects of L-alpha-glycerylphosphorylcholine: influence on cognitive mechanisms in the rat. Pharmacol Biochem Behav 1992, 41:445-448.

4.         Walesiuk A, Trofimiuk E, Braszko JJ: Gingko biloba extract diminishes stress-induced memory deficits in rats. Pharmacol Rep 2005, 57:176-187.

5.         Klein AM, Ferrante RJ: The neuroprotective role of creatine. Subcell Biochem 2007, 46:205-243.

6.         Benton D, Donohoe R: The influence of creatine supplementation on the cognitive functioning of vegetarians and omnivores. Br J Nutr 2011, 105:1100-1105.

7.         Rae C, Digney AL, McEwan SR, Bates TC: Oral creatine monohydrate supplementation improves brain performance: a double-blind, placebo-controlled, cross-over trial. Proc Biol Sci 2003, 270:2147-2150.

8.         Ling J, Kritikos M, Tiplady B: Cognitive effects of creatine ethyl ester supplementation. Behav Pharmacol 2009, 20:673-679.

9.         McMorris T, Mielcarz G, Harris RC, Swain JP, Howard A: Creatine supplementation and cognitive performance in elderly individuals. Neuropsychol Dev Cogn B Aging Neuropsychol Cogn 2007, 14:517-528.

10.       McMorris T, Harris RC, Swain J, Corbett J, Collard K, Dyson RJ, Dye L, Hodgson C, Draper N: Effect of creatine supplementation and sleep deprivation, with mild exercise, on cognitive and psychomotor performance, mood state, and plasma concentrations of catecholamines and cortisol. Psychopharmacology (Berl) 2006, 185:93-103.

11.       Watanabe A, Kato N, Kato T: Effects of creatine on mental fatigue and cerebral hemoglobin oxygenation. Neurosci Res 2002, 42:279-285.

12.       Sakellaris G, Nasis G, Kotsiou M, Tamiolaki M, Charissis G, Evangeliou A: Prevention of traumatic headache, dizziness and fatigue with creatine administration. A pilot study. Acta Paediatr 2008, 97:31-34.

13.       Allah Yar R, Akbar A, Iqbal F: Creatine monohydrate supplementation for 10 weeks mediates neuroprotection and improves learning/memory following neonatal hypoxia ischemia encephalopathy in female albino mice. Brain Res 2015, 1595:92-100.

14.       Iqbal S, Ali M, Iqbal F: Long term creatine monohydrate supplementation, following neonatal hypoxic ischemic insult, improves neuromuscular coordination and spatial learning in male albino mouse. Brain Res 2014.

15.       Cunha MP, Martin-de-Saavedra MD, Romero A, Egea J, Ludka FK, Tasca CI, Farina M, Rodrigues AL, Lopez MG: Both creatine and its product phosphocreatine reduce oxidative stress and afford neuroprotection in an in vitro Parkinson’s model. ASN Neuro 2014, 6.

 

Out-Supplement a Bad Diet

 

By Jose Antonio PhD FISSN FNSCA

Key points if you are too lazy to spend 7 minutes reading this:shutterstock-couch-potato

  1.  Virtually every study on effective ergogenic aids have not controlled for diet.
  2. You can improve exercise performance with no change in diet.
  3. Diet is however key to looking pretty.
  4. Goals determine strategies – endurance athletes can get away with eating the kitchen sink.
  5. It is always best to implement strategies of eating well, effective supplementation, and proper exercise to achieve your goal(s).
  6. I really don’t give a shit what you eat.
  7. Read the references at the end.

You’re familiar with the saying that “if you tell a lie big enough and keep repeating it, people will eventually come to believe it.”  Was it Joseph Goebbels who said that?  Nevertheless, how out train a bad dietmany times have you seen the internet meme, popularized by Facebook fitness aficionados, that states the following: “You Can’t Out Train a Bad Diet.”  Or it might go something like these:  “If you take supplements on a crappy diet, you still have a crappy diet.”  Or “you must clean up your diet first before you take supplement(s).”  Certainly, the fortune cookie sayings sound good.  But are they in fact true?

I remember when President Bill Clinton said “I did not have sexual relations with that woman…”  Perhaps he even believed it.repeat3

Getting back to the bad diet and training stuff.  If your goal is to look purrrty, then your diet is probably the single most important factor.  So for all of you physique athletes who were ready to tar and feather me for this dietary blasphemy, rest assured you can get back on Instagram and post your 132nd selfie of the year.  On the other hand, if your goal is performance, particularly in the endurance realm, then it’s certainly possible to out train a ‘bad diet.’ Endurance athletes expend an ungodly amount of energy just with training alone.  For instance, the average energy intake of male cyclists riding 15-18 hours a day for 10 days was over 7,000 calories![1]  In fact, 44% of the carbohydrate calories came from simple sugars, cookies, sweetened drinks, and candy. Try getting those calories by eating broccoli and chicken.  The total energy expenditure of female swimmers during a eating hot dogparticular training period averaged ~5,600 calories.[2]   What’s the commonality with these athletes?  Their paramount dietary concern is getting enough calories.  That means eating anything and everything:  ice cream, peanut butter, steak, eggs, rice, apple pie, sushi, fish oil, Krispy Kreme donuts, bread with butter, hot dogs, blah blah blah.  Of course, if you have no plans to cycle all day, swim from Cuba to Florida, or train for the Ironman triathlon (i.e. swim 2.4 miles, bike 112 miles and then run 26.2 miles) then perhaps you can’t out train a ‘bad’ diet.

Moreover, let’s look a corollary of this.  I do think that you can out-supplement a bad diet. Or put another way, do you have to clean up your diet before you take a supplement(s)?  That depends on whether you use science to answer your question or your grandma’s voodoo logic from the old country.  In fact, for all of you ‘do you even science’ enthusiasts, I’d suggest you check out the science. And oh by the way, science is a noun, not a verb.

trivia crackLet’s play a little bit of Trivia Crack.  So turn on that cortex and answer the following question:  Which of the following strategies can produce the quickest and measurable increases in exercise performance and/or body composition?  A) Changes in Training.  B) Changes in Diet.  C) Changes in Supplementation.  D) All of the above are equally effective.

If you answered A, B or D, you need to go back to school.  If you answered C, then you’re the teacher’s pet.  In general, changes in diet or training take roughly 4 weeks to produce measurable changes in performance or body composition.  Taking the right supplements can take minutes to a few days to produce a robust ergogenic effect.  In fact, let’s look at the current science and see what strategies (diet vs supplements) increase muscular power, strength and lean body mass better and quicker.

But before we do that, let me kill another stinkin’ cliché that I see more often than I hear that annoying “Shake it off” song by Taylor ‘twiggy’ Swift.  It goes like this: Foods are always better than supplements.  Clinical types just loooooove saying this.  Actually, pretty much everyone clings to this with the same enthusiasm that a fat boy in Texas clings to his cotton candy at the State Fair.

The “foods are always better than supplements” and the “you can’t out-supplement a bad diet” really go hand in hand.  To wit:

  • Branched-chain amino acids consumed immediately before a killer workout can reduce muscle damage and accelerate recovery [3].  Is there a food that can do that?  Heck, would you want to eat food prior to such a hard workout?
  • Creatine supplementation can increase muscle mass and sprint performance in as little as three days.[4]  Is there a food that can do that?  Don’t think so.
  • Betaine supplementation can increase power output in as little as seven days.[5]  Is there a food that can do that?  Yeah.  Can’t find one can you?
  • Beta-alanine supplementation for 1 month can increase training volume and lower the sensation of fatigue.[6]  Are there any scientific studies to show that a whole food can do that same?  Uh.  Guess not.
  • There is a dearth of foods that show promise as ergogenic aids.  One that is equal to a supplement in terms of a rapid ergogenic effect is coffee (vs caffeine).[7] Also, low fat chocolate milk is as good as your typical sports drink for promoting recovery.[8]  But other than that, there ain’t much science out there (in terms of foods and an ergogenic effect).

dont give a fuck“The beauty of science is that it doesn’t care what you believe.”

Indeed.  There are few foods that have the profound effect that certain dietary supplements have.  If you read the 1000 plus peer-reviewed studies on sports supplements (e.g. creatine, caffeine, beta-alanine, BCAAs, protein, etc), virtually NONE of them have controlled for diet.

Meaning, it doesn’t matter if you eat as clean as a cloistered nun or as cruddy as a beer-drinkin’ New England Deflatetriots fan.  You don’t have to clean up your diet to take supplements.

pauline-nordin-5

This photo, courtesy of Pauline Nordin (Fighter Diet) has nothing to do with this article. I just like the pic. Booyah!

HOWEVER, that doesn’t mean you SHOULDN’T clean up your diet.  Certainly it is best that you eat well, take supplements, and train harder than a hamster on a wheel.  But the notion that foods trump supplements all the time has no basis in fact.  In fact, the supportive data shows that certain supplements can indeed produce a robust ergogenic effect even with no change in diet.

So enough of the fortune cookie sayings.

Yes.  You do not have to clean up your diet before you take a supplement(s).  You can out-supplement a bad diet. 

And depending on your athletic endeavor, yes you can out-train a bad diet.

And yes.  It is better if you take supplements and are on a good diet.

I’d suggest you also work out hard.  And sweat a lot.

BIO – Dr. Jose Antonio earned his PhD at the University of Texas Southwestern Medical Center.  If you want to buy him beer and sushi, please meet him at the ISSN Conference. Thank you.

References

1.            Gabel KA, Aldous A, Edgington C: Dietary intake of two elite male cyclists during 10-day, 2,050-mile ride. Int J Sport Nutr 1995, 5:56-61.

2.            Trappe TA, Gastaldelli A, Jozsi AC, Troup JP, Wolfe RR: Energy expenditure of swimmers during high volume training. Med Sci Sports Exerc 1997, 29:950-954.

3.            Howatson G, Hoad M, Goodall S, Tallent J, Bell PG, French DN: Exercise-induced muscle damage is reduced in resistance-trained males by branched chain amino acids: a randomized, double-blind, placebo controlled study. J Int Soc Sports Nutr 2012, 9:20.

4.            Ziegenfuss TN, Rogers M, Lowery L, Mullins N, Mendel R, Antonio J, Lemon P: Effect of creatine loading on anaerobic performance and skeletal muscle volume in NCAA Division I athletes. Nutrition 2002, 18:397-402.

5.            Pryor JL, Craig SA, Swensen T: Effect of betaine supplementation on cycling sprint performance. J Int Soc Sports Nutr 2012, 9:12.

6.            Hoffman JR, Ratamess NA, Faigenbaum AD, Ross R, Kang J, Stout JR, Wise JA: Short-duration beta-alanine supplementation increases training volume and reduces subjective feelings of fatigue in college football players. Nutr Res 2008, 28:31-35.

7.            Wiles JD, Bird SR, Hopkins J, Riley M: Effect of caffeinated coffee on running speed, respiratory factors, blood lactate and perceived exertion during 1500-m treadmill running. Br J Sports Med 1992, 26:116-120.

8.            Spaccarotella KJ, Andzel WD: The effects of low fat chocolate milk on postexercise recovery in collegiate athletes. J Strength Cond Res 2011, 25:3456-3460.