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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:


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


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


  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.


The Case for Carbs – Part 1


by Kedric Kwan CISSN. The world of carbohydrates can be one plague with controversy. It seems like people tend to polarize the intake of carbohydrates from either completely low to no carbohydrate or having a high carb diet all day, every day. It’s either cotton candy or some gross sugar-free substitute. And somewhere in that morass of social media confusion, lies the truth.sport_drinks

When the role of carbohydrate is concerned, it is mainly involved in keeping muscle glycogen and blood glucose elevated to facilitate exercise performance.

Classic studies have shown the role skeletal muscle glycogen content plays in sustaining exercise or sporting performance. My favourite one in particular is this study done in soccer players. The finding of the summary is in the table below:

High Glycogen Low Glycogen
Muscle glycogen at start of game: 100% 50%


Muscle glycogen at half time: 40% 7%
Muscle glycogen at full time: 10% 0%
Distance covered first half 6,100m 5,600m
Distance covered second half 5,9000m 4,1000m
Total distance covered 12,000m 9,7000m
Percentage walking 27% 50%
Percentage sprinting 24% 15%

This study basically showed that the football players with higher glycogen covered a staggering 1,300m more and sprinted more and walked less compared to the ones who had low muscle glycogen (Saltin 1973).

I don't like white rice said no Asian ever.

I don’t like white rice said no Asian ever.

You should be convinced now that carbohydrates do play a huge role in both exercise and sporting performance. However, just because something is good doesn’t mean that constantly consuming a ton if it will bring additional benefits.

In the endurance world, performance is definitely affected by carbohydrates and recent studies have indeed demonstrated that (Leckey et al., 2015, Torrens et al., 2016). However, in 8 longitudinal studies evaluating the relationship between a high carbohydrate diet (HCHO) and moderate carbohydrate diet (MCHO), 5 studies showed no difference in performance improvement of HCHO compared to MCHO when it came to the actual performance test (Burke et al., 2004).

This leaves us with the question, is constantly having high carbohydrate availability the best way to maximize endurance performance? Or could strategically periodizing phases of training with low carbohydrate availability enhance performance to a greater extent?

Mitochondrial physiology

In order to fully understand the content of this article we need to understand a little physiology of endurance performance. Besides the role the heart plays, the two ways someone can increase their endurance performance is by increasing the number of mitochondria also known as mitochondria volume density or by improving mitochondrial function. This article will focus mainly on the increasing of mitochondrial volume density also known as mitochondrial biogenesis, instead of its function.

Mitochondria is the site where energy in the form of ATP is produced so the more mitochondria we have, the more ATP we can produce which theoretically leads to an improvement of performance. Since the improvement of performance could be thought of the accumulated response from an acute exercise bout, constant training would result in an improvement of endurance performance through increased mitochondrial volume.outrigger-canoe

Something that governs the increase of mitochondria is the transcription factor called Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α). This has been labelled as the “master regulator” of mitochondrial biogenesis and training in a state of reduced carbohydrate availability seems to augment this by upregulation upstream regulators and protein kinases that are involved in the signalling pathway for mitochondrial biogenesis.

One of the major protein kinases that up regulates PGC-1α is the protein kinase called AMP- activated protein kinase (AMPK). This protein responses mainly to energy availability and the ratio of AMP to ATP, a higher level of AMP concentration simply signals that energy availability is low and AMPK will be upregulated (Alexander and Walker, 2011). Another protein kinases is the p38 mitogen-activated protein kinase (p38 MAPK) which is a protein that is sensitive to stress that takes place during exercise mainly in the form of cellular perturbation and oxidative stress. This two proteins act downstream on PGC-1α, increasing it’s activity hence up regulating mitochondrial biogenesis.

Besides PGC-1α, another protein called p53 has also been implicated in the role of mitochondrial biogenesis. Similar to how PGC-1α is upregulated by AMPK and p38 MAPK, p53 is also one of the downstream targets of those proteins.

Training with low carbohydrate availability – the evidence.

One of the most common ways to reduce carbohydrate availability is to train twice a day without ingesting any form of carbohydrate after the first exercise bout. What happens when exercise is commenced with low carbohydrate availability is that the cellular perturbation is increased and energy availability would be greatly reduced hence AMPK and p38 MAPK activity would increase and act on it’s downstream targets. This was first seen in a study done by Hansen and workers (2005) in which they recruited a group of seven untrained males and have them perform single leg knee extensions at 75% maximal power out (Pmax). One leg trained twice a day, every other day (LOW) while the other once a day, every day (HIGH). This training runningprotocol lasted 10 weeks. Only water was ingested while training the LOW leg to ensure that the second bout of training was commenced with lower glycogen stores while the HIGH leg that was trained once every other day trained with regular glycogen levels. After 10 weeks the LOW leg showed higher a increase of Citrate Synthase (CS) which is a marker of increased mitochondrial volume and HAD which shows greater oxidative capacity, compared to the HIGH. The LOW leg also performed better in a time to exhaustion test (TTE) compared to the HIGH.

This study was definitely a huge pain to go through and in most countries, it wouldn’t even get approved by ethics. Hence ecological validity isn’t particularly high but this was simply a “proof of principle” study that eventual lead to more studies being done. Another thing to take note of is that this study was done with untrained population and the effects on trained population might be different

To create a study that had greater real world application, a similarly study was done using a cycling model on 12 endurance trained cyclist or triathletes. Using a similar design in a cycling model, one group trained twice a day with both steady state (SS) and high intensity interval training (HIIT) done on the same day (LOW) every other day while the other group once a day, every day (HIGH) alternating between SS and HIIT for 3 weeks. Participants cycled for an initial 100 minute of SS cycling followed by 8 x 5 minutes of HIIT at 75-80% Pmax (Yeo et al., 2008).

The LOW group was given only water while the high group had no nutritional restriction. In the first two weeks, the LOW group had reduced power output compared to the HIGH but that stabilized in the third week. After 3 weeks, biopsies showed a higher increase in CS and β-HAD in the LOW in agreement to the results reported by Hansen et al. The LOW group also had 12473749_10156454930670440_2801202052687652102_ohigher lipid oxidation compared to the HIGH. A 60 minute time trial was also performed to measure performance improvement but there was no difference between groups. Unlike the study done by Hansen et al which showed an improvement in both mitochondrial adaptation and performance (TTE) Yeo et al couldn’t display an additional performance benefit despite enhance mitochondrial adaptation in the LOW group.

Hulston and colleagues (2010) performed what was almost a replication of the study conducted by Yeo et al with small changes in different training parameters and what they showed was consistent with the previous findings, as markers of mitochondrial adaptation (CS and β-HAD) and lipid oxidation increased while a drop in power output was seen in the low group and both groups showed similar improvement in a time trial test.

Despite the lack of performance improvement, most acute studies done would be in agreement with the chronic studies showing additional improvement in markers of mitochondrial adaptation (some acute studies did not show improvements but will be touched on below). Using a cycling model, Psilander and colleagues (2013) recruited 10 subjects to investigate the acute response to training with reduced glycogen availability on highly trained athletes. They performed exercise either in a high glycogen session or low glycogen session with at least a week in between sessions. On the first day, a protocol to deplete glycogen was done for both high and low sessions. The high session then consumed two high carbohydrates meal and returned for the exercise test 14 hours later, whereas the low session was commenced 14 hours later after consuming two low carbohydrate meal. The exercise test consist of 6 intervals of 10 minutes with 4 minutes of active rest in between intervals. The first interval started at 72.5% Vo2 max and subsequent intervals were reduced by 2.5% making the last interval 60% of Vo2 max. A muscle biopsy obtained 3 hours post test showed a greater increase in PGC-1α expression with also an increase of the mitochondrial enzyme pyruvate dehydrogenase lipoamine kinase isoenzyme 4 (PDK-4).keto-diets-suck

In a different study, increases of PDK- 4 and Carnitine palmitoyltransferase I (CPT-1), another mitochondrial enzyme was higher in the group that performed exercise in a lower glycogen state (Bartlett et al., 2013). 8 participants performed a glycogen depletion protocol in the evening lasting 68 minutes. Participants returned the next morning to perform High Intensity Training (HIT) running for 6 x 3 minutes at 90% Vo2 max. Participants exercised either in a high (HIGH) carbohydrate state or low (LOW) carbohydrate state. In the HIGH state, participants were fed carbohydrate before, during and after HIT while in the LOW state, no carbohydrate was fed before, during and after HIT. Participants switched groups (HIGH to LOW or LOW to HIGH) and repeated the protocol with a minimum of 7 days rest between protocols. Phosphorylation of p53 was also higher in LOW compared to HIGH but the increase of PGC-1α was similar between both groups.

So far every exercise protocol here has been done using an endurance exercise model, for all the meat heads out there, don’t lose hope as there is one study that used resistance training to investigate similar hypothesis.

Low carbohydrate availability and resistance exercise.

In this study, Camera and workers (2015) recruited participants to perform resistance exercise to investigate the acute response on mitochondrial adaptation. A group of 8 healthy fit males were recruited and they performed a glycogen depletion protocol on one leg. Participants then consumed a low carbohydrate dinner and returned the next morning to perform resistance exercise after an overnight fast to ensure one leg would perform the exercise in a low glycogen state. Participants then performed 8x 5 minutes at 80% of their 1RM with 3 minutes rest in

Check out Pauline's glycogen filled skeletal muscles.

Check out Pauline’s glycogen filled skeletal muscles.

between legs. The leg that performed resistance exercise in a low glycogen state had greater phosphorylation of p53 compared to the normal leg and PGC-1α also had a higher increase in the low glycogen leg.

As far as the acute and chronic changes in mitochondrial adaptation is concerned, it’s safe to say that training in a low glycogen/carbohydrate state definitely enhances this response. When it comes to performance, it’s not so clear cut.

Two other studies showed increases in both mitochondrial adaptations but when it came to the actual performance test, improvements were similar across both groups with no additional performance outcome (Morton et al., 2009, Van Proeyen et al., 2011).

Low carbohydrate availability and greater performance improvement.

However there are two studies that have been published recently that shows an improvement in performance. The first was done by Cochran and workers (2015) which showed that high intensity interval training (HIIT) performed twice a day with the second bout in a glycogen reduced state showed an improvement in a 250kj time trial compared the control group. This training protocol lasted 2 weeks. Another study was published early this year that showed that by simply altering the timing of intake of carbohydrate resulted in both a reduction in body fat and improved performance in a stimulated triathlon test (Marquetz et al., 2016).

In brief, both groups performed two bouts of exercise. The first bout of exercise took place in the evening and consisted of 8 x 5 minutes of maximum aerobic power followed by 60 minutes of cycling at 65% maximum aerobic power. The sleep low group restricted carbohydrate from their meals after the first bout of exercise up till the second bout of exercise whereas the Science rocks piccontrol group maintained carbohydrate availability with throughout the recovery period up till the second exercise bout and a carbohydrate drink was consumed during the second bout of exercise. After the second bout of exercise, the sleep low group then consumed large amount of carbohydrates to match the amount consumed by the control group. Both groups were given a protein drink before bed and total energy intake was matched between groups.

Improvements in triathlon simulated trial, decreased in heart rate and rate of perceived exertion took place only in the sleep low group whereas the control group showed no noticeable difference. This study is significant because it’s the first and only study that showed an improvement in performance in a group of highly trained athletes whereas the previous studies (Hansen et al and Cochran et al) was done in untrained individuals.

This is almost all the evidence there is on training with low carbohydrate availability and I hope that it has given some insight on the mechanism on how it works.

I’ve purposefully left out some evidence from the literature because I plan to include that in the next part where we will touch on the implementation of low carbohydrate availability training and how to optimise it to get a performance outcome.  Part 2 coming soon!


Alexander, A. and Walker, C. (2011). The role of LKB1 and AMPK in cellular responses to stress and damage. FEBS Letters, 585(7), pp.952-957.

Bartlett, J., Louhelainen, J., Iqbal, Z., Cochran, A., Gibala, M., Gregson, W., Close, G., Drust, B. and Morton, J. (2013). Reduced carbohydrate availability enhances exercise-induced p53 signaling in human skeletal muscle: implications for mitochondrial biogenesis. AJP: Regulatory, Integrative and Comparative Physiology, 304(6), pp.R450-R458.

Burke, L., Kiens, B. and Ivy, J. (2004). Carbohydrates and fat for training and recovery. Journal of Sports Sciences, 22(1), pp.15-30.

Camera, D., Hawley, J. and Coffey, V. (2015). Resistance exercise with low glycogen increases p53 phosphorylation and PGC-1α mRNA in skeletal muscle. European Journal of Applied Physiology, 115(6), pp.1185-1194.

Cochran, A., Myslik, F., MacInnis, M., Percival, M., Bishop, D., Tarnopolsky, M. and Gibala, M. (2015). Manipulating Carbohydrate Availability Between Twice-Daily Sessions of High-Intensity Interval Training Over 2 Weeks Improves Time-Trial Performance. IJSNEM, 25(5), pp.463-470.

Hansen, A., Fischer, C., Plomgaard, P., Andersen, J., Saltin, B. and Pedersen, B. (2005). Skeletal muscle adaptation: training twice every second day versus training once daily. Scand J Med Sci Sports, 15(1), pp.65-66.

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.

Leckey, J., Burke, L., Morton, J. and Hawley, J. (2015). Altering fatty acid availability does not impair prolonged, continuous running to fatigue: evidence for carbohydrate dependence. Journal of Applied Physiology, 120(2), pp.107-113.

Marquet, L., Brisswalter, J., Louis, J., Tiollier, E., Burke, L., Hawley, J. and Hausswirth, C. (2016). Enhanced Endurance Performance by Periodization of CHO Intake. Medicine & Science in Sports & Exercise, p.1.

Morton, J., Croft, L., Bartlett, J., MacLaren, D., Reilly, T., Evans, L., McArdle, A. and Drust, B. (2009). Reduced carbohydrate availability does not modulate training-induced heat shock protein adaptations but does upregulate oxidative enzyme activity in human skeletal muscle. Journal of Applied Physiology, 106(5), pp.1513-1521

Psilander, N., Frank, P., Flockhart, M. and Sahlin, K. (2012). Exercise with low glycogen increases PGC-1α gene expression in human skeletal muscle. European Journal of Applied Physiology, 113(4), pp.951-963.

Saltin, B. (1973). Metabolic fundamentals in exercise. Medicine & Science in Sports & Exercise, 5(3), pp.137-146.

Torrens, S., Areta, J., Parr, E. and Hawley, J. (2016). Carbohydrate dependence during prolonged simulated cycling time trials. European Journal of Applied Physiology.

Van Proeyen, K., Szlufcik, K., Nielens, H., Ramaekers, M. and Hespel, P. (2010). Beneficial metabolic adaptations due to endurance exercise training in the fasted state. Journal of Applied Physiology, 110(1), pp.236-245.

Yeo, W., Paton, C., Garnham, A., Burke, L., Carey, A. and Hawley, J. (2008). Skeletal muscle adaptation and performance responses to once a day versus twice every second day endurance training regimens. Journal of Applied Physiology, 105(5), pp.1462-1470.

About the Author: Kedric Kwan CISSN

Kedric is a performance nutritionist (CISNN) certified through the International society of sports nutriKedric Kwantion (ISSN) and is currently pursuing his MSc. His researc
h is currently focusing on
carbohydrate and it’s effect on sports performance with a particular interest in the molecular signalling pathways. He has worked with professional football players, powerlifters and endurance athletes but his current clientele consist of strength/power athletes and the general weekend warrior. His aim is to able to translate the ABC soup of complex science into something palatable for the general population. He is also a competitive powerlifter and when he is not spending time nerding over science or lifting heavy weights, he enjoys indulging in ice cream and reading about superheroes. If you enjoy any of the aforementioned things, feel free to drop him a holla!

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


  • 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.


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.


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.


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.


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.


Skeletal Muscle Fiber Hyperplasia


by Jose Antonio PhD.   PREFACE –  It has been about a score (that’s 20 years for those who slept through English 101) since I’ve plastered my myopic eyeballs on to a dissecting microscope and counted skeletal muscle fibers.  Counting muscle fibers is as painful as watching the afternoon gabfest known as The View (yeah, you understand). Actually scratch that.  The View is much more painful.  Either way, I wanted to shed light on a topic that is of interest to many; yet very few are aware of the research that has been published.  I’m one of a handful (perhaps a half-dozen or less) of science nerds that has actually done research on muscle fiber hyperplasia.  To do that, you got to count.  And believe me my friends, you are counting all day and frickin’ night.  It’s like watching ants march in a line.  If you stare at them long enough, you’ll go cross-eyed and eventually blind.  Okay, maybe not blind.  Seriously, why do we do this kind of research?  Ultimately, the question that is always asked is as follows:  Do human beings have the capacity to increase the number of skeletal muscle fibers?  And if so, what’s the mechanism?  For answers to that, read on my friend.

WHAT IS HYPERPLASIA?  Hypertrophy refers to an increase in the size of the cell while hyperplasia refers to an increase in the number of cells or fibers. A single muscle cell is usually called a fiber, muscle fiber or myofiber.  Ok.  You passed Cell Biology 101.  Whew.hyperplasia pics 2_Page_4

HOW DO MUSCLE FIBERS ADAPT TO DIFFERENT TYPES OF EXERCISE?  If you look at a good marathon runner’s physique and compared him/her to a bodybuilder it becomes obvious that training specificity has a profound effect. We know that aerobic training results in an increase in mitochondrial volume/density, oxidative enzymes, and capillary density [1]. Also, in some elite endurance athletes the trained muscle fibers may actually be smaller than those of a completely untrained person. Bodybuilders and other strength-power athletes, on the other hand, have much larger muscles [2, 3]. That’s their primary adaptation; their muscles get bigger. All the cellular machinery related to aerobic metabolism (i.e., mitochondria, oxidative enzymes, etc.) isn’t necessary for maximal gains in skeletal muscle force output; in essence, you just need more contractile protein. We know that this muscle mass increase is due primarily to fiber hypertrophy; however, are there situations where muscles also respond by increasing fiber number?  Ok, you now know the basics of training specificity.  For now, go to the head of the class.  

EVIDENCE FOR SKELETAL MUSCLE FIBER HYPERPLASIA – Scientists have come up with all human-sacrifice-aztecssorts of methods to study muscle growth in laboratory animals. You might wonder what relevance this has to humans. Keep in mind that some of the procedures which scientists perform on animals simply can’t be done on humans due to ethical and logistical reasons. Unless of course you support human sacrifice like the ancient Aztecs.  Nonetheless,  the more convincing data supporting muscle fiber hyperplasia emerges from animal studies. Some human studies have also suggested the occurence of muscle fiber hyperplasia. I’ll address those studies later.  Unless you fall asleep first.

DOES “STRETCH” INDUCE FIBER HYPERPLASIA? Please don’t confuse ‘stretch’ with doing yoga in your Lululemon pants.  Not THAT kind of stretching.  Instead, it’s a more painful type we’re talking about here.  The avian stretch model was first used by Sola et al. in 1973 [4]. In essence, you put a weight on one wing of a bird (usually a chicken or quail) and leave the other wing alone. By putting a weight on one wing (usually equal to 10% of the bird’s weight), a weight-induced stretch is imposed on the back muscles. The muscle which is usually hyperplasia pics 2_Page_2examined is the anterior latissimus dorsi or ALD (unlike humans, birds have an anterior and posterior latissimus dorsi). Besides the expected observation that the individual fibers grew under this stress, Sola et al. found that this method of overload resulted in a 16% increase in ALD muscle fiber number. Since the work of Sola, numerous smarty-pants science types have used this model [5-20]. For example, Alway et al. [5] showed that 30 days of chronic stretch (i.e., 30 days with the weight on with NO REST) resulted in a 172% increase in ALD muscle mass and a 52-75% increase in muscle fiber number! Imagine if humans could grow that fast.  Yeah.  And imagine if Kate Upton shows up at your next birthday party.

I also performed a study using the avian stretch model. However, I put a significant twist on this model [10].  I used a progressive overload scheme whereby the ALD was initially loaded with a weight equal to 10% of the bird’s body weight followed by increments of 15%, 20%, 25%, and 35% (of the bird’s body weight) (5). Each weight increment was interspersed with a 2-day rest. The total number of stretch days was 28.  Using this approach produced the greatest gains in muscle mass EVER recorded in an animal or human model of tension-induced overload, up to a 334% increase in muscle mass with up to a 90% increase in fiber number.  I was also able to uncouple the hypertrophic and hyperplastic responses.  Meaning that the muscle fibers undergoing progressive stretch overload actually increased muscle fiber size at first, and then underwent hyperplasia secondarily.  Perhaps the muscle fibers reached a critical cell size (upon which further increases in muscle fiber cross-sectional areas would have compromised the ability of the cell to obtain nutrients).  If you look at the light micrograph below, you will see that ginormous fiber in panel “B” labeled with an asterisk.  Just think.  Back then, the word ginormous didn’t exist.  Now I actually have an excuse to use the word.  Anyhow, that muscle fiber is the largest EVER in the published literature.  But you’ll notice the fissures in it (see the arrow pointing at the fissure).  Perhaps it’s splitting into smaller parts. That’s evidence of muscle fiber splitting.   I mean come on.  You can only get SO BIG.Muscle fiber hyperplasia pic

But you might ask yourself, what does hanging a weight on a bird have to do with humans who lift weights? So who cares if birds can increase muscle mass by over 300% and fiber number by 90%.  To the naked eye, you seem to have a good point.  But if you care about the mechanisms that regulate skeletal muscle size, than I would highly recommend you drink a bit more coffee and pay attention.   Certainly, nobody out there hangs weights on their arms for 30 days straight or even 30 minutes for that matter. Maybe you should try it and see what happens. This could be a different albeit painful way to “train.” But actually the physiologically interesting point is that if presented with an appropriate stimulus, a muscle can produce more fibers. What is an appropriate stimulus? I think it is one that involves subjecting muscle fibers to high tension overload (enough to induce injury) followed by a regenerative period.  Can you get hypertrophy without injury or damage?  Yes.  I’d surmise that inducing actual damage to the sarcolemma, Z-lines, etc is the ‘best’ way to ultimately promote growth.

SIDE BAR – Intraset Stretching by Jacob Wilson PhD – Dr Wilson (at the University of Tampa) has taken the basic science work that I’ve done and applied it to the human condition. Check this out! http://www.bodybuilding.com/fun/jake-wilsons-project-mass-intraset-stretching.html

WHAT ABOUT EXERCISE? The stretch induced method is a rather unusual stimulus compared to normal muscle activity. What about “normal” muscular exercise? Several scientists have used various models of  ‘tension overload’ to study the role of muscle fiber hyperplasia in muscular growth [5-11, 18-39]. Dr. William Gonyea was the first to demonstrate exercised-induced muscle fiber hyperplasia using weight-lifting cats as the model [25, 28, 29, 40]. Cats were trained to perform a wrist flexion exercise with one forelimb against resistance in order to receive a food reward. The non-trained forelimb thus served as a control for comparison. Resistance was increased as the training period progressed. He found that in addition to hypertrophy, the forearm muscle (flexor carpi radialis) of these cats increased fiber number from 9-20%. After examining the training variables that predicted muscle hypertrophy the best, scientists from Dr. Gonyea’s laboratory found that lifting speed had the highest correlation to changes in muscle mass (i.e., cats which lifted the weight in a slow and deliberate manner made greater muscle mass gains than cats that lifted ballistically) [41].

Keep in mind that these cats trained in a normal manner.  It wasn’t like they were doing crazy high volume or weight.  Thus, it would seem reasonable that heavy resistance training (when done reasonably hard) in humans could also result in gains in muscle fiber number.  To suggest that you need to kill yourself by training like a maniac just isn’t supported by the cat weight-lifting data.hyperplasia pics 2_Page_1

Rats have also been used to study muscle growth [32, 34, 42]. In a model developed by Japanese researchers [34], rats performed a squat exercise in response to an electrical stimulation. They found that fiber number in the plantaris muscle (a plantar flexor muscle on the posterior side of the leg) increased by 14%. Moreover, an interesting observation has been made in hypertrophied muscle which suggests the occurrence of muscle fiber rat lifting weightshyperplasia [16, 22, 23, 42, 43]. Individual small fibers have been seen frequently in enlarged muscle. Initially, some researchers believed this to be a sign of muscle fiber atrophy. However, it doesn’t make any sense for muscle fibers to atrophy while the muscle as a whole hypertrophies. Instead, it seems more sensible to attribute this phenomenon to de novo formation of muscle fibers (i.e., these are newly made fibers). I believe this is another piece of evidence, albeit indirect, which supports the occurrence of muscle fiber hyperplasia.

EXERCISE-INDUCED GROWTH IN HUMANS – The main problem with human studies to determine if muscle fiber hyperplasia contributes to muscle hypertrophy is the inability to make direct counts of human muscle fibers. Some would rather stick a fork in their eye than count muscle fibers.  And a mere perusal through the published literature shows indeed how rare studies are that do direct muscle fiber counts or count the fibers in an entire histological cross-section(s).  Heck, you’d have a better chance of finding a McDonalds in North Korea than finding a graduate student or PhD willing to do muscle fiber counts.   For instance, one study how-to-build-arm-muscles1determined that the tibialis anterior muscle contains approximately 160,000 fibers. Imagine counting 160,000 fibers [44] for just one muscle! The biceps brachii muscle contains roughly a quarter of a million muscle fibers [45].  One study found it to be as high as 418,884 [46].

SIDE BAR – Do we lose muscle fibers with age? Apparently we don’t.  Amen to that!  According to a study by Klein et al:  “We have compared the number of muscle fibers in the biceps brachii muscle (BB) of six old men (82.3 +/- 4.3 years) and six young men (21.2 +/- 1.9 years). Muscle fiber number was estimated by dividing the maximal area of the BB, determined with magnetic resonance imaging, by the mean fiber area of the BB determined in a muscle biopsy. The percentage of type II fibers in the BB (approximately 60%) and the type I fiber area were not different between the groups. The BB area (-26%), type II fiber area (-24%), mean fiber area (-20%), and maximal voluntary contraction strength (MVC) of the elbow flexor muscles (-27%) were lower in the old than young group. However, the estimated number of muscle fibers was not significantly different between the young (253000) and old (234000) men. Consequently, the smaller BB area of the old men could be explained primarily by a smaller type II fiber size. These findings suggest that old age is not associated with a reduced number of muscle fibers in the BB. The relative contribution of a reduction in fiber number to age-related muscle atrophy may be muscle-dependent[45].”

So how do human studies come up with evidence for hyperplasia? It’s arrived at in an indirect fashion. For instance, one study showed that elite bodybuilders and powerlifters had arm circumferences 27% greater than normal sedentary controls yet the size (i.e., cross-sectional area) of athlete’s muscle fibers (in the triceps brachii m.) were not different than the control group. The investigators stated that “Despite large differences in elbow extension strength and arm girth there was no significant difference in fibre areas or percentages of fibre types between the elite group and the trained controls[47].”  This of course suggests that the elite group had a greater number of skeletal muscle fibers.Mike_Ashley_fullbody  Nygaard and Neilsen [48] did a cross-sectional study in which they found that swimmers had smaller Type I and IIa fibers in the deltoid muscle when compared to controls despite the fact that the overall size of the deltoid muscle was greater. Larsson and Tesch [49] found that bodybuilders possessed thigh circumference measurements 19% greater than controls yet the average size of their muscle fibers were not different from the controls. Furthermore, Alway et al. [26] compared the biceps brachii muscle in elite male and female bodybuilders. They showed that the cross-sectional area of the biceps muscle was correlated to both fiber area and number. Other studies, on the other hand, have demonstrated that bodybuilders have larger fibers instead of a greater number of fibers when compared to a control population [46, 50, 51]. Some scientists have suggested that the reason many bodybuilders or other athletes have muscle fibers which are the same size (or smaller) versus untrained controls is due to a greater genetic endowment of muscle fibers. That is, they were born with more fibers. If that was true, then the intense training over years and decades performed by elite bodybuilders has produced at best average size fibers. That means, some bodybuilders were born with a bunch of below average size fibers and training enlarged them to average size. I don’t know about you, but I’d find that explanation rather tenuous. Actually, that explanation is just plain dopey.  It would seem more plausible (and scientifically defensible) that the larger muscle mass seen in bodybuilders is due primarily to muscle fiber hypertrophy but also to fiber hyperplasia. So the question that needs to be asked is not whether muscle fiber hyperplasia occurs, but rather under what conditions does it occur. I believe the the scientific evidence shows clearly in animals, and indirectly in humans, that fiber number can increase. Does it occur in every situation where a muscle is enlarging? No. But can it contribute to muscle mass increases? Yes.

HOW DOES MUCLE FIBER HYPERPLASIA OCCUR? There are two primary mechanisms in

Check out these 'split' or branching fibers.

Check out these ‘split’ or branching fibers.

which new fibers can be formed. First, large fibers can split into two or more smaller fibers (i.e., fiber splitting) [8, 10, 32, 34].  And perhaps the primary mechanism is via the activation and proliferation of satellite cells [18-20, 23, 52, 53].  Satellite cells are myogenic stem cells which are involved in skeletal muscle regeneration. When you injure, stretch, or severely exercise a muscle fiber, satellite cells are activated [18-20, 53]. Satellite cells proliferate (i.e., undergo mitosis or cell division) and give rise to new myoblastic cells (i.e., immature muscle cells). These new myoblastic cells can either fuse with an existing muscle fiber causing that fiber to get bigger (i.e., hypertrophy) or these myoblastic cells can fuse with each other to form a new fiber (i.e., hyperplasia).

ROLE OF MUSCLE FIBER DAMAGE – There is robust evidence which has shown the importance of eccentric contractions in producing muscle hypertrophy [54-57]. It is known that eccentric contractions produces greater injury than concentric or isometric contractions. We also know that if you can induce muscle fiber injury, satellite cells are activated. Both animal and human studies point to the superiority of eccentric contractions in increasing muscle mass [55-57]. However, in the real world, we don’t do pure eccentric, concentric, or isometric contractions. We do a combination of all three. So the main thing to keep in mind when performing an exercise is to allow a controlled descent of the weight hyperplasia pics 2_Page_3being lifted. And on occasion, one could have his/her training partner load more weight than can be lifted concentrically and spot him/her while he/she performs a pure eccentric contraction. This will really put your muscle fibers under a great deal of tension causing microtears and severe delayed-onset muscle soreness. Thus, the repeated process of injuring your fibers (via weight training) followed by a recuperation or regeneration may result in an overcompensation of protein synthesis resulting in a net anabolic effect [58][59].

SIDE BAR:  THE MYTH OF SARCOPLASMIC VS MYOFIBRILLAR HYPERTROPHY – This is perhaps one of the more annoying and contrived controversies in the field of skeletal muscle plasticity.  Was it Joseph Goebbels who said that “if you repeat a lie often enough, it becomes the truth”? This is a perfect example of this maxim.   Frankly, I don’t give a shit who started this mythical beast known as sarcoplasmic hypertrophy.  The fact of the matter is there has never been evidence to suggest that increases in skeletal muscle size can be the result of selective hypertrophy of the sarcoplasm.  It’s not like you can train to increase the sarcoplasm one day; and then the next day, train for myofibrillar growth.  Roughly 70-80% of the volume of a muscle fiber is the myofibrillar component.  It should be as clear as the Montana sky that gains in muscle size are largely due to increases in contractile protein.  In fact there is a classic paper by Claassen et al. (Journal of Physiology, 1989, 409: 491-495) entitled “Muscle Filament Spacing and Short-term Heavy-Resistance Exercise in Humans.”  They found that the “linear distance between myofilaments as well as the ratio of actin to myosin filament did not change with training.”  Mythbusters (1)So the next time you hear a bodybuilder or training guru talk about achieving greater ‘muscle density,’ they’re just making shit up.  And while you’re at it, if you like your doctor you can keep your doctor.  And if you like your healthcare plan, you can keep it. Moreover, don’t confuse gains in strength without gains in skeletal muscle size as evidence for sarcoplasmic hypertrophy.  As my teenage daughter would say, ‘isn’t it obvy?’  Yes, it is obvy (obvious) that improvements in rate coding, muscle activation patterns and motor unit recruitment do indeed account for changes in strength without a concomitant increase in skeletal muscle size.  However, if someone shows me evidence that an enlarged muscle or muscle fiber has an increase in cytoplasm with no change in the volume of actin and myosin, then I’ll alter my conclusions.  Until then, show me the evidence.  And if it doesn’t exist, then quit bs’ing everyone about ‘sarcoplasmic’ hypertrophy.  What’s next?  Pigs flying, unicorns trotting, the Jets winning?  For another opinion, check out Stu Phillips PhD little ditty:  https://twitpl.us/t/4Xeb

HAS THE HYPERPLASIA DEBATE BEEN SETTLED?  To quote the genius of Yogi Berra, “I wish I had an answer to that because I’m tired of answering that question.”  In my scientific opinion, this issue has already been settled. Muscle fiber hyperplasia can contribute to whole muscle hypertrophy. There is human as well as rat, cat, and bird data which support this proposition [6-10, 20, 23, 25, 28, 32-34, 47, 60-66], a veritable wild kingdom of evidence. Does muscle fiber hyperplasia occur under all circumstances? No. There are several studies which show no change in fiber number despite significant increases in muscle mass [11, 13, 37, 67]. Is it possible that certain muscles can increase fiber number more so than others? Maybe. Can any Joe Schmoe off the street who lifts weights to get in better shape increase the number of fibers for instance in their biceps? Maybe, maybe not. What about the elite bodybuilder who at 5’8″ tall is ripped at a body weight of 250 lbs.? Are his large muscles purely the result of muscle fiber hypertrophy? I think it would be extremely naive to think that the massive size attained by elite bodybuilders is due solely to fiber hypertrophy.  Despite the contention that fiber number is constant once you’re born, there is an abundance of evidence which shows that muscle fiber number can increase post-natally.

Always wondered how much hyperplasia could occur in the gluteus maximus.  Hmmm...

Always wondered how much hyperplasia could occur in the gluteus maximus. One, two, 5999, 190000, 699699, oh my…keep counting.

Besides, there is nothing magical at birth which says that now that you’re out of the womb, you can no longer make more muscle fibers. A mechanism exists for muscle fiber hyperplasia and there is plenty of reason to believe that it occurs. Of course, the issue is not whether fiber number increases after every training program, stress, or perturbation is imposed upon an animal (or human). The issue is again, under which circumstances is it most likely to occur. For humans, I’d surmise that the average person who lifts weights and increases their muscle mass moderately probably won’t induce fiber hyperplasia in their exercised muscle(s).  Yet I imagine there are exceptions.  However, the elite bodybuilder who attains the massive muscular development now seen may be the more likely candidate for exercise-induced muscle fiber hyperplasia. If you are interested in a comprehensive scientific treatise on this subject, read a scientific review article that I wrote way back when Bill Clinton was President of the USA [9].  It still holds true today.


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63.     Alway SE: Stretch induces non-uniform isomyosin expression in the quail anterior latissimus dorsi muscle. Anat Rec 1993, 237:1-7.

64.     Alway SE: Perpetuation of muscle fibers after removal of stretch in the Japanese quail. Am J Physiol 1991, 260:C400-408.

65.     Sjostrom M, Lexell J, Eriksson A, Taylor CC: Evidence of fibre hyperplasia in human skeletal muscles from healthy young men? A left-right comparison of the fibre number in whole anterior tibialis muscles. Eur J Appl Physiol Occup Physiol 1991, 62:301-304.

66.     Tamaki T, Akatsuka A, Tokunaga M, Ishige K, Uchiyama S, Shiraishi T: Morphological and biochemical evidence of muscle hyperplasia following weight-lifting exercise in rats. Am J Physiol 1997, 273:C246-256.

67.     McCall GE, Byrnes WC, Dickinson A, Pattany PM, Fleck SJ: Muscle fiber hypertrophy, hyperplasia, and capillary density in college men after resistance training. J Appl Physiol (1985) 1996, 81:2004-2012.

About the Author – Jose Antonio PhD is the CEO of the ISSN, www.theissn.org.  His published work is in the area of sports nutrition and skeletal muscle plasticity.  When he’s not writing, he’s probably watching football or MMA. Or better yet, he’s probably on the ocean paddling like a ninja master.  Doug me and Staci Aug 2009 paddling

HMB Free Acid and The Misunderstood Relationship Between Training and Supplements


By Jacob M. Wilson, Ph.D., CSCS*D and Ryan Lowery, B.S., CSCS.   Ryan Lowery and I are speaking at this years ISSN, and we have to admit that the lineup is stellar.  Our discussion will focus on novel methods to enhance fat metabolism on Saturday morning at 11:00 AM.  Prior to our discussion at 9:00 AM on Saturday, Dr. Gabe Wilson and Shawn Wells  will be talking about one of the most heated, and highly debated subjects in sports nutrition for the last decade.  The title of their talk is “Leucine, HMB, and Amino Acid Metabolites Support Muscle Growth and Athletic Performance.”  One of the key controversial components is in bold letters – that’s right, HMB.MT-HMB3

Part of the controversy stems from how the companies marketed the product years ago and mis-portrayed the practicality of the supplement at hand.  For instance, advertisers claiming that HMB “feels like DECA” or works like testosterone. Additional issues lie in contradictory results between studies, with some showing improvements in performance markers, and others showing no benefit from HMB. This subject is of great interest to us, which is why we have spent literally the last decade studying this topic.  In fact, we have studied HMB in trained (6, 13, 14) and untrained humans (12); the elderly (8); rats and mice (3, 11), and yes, even hamsters! There is certainly a complicated history to this supplement…so sit back and get ready to hear the full story.

HMB was first introduced to the market in the early 90s by EAS.  Fast forward a few decades later, and the supplement has been studied in virtually every condition possible.  What has been demonstrated from our research and others is that HMB works by improving protein synthesis and reducing protein breakdown that occurs within the muscle following intense exercise; thereby, accelerating the recovery process.  Adel from Suppversity suggests that often times the anabolic effects of HMB are mistaken for its anti-catabolic properties, which are fully realized under novel conditions.  The major problem, from people who misinterpret the HMB literature, is that they view supplements as independent from the training stimulus itself.  HOWEVER, this is a major flaw and misconception.  In reality, the field of sports nutrition is all about how the supplement interacts with the training stimulus.  Take HMB for example, it has anti-catabolic and recovery properties.  We can virtually guarantee that if you are taking HMB as a sedentary young, healthy individual, or as someone who does not train hard that you will see virtually no benefits (10).  In fact, it is these people who are most likely to state that “they didn’t feel anything” while taking HMB. Considering that HMB is not a stimulant and they had no muscle damage to recover from, we are not surprised at this comment.

Before we can delve deeper into HMB supplementation, we need to discuss the training stimulus itself. As eluded too, HMB works ideally under novel training conditions.  Most people view gains in muscle and strength as a linear process over time.  However when examining long-term training studies, it is clear that people do not make linear gains –  rather, they make large gains in short bursts of time with the remainder of time spent in maintenance(2).  What triggers these growth spurts is the introduction of novel training variables.  Periodization is defined as programed variation and rest to reach a physiological peak.  Research indicates that periodized training, regardless of the form results in greater neuromuscular gains than non periodized protocols.

Intriguingly enough HMB has been studied in both untrained and trained individuals using periodized as well non periodized training programs.  In the 90s, it was demonstrated that untrained individuals attained greater muscle and strength gains while taking HMB (7), but this should be expected because even looking at a squat rack in an untrained population provides a novel stimulus for growth! However, early studies on HMB in trained individuals failed to find a beneficial result (5).  If you carefully examine the landmark papers on this topic, the reason for a lack of benefit from HMB, may be that the novelty of the training stimulus was inadequate.  In fact, in these studies, investigators told subjects to not alter their training programs (5).  This is great research because it led us to the understanding that HMB likely interacts with the training stimulus itself (10).  Our hypothesis was supported by William Kraemer’s lab, which demonstrated that HMB given during a 12-week periodized training program resulted in ~ 9 kg gains in lean body mass compared to only ~ 2 kg in the placebo group (4). In this scenario where the training stimulus is altered continually, HMB’s regenerative and anti-catabolic properties are able to improve neuromuscular adaptations.  It is important to emphasize here that it is the interaction between optimal training variables and HMB supplementation that triggers the growth and strength adaptations (4).  In so much as, HMB will support recovery so that the athlete is better prepared to workout during each successive bout compared to their non-supplemented counterparts.

HMB-Free-AcidModern research has sought to improve the delivery of HMB supplementation (1).  Specifically, HMB has historically been administered as calcium bound to HMB, which results in peak plasma concentrations in 90 to 120 minutes (9).  However, recent research has used an HMB free acid (HMB separated from calcium) which peaks in as little as 30 minutes and results in a 100% greater total increases in plasma HMB than the HMB-calcium bound supplement (1).  Theoretically, HMB free acid (trademarked BetaTOR) may result in improved anabolic effects relative to the calcium salt. Therefore, our lab recently published a paper in the British Journal of Nutrition, which investigated HMB free acid’s impact on skeletal muscle recovery following a strenuous training session, in advanced resistance trained individuals (14). Results showed that BetaTOR was able to cut muscle damage and soreness in half relative to placebo as well as lower protein breakdown. To follow up on these findings, our lab published work in the European Journal of Applied Physiology, using a long-term periodization program (13). In this experiment, we sought to use advanced athletes, as this is one of the most controversial populations in terms of HMB’s effectiveness.  Indeed, our criteria were quite stringent, and in fact took a full school semester to recruit the desired population. In the end, elite athletes – many of which were able to squat over 500 lbs, and deadlift over 600 lbs – were identified, and put through a rigorous 12-week training program, while taking BetaTOR or a placebo.

To elaborate, we used a 3-phase training protocol.  Phase one (weeks 1-8) consisted of periodization in which subjects trained each body part 3 times weekly, while varying the repetitions, intensity, and rest period lengths daily. We also provided slight variations in the way in which the exercise was executed every 4 weeks (e.g. overhand vs. underhand bent over rows).  Results demonstrated that this training stimulus was enough to maintain muscle damage for a period of 8 weeks, suggesting that the training load was novel to these athletes.  However, at week 8, the athletes began to adapt to the training stimulus.  At this point, we had them train every body part 5 days a week for 2 weeks straight (phase 2).  In fact, some subjects lifted over 200, 000 lbs of total volume in a given week! Lastly, we decreased volume by 60% (tapered – phase 3), while maintaining training intensity and frequency, in order to allow them to recover before final testing.  We found that during weeks 1-8, both groups made improvements; however, the BetaTOR group made greater gains (5 vs. 3 kg of lean mass). However, phase two is where separation really occurred between groups.  In fact, the placebo group regressed in performance and lean mass from weeks 8-12, while the BetaTOR group continued to increase!  Thus, a training load, which was catabolic in nature, became stimulatory when consuming BetaTOR.  For this reason, we would argue that HMB is not necessarily making individuals huge by itself.  Rather, HMB is allowing an individual to train at higher intensities more frequently.  Thus, allowing for a greater training stimulus and improved recovery! It is the ability to train more, and recover faster that allows individuals to make greater gains with HMB. Clearly, if you are not pushing yourself to this limit, HMB will not be an effective supplement.

In conclusion, we hope to educate the consumer of what it truly takes in order to optimize HMB’s and BetaTOR’s effects.  Research indicates that HMB has little benefit for the everyday individual just looking to go in the gym and train their arms and calves every other workout. Rather, HMB is most effective for athletes undergoing difficult and novel training demands.  For more information on this exciting and controversial topic, as well as leucine and other metabolites of the amino acid leucine, we suggest that you attend Dr. Gabe Wilson and Shawn Wells lecture at the annual ISSN conference on Saturday morning at 9:00 AM.


1.           Fuller JC, Jr., Sharp RL, Angus HF, Baier SM, and Rathmacher JA. Free acid gel form of beta-hydroxy-beta-methylbutyrate (HMB) improves HMB clearance from plasma in human subjects compared with the calcium HMB salt. The British journal of nutrition 105: 367-372, 2011.

2.           Hakkinen K, Pakarinen A, Alen M, Kauhanen H, and Komi PV. Neuromuscular and hormonal adaptations in athletes to strength training in two years. J Appl Physiol 65: 2406-2412, 1988.

3.           Henning PC, Park B-S, Lee S-R, Wilson JM, Park Y-M, Arjmandi BH, Grant SC, and Kim J-S. β-hydroxy-β-methylbutyrate (HMB) Improves Muscle Mass And Protein Turnover In Male Mice During A 6-week Catabolic Condition.  , in: American College of Sports Medicine. Washington D.C.: Medicine and Science in Sports and Exercise 2011, p 137.

4.           Kraemer WJ, Hatfield DL, Volek JS, Fragala MS, Vingren JL, Anderson JM, Spiering BA, Thomas GA, Ho JY, Quann EE, Izquierdo M, Hakkinen K, and Maresh CM. Effects of amino acids supplement on physiological adaptations to resistance training. Med Sci Sports Exerc 41: 1111-1121, 2009.

5.           Kreider RB, Ferreira M, Wilson M, and Almada AL. Effects of calcium beta-hydroxy-beta-methylbutyrate (HMB) supplementation during resistance-training on markers of catabolism, body composition and strength. Int J Sports Med 20: 503-509, 1999.

6.           Lowery RP, Joy JM, Rathmacher JA, Baier SM, Fuller J, Jr., Shelley MC, 2nd, Jaeger R, Purpura M, Wilson SM, and Wilson JM. Interaction of Beta-Hydroxy-Beta-Methylbutyrate Free Acid (HMB-FA) and Adenosine Triphosphate (ATP) on Muscle Mass, Strength, and Power in Resistance Trained Individuals. Journal of strength and conditioning research / National Strength & Conditioning Association, 2014.

7.           Nissen S, Sharp R, Ray M, Rathmacher JA, Rice D, Fuller JC, Jr., Connelly AS, and Abumrad N. Effect of leucine metabolite beta-hydroxy-beta-methylbutyrate on muscle metabolism during resistance-exercise training. Journal of applied physiology 81: 2095-2104, 1996.

8.           Stout JR, Smith-Ryan AE, Fukuda DH, Kendall KL, Moon JR, Hoffman JR, Wilson JM, Oliver JS, and Mustad VA. Effect of calcium beta-hydroxy-beta-methylbutyrate (CaHMB) with and without resistance training in men and women 65+yrs: a randomized, double-blind pilot trial. Experimental gerontology 48: 1303-1310, 2013.

9.           Vukovich MD, Slater G, Macchi MB, Turner MJ, Fallon K, Boston T, and Rathmacher J. beta-hydroxy-beta-methylbutyrate (HMB) kinetics and the influence of glucose ingestion in humans. The Journal of nutritional biochemistry 12: 631-639, 2001.

10.         Wilson JM, Fitschen PJ, Campbell B, Wilson GJ, Zanchi N, Taylor L, Wilborn C, Kalman DS, Stout JR, Hoffman JR, Ziegenfuss TN, Lopez HL, Kreider RB, Smith-Ryan AE, and Antonio J. International Society of Sports Nutrition Position Stand: beta-hydroxy-beta-methylbutyrate (HMB). Journal of the International Society of Sports Nutrition 10: 6, 2013.

11.         Wilson JM, Grant SC, Lee SR, Masad IS, Park YM, Henning PC, Stout JR, Loenneke JP, Arjmandi BH, Panton LB, and Kim JS. Beta-hydroxy-beta-methyl-butyrate blunts negative age-related changes in body composition, functionality and myofiber dimensions in rats. Journal of the International Society of Sports Nutrition 9: 18, 2012.

12.         Wilson JM, Kim JS, Lee SR, Rathmacher JA, Dalmau B, Kingsley JD, Koch H, Manninen AH, Saadat R, and Panton LB. Acute and timing effects of beta-hydroxy-beta-methylbutyrate (HMB) on indirect markers of skeletal muscle damage. Nutrition & metabolism 6: 6, 2009.

13.         Wilson JM, Lowery RP, Joy JM, Andersen JC, Wilson SM, Stout JR, Duncan N, Fuller JC, Baier SM, Naimo MA, and Rathmacher J. The effects of 12 weeks of beta-hydroxy-beta-methylbutyrate free acid supplementation on muscle mass, strength, and power in resistance-trained individuals: a randomized, double-blind, placebo-controlled study. Eur J Appl Physiol 114: 1217-1227, 2014.

14.         Wilson JM, Lowery RP, Joy JM, Walters JA, Baier SM, Fuller JC, Jr., Stout JR, Norton LE, Sikorski EM, Wilson SM, Duncan NM, Zanchi NE, and Rathmacher J. beta-Hydroxy-beta-methylbutyrate free acid reduces markers of exercise-induced muscle damage and improves recovery in resistance-trained men. The British journal of nutrition 110: 538-544, 2013.

About the authors:

Jacob WJacob Wilson, Ph.D., CSCS*D is an assistant professor and runs the strength & sports nutrition laboratory at the University of Tampa.  Dr. Wilson’s research has covered the cellular, molecular, and whole body changes in muscle size, strength, and power in response to resistance training and nutritional supplementation interventions.  On these topics he has published over 100 peer-reviewed papers, book chapters and abstracts.  He has recently established a new graduate program at University of Tampa dedicated to Sports Nutrition and has previously been awarded the NSCA’s Terry J. Housh young investigator of the year award.

Ryan LRyan P. Lowery, B.S., CSCS is completing his masters degree in sports nutrition at the University of Tampa.  In 2013, Ryan won the National Championship in baseball with the University of Tampa Spartans. Ryan lowery has served as the senior researcher in Dr. Jacob Wilson’s lab the past four years.  Ryan currently has 22 published manuscripts, 3 book chapters, and over 60 published abstracts, and serves as a reviewer for JISSN.  He has received the Exercise Science Student of the Year Award, NSCA Award for Outstanding Presentation, and most recently the National AAHPERD Exercise Science Major of the Year Award.  Ryan’s main areas of focus are sports nutrition and supplementation.




Why Not Fat?

Jordan M. Joy CISSN.  What do we think of when we think of “bad” food? No, not the tastes bad Fear Factor type foods, but the naughty foods we’re discouraged from eating. Desserts, potato chips, hot dogs, deep fried mayonnaise balls, and the list goes on. Generally speaking, we classify fats as “bad,” and we classify sugars as “bad.” I can get behind sugar as bad for the most part (it is beneficial in some situations), but fat as bad? That’s a notion I can’t support.

Why do we, as a society, criminalize dietary fat? Well its NAME is FAT! If we were to just call healthy_high_fat_foods_draft_2them lipids from the get go, they would probably be more accepted. Nomenclature aside, the United States used to support an “eat more” diet, as nutrient deficiencies were highly prevalent in the early 1900’s. However, the progression into our current, overweight society became a concern around the 1960’s, and a globally conducted study associated fat with death rates, while complex carbohydrates were negatively associated. Thus, we now have the recommendation that ~50% of daily calories should come from carbohydrates. Unfortunately, the “complex” portion of carbohydrates has been lost for most individuals, and if trends mean anything, we’re likely worse off than before.

Interestingly, 150g had, at least at one time, been determined to be the minimum amount of carbohydrate necessary for maintenance of health. However, carbohydrates are not an essential nutrient soooo… uhh what? You don’t need them! Your body can actually produce up to 200g of its own carbohydrate per day. Moreover, that global study from I mentioned doesn’t translate to the good ol’ US of A, and the replacement of saturated fat with carbohydrate does NOT lower risk for CHD whereas the replacement of saturated fat with polyunsaturated fat does lower risk for CHD. In addition, there is overwhelming support for a very low carbohydrate, ketogenic diet for improving symptoms of metabolic syndrome. Of course while following a ketogenic diet, dietary fat is much higher than recommended. Fat is not bad on its own. However, fat in combination with sugar reduces fatty acid oxidation. So for the desserts or the potato chips or the hot dogs, is it any one of the nutrients or is it the combination? More evidence is necessary to fully clarify, but so far it seems that it is the combination. So really, why not fat as a primary fuel source?

For most of you or someone you know, the answer is energy systems, and most athletes tend to care about their performance during the ~10-120 second range. Outside the population of competitive athletes, fats are perfectly suitable for composing the primary energy source, and they’re likely beneficial. Thinking of the roles between the two, carbohydrates supply energy and not very much of anything else, while fats have a role in hormone synthesis, vitamin absorption, neural function, and so on. All of these things are critical for athletic performance. The thing about carbohydrates are they’re only needed for high intensity exercise. For the casual 5k runner, they’re not all that important (evidence demonstrates low intensity exercise is not altered by a ketogenic diet), but a soccer player absolutely would benefit. Still, how useful is your mouth guard from pee wee football? Not very because you only need it when you need it. Sugars are the same way; have them during periods of activity and “load” other carbohydrates prior to competition. Have your fat separate from carbohydrates when possible, but certainly don’t fear it.

In short, dietary fat is not to be feared. In all actuality, it seems that sugar exacerbates health problems more so than fat, and it may possibly make fat bad, so just like picking your friends nose, you can have your bacon, and you can have your bagel (whole grain, of course), but you might not want to put your bacon on your bagel.

BIO – Jordan Joy is currently a Research Coordinator at MusclePharm Sports Science Institute. He is a CISSN certified sport nutritionist and CSCS certified strength coach. He has his BS in Exercise Science from the University of Tampa and is pursuing his MS in Applied Nutrition with Northeastern University.


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  • Westman, E. C. (2002). Is dietary carbohydrate essential for human nutrition? The American journal of clinical nutrition, 75(5), 951-953.
  • Astrup, A., Dyerberg, J., Elwood, P., Hermansen, K., Hu, F. B., Jakobsen, M. U. & Willett, W. C. (2011). The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010 The American journal of clinical nutrition, 93(4), 684-688.
  • Volek, J. S., & Feinman, R. D. (2005). Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction. Nutr Metab (Lond), 2(1), 31.
  • Phinney, S. D. (2004). Ketogenic diets and physical performance. Nutr Metab (Lond), 1(1), 2.

An Ode to Nutrient Timing


By Jose Antonio PhD FISSN FNSCA CSCS.  A few weeks back, one of my students asked me about a recent meta-analysis published in the Journal of the International Society of Sports Nutrition.  It was a well-written piece authored primarily by Brad Schoenfeld who is perhaps better known for his Lookgreatnaked.com website.  I mean who wouldn’t want to look frickin’ great naked, right?  Like the old Seinfeld comedy TV show demonstrated so poignantly, there’s ‘good naked’ and ‘bad naked.’  I’m a big fan of ‘good naked.’  Anyhow, the student posited the following:  “I read that nutrient timing doesn’t work according to that study published in the JISSN.”  JISSN is aka the Journal of the International Society of Sports Nutrition.  It’s an awesome scientific journal.  Besides, I’m the Editor in Chief.  And that’s reason enough to read it. :-)  Anyhow, getting back to my student’s query.  So much to learn, so little time.  Without delving into the minutae of different types of studies, I replied “that was a meta-analysis, not an original investigation.”  Mainstream journalists don’t realize that a meta-analysis does not provide new data.  It is merely a statistical analysis of existing data.  This is a huge difference.  The gold standard of scientific inquriy is the randomized controlled trial.   Either way.  This Millennial generation seems to believe everything they read; until of course they read something contrary.  No wonder they can’t make up their minds.

Bruce Lee says, "Timing is everything.  Especially when kicking someone's ass."

Bruce Lee says, “Timing is everything. Especially when kicking someone’s ass.”

So what gives?  What’s the devil in the details?  First, to summarize that meta-analysis, it stated in essence: “These results refute the commonly held belief that the timing of protein intake in and around a training session is critical to muscular adaptations and indicate that consuming adequate protein in combination with resistance exercise is the key factor for maximizing muscle protein accretion.[1]  In English, that means that protein timing is of no benefit and that the key factor is total protein intake.  Interestingly, in their Discussion, it is also stated that they “must acknowledge the possibility that protein timing was in fact responsible for producing a positive effect and that the associated increase in protein intake is merely coincidental.”  It makes sense that both timing and total protein intake are important.

Take the hypothetical scenario of a 180 pound man who consumes 180 grams of protein daily (to meet his athletic needs etc).  Would consuming all 180 grams at breakfast be as effective as spreading it out over 6 meals (30 grams every 3 hours)?  Uh hell no. What fool would eat like that? So when you eat (i.e. timing) is a critical factor.

Please note the distinction between protein timing with the sole purpose of promoting skeletal muscle hypertrophy and nutrient timing, which encompasses a variety of strategies that are related to performance and recovery.  I’ll get to what constitutes nutrient timing later.  But first let me shed some light on the issue of protein timing specifically.nutrient timing photo

In reality, there are only two studies, using resistance-trained subjects, whose protein intake was sufficiently high (1.8-1.9 g per kg per day) and matched, that employed a ‘protein timing’ strategy.  Please note however that most studies, for reasons that are too detailed to be covered here, typically compared protein to carbohydrate.  Those studies are quite important for historical reasons.  One day I’ll explain why over some beer and sushi.

Nevertheless, these two ‘protein timing’ studies were done by Paul Cribb PhD FISSN and Jay Hoffman PhD FISSN, respectively.  These were ‘apples to apples’ comparisons.  Not aardvark to orangutan comparisons (which in reality is most of what is called ‘protein timing’).  The Cribb study did indeed show a significant effect of immediate PRE and POST training supplementation working quite well (i.e. increased lean body mass and type IIA and IIX muscle fiber cross-sectional areas) in comparison to a Morning and Evening consumption strategy.  So in this case, timing matters.  Dr. Cribb concluded that “supplement timing represents a simple but effective strategy that enhances the adaptations desired from RE-training.[2]”  On the other hand, Dr. Hoffman basically replicated this study design and found that the “time of protein-supplement ingestion in resistance-trained athletes during a 10-wk training program does not provide any added benefit to strength, power, or body-composition changes.[3]”  So it either helps or has no effect, right? If you answered yes, you get 5 extra credit points on your final exam.

A simple maxim that I teach my students to follow vis a vis sports nutrition strategies is as follows:  “If it helps or has a neutral effect, try it.” Or better yet, do it.  So if you go beyond the mere dotting of i’s and crossing of t’s, you’d ask yourself the following questions.  1)  Is there any advantage to NOT utilizing a protein timing strategy?  Answer: No.  2) Is there a potential benefit to using a protein timing strategy? If you answered ‘yes,’ then go to the head of the class.  There is no downside to protein timing as a strategy.  In fact, take the common scenario of eating every three hours.  Let’s say meal 1, 2, and 3 are at 6am, 9am and 12noon.  Then you train at 3pm-4pm.  Wouldn’t it make sense to consume a protein-containing meal immediately after training?  That would make your fourth meal of the day consumed at 4pm.  Not quite every three hours.  However imagine waiting four hours post-training?  Why on Earth would anyone do that?  Hence, follow my advice and consume your meal immediately post-training at 4pm.  Then eat your regular dinner (i.e. meal #5) around 6-7pm.  Then around 9-10pm, have another small casein-based protein meal.

To give the ‘advice’ that it is useless or ineffective is a bit of an untruth (that’s Washington DC political-speak if you get my drift).  Even if something is marginally helpful, it is still helpful.  If one’s goal is to promote muscle hypertrophy, why wouldn’t you employ every possible tactic to get to your goal?  From a purely pragmatic standpoint, you should employ protein timing.

Now getting back to ‘nutrient timing.’   Folks have summarily dismissed nutrient timing because of their confusion with protein timing as it relates to skeletal muscle hypertrophy.  Nutrient timing is a very effective strategy.  To wit:

Consuming caffeine (in the form of a chewing gum) enhances cycling performance when administered immediately prior to, but not 1 or 2 hours before cycling.[4]

A 20 gram bolus of whey protein consumed every three hours is superior to other temporal patterns of feeding for the purpose of stimulating muscle protein synthesis and thus “has the potential to maximize outcomes of resistance training for attaining peak muscle mass.[5]”whey-protein-drinks-06

Consuming a sports drink 30 minutes before exercise improved performance better than consuming it 120 minutes prior. “This study provides new evidence to suggest that timing of carbohydrate intake is important in short duration high-intensity exercise tasks, but a concentration effect requires further exploration.[6]”  Certainly, it is well known that consuming a sports drink during exercise is better than drinking water. Thus, a “carbohydrate-electrolyte drink can increase endurance performance as well as enhance lactate removal and thereby delaying the onset of fatigue.[7]”

Another study showed that casein “protein ingested immediately before sleep is effectively digested and absorbed, thereby stimulating muscle protein synthesis and improving whole-body protein balance during postexercise overnight recovery.[8]”

In overweight individuals, shifting more of your calories towards breakfast versus later in the day is better for weight loss.[9]

Heck, common sense tells you that drinking water during a half-marathon run in the heat is better for performance than drinking after the run.  That’s a simple example of nutrient timing.

Thus, it is virtually impossible to escape the fact that nutrient timing plays an important role in many circumstances vis a vis the acute and chronic response to exercise.

I’d posit that not eating is the worst thing you can do.  Let’s face, there is nothing anabolic about not eating for 4 hours after training.  When in doubt, consume a protein-containing meal.  A meal doesn’t have to be a Thanksgiving-size portion.  A protein shake of 200 kcals or so constitutes a meal.  In essence, nutrient timing incorporates the use of methodical planning and eating of whole foods, beverages and supplements with the express purpose of enhancing recovery, performance, or body composition.[10]

One last note.  Science often reminds me of the tale of the six blind men and the elephant.  The tale goes like this.  One blind man feels the trunk and says it’s a snake.  Another touches the tail and says it’s a rope.  Another touches the legs and says it’s a tree. Another touches the ear and says it’s a fan.  Another touches the side of the animal and says it’s a wall.  While another grabs the tusks and says it’s a spear.  All of them are right…and wrong.  Don’t lose sight of the forest for the trees.

Our field is ultimately one governed by pragmatism.  Having done quite a bit of basic science (animal work particularly) research in my day, I can attest to its importance in understanding the underlying mechanisms that govern why things work the way they do.  However, our field is, when you get down to the nuts and bolts of it, an advice-driven one.  As scientists, we can argue over crossing t’s and dotting i’s, but in the end, we have to give the best advice we know based on the current data of the time.

If it helps or has a neutral effect, do it.


1.           Schoenfeld BJ, Aragon AA, Krieger JW: The effect of protein timing on muscle strength and hypertrophy: a meta-analysis. J Int Soc Sports Nutr 2013, 10:53.

2.           Cribb PJ, Hayes A: Effects of supplement timing and resistance exercise on skeletal muscle hypertrophy. Med Sci Sports Exerc 2006, 38:1918-1925.

3.           Hoffman JR, Ratamess NA, Tranchina CP, Rashti SL, Kang J, Faigenbaum AD: Effect of protein-supplement timing on strength, power, and body-composition changes in resistance-trained men. Int J Sport Nutr Exerc Metab 2009, 19:172-185.

4.           Ryan EJ, Kim CH, Fickes EJ, Williamson M, Muller MD, Barkley JE, Gunstad J, Glickman EL: Caffeine gum and cycling performance: a timing study. J Strength Cond Res 2013, 27:259-264.

5.           Areta JL, Burke LM, Ross ML, Camera DM, West DW, Broad EM, Jeacocke NA, Moore DR, Stellingwerff T, Phillips SM, et al: Timing and distribution of protein ingestion during prolonged recovery from resistance exercise alters myofibrillar protein synthesis. J Physiol 2013, 591:2319-2331.

6.           Galloway SD, Lott MJ, Toulouse LC: Pre-Exercise Carbohydrate Feeding and High-Intensity Exercise Capacity: Effects of Timing of Intake and Carbohydrate Concentration. Int J Sport Nutr Exerc Metab 2013.

7.           Khanna GL, Manna I: Supplementary effect of carbohydrate-electrolyte drink on sports performance, lactate removal & cardiovascular response of athletes. Indian J Med Res 2005, 121:665-669.

8.           Res PT, Groen B, Pennings B, Beelen M, Wallis GA, Gijsen AP, Senden JM, LJ VANL: Protein ingestion before sleep improves postexercise overnight recovery. Med Sci Sports Exerc 2012, 44:1560-1569.

9.           Jakubowicz D, Barnea M, Wainstein J, Froy O: High Caloric intake at breakfast vs. dinner differentially influences weight loss of overweight and obese women. Obesity (Silver Spring) 2013, 21:2504-2512.

10.         Kerksick C, Harvey T, Stout J, Campbell B, Wilborn C, Kreider R, Kalman D, Ziegenfuss T, Lopez H, Landis J, et al: International Society of Sports Nutrition position stand: nutrient timing. J Int Soc Sports Nutr 2008, 5:17.

About the Author – Jose Antonio is the CEO and Co-founder of the International Society of Sports Nutrition and the Editor-in-Chief of the JISSN (www.jissn.com).  Check out the latest ISSN Conferences at www.theissn.org. If you’re ever in South Florida, he’d be happy to take you outrigger paddling.




Tips for Big Guns

by Ramsey Rodriguez CSCS CISSN. Building big arms has been a fascination and/or an obsession for those of us who lift weights.   My bodybuilding and personal training career spans over three decades and I can truly say I learned the most about building big arms while working with Professor Angel Spassov who is one of the best Strength Coaches in the World!  He told me, “I have conquered every sport in the world and Bodybuilding is no different.”  I don’t want to bore you with describing more of the same exercises you have done for your arms.  But, what I will do is offer you some insight that may be new to you and that will help you build your arms.  Before you can build the arms you want; you need to understand what stimulates your arms for growth. The secret is in knowing that the muscle fiber types in the arms, which are composed mostly of slow twitch muscles, are stimulated best with higher reps and lower weights. They do assist in strength exercises like the bench press or power exercises such as the Power Clean; however, when performing an isolation arm exercise such as tricep extensions or bicep curls they function as endurance muscles; therefore, higher reps should be used.

3  Tips to Build Big Arms

  • Use High Rep Sets ((20-25 reps)

(12-15 rep sets  if you are new to using higher rep sets)

  • 6-8total sets (per muscle group) in order to prevent over-training.

NOTE: Only 1-2 exercises should be used.

  • Use Heavy Bench Press work followed by Tricep work for a greater effect (not supersets). The combination of the two provides for greater stimulation and recovery.

3 Mistakes People Make

  • Going Too Heavy! We have all seen the picture of a bodybuilder performing a 225 lb curl – this is just for show and it is definitely not part of his workout-besides it’s not realistic because they are probably using lots of steroids.
  • Too Much Arm Work– Overload the muscles too much and you will not recover!
  • Not Including enough Strength Exercises like pull ups, chin ups, bench press, and dips into your workout.

***Quick Note:  How do you know if its time to change your exercise or sets/reps?  The arms are no longer getting the “pump sensation” while doing your workout.

Now that I have made my opinion based on the education and experience from working closely with one of the smartest Coaches in the World of strength- we need to address the Power of Program design.  People talk a lot about exercises however little seems to be discussed about how it is implemented in a workout program. To do this we need to create a specialized training program for the arms. In order to do this we need to carefully implement acute training variables necessary to create a program of at least 6 weeks (Meso-Cycle).

 Program Design- here is some guidelines in designing a workout program.

Beginner- (0-6 months of serious lifting)


Exercise- Barbell Curls – 3 sets of 12-15 reps

Incline Dumbbell Curls – 3 sets of 12-15 reps

(use only a slight incline-most people create too much angle).


Exercises   Lying Triceps Extensions – 3 sets of 12-15 reps

Seated Triceps Dumbbell Extensions – 3 sets of 12-15 reps

Rest Interval:  60-90 seconds between sets.

Frequency- once a week

Intermediate- 6 months/1 yr. of serious lifting


Exercises- Barbell Curls  3-4 sets of 15-20 reps

Dumbbell Incline Curls – 3-4 sets of 15-20 reps


Exercises- Lying Triceps Extension – 3-4 sets of 15-20 reps

Seated Dumbbell Extension – 3-4 sets of 15-20 reps

Rest Interval:: 1.5-2 minutes between sets.

Frequency:  2 times/week

Note- AA lot of people fall into the category of intermediate training.  Keep.  K in mind while performing these protocols you will need to use lighter weight and rest between sets (rest intervals) of 1.5 minutes (90 sec.)  up to 2 minutes for proper recovery.  These higher reps create an increase of “workload“”; therefore requiring more rest between sets! Only 85% of the ATP energy source is restored in this time, however intensity work of 65-75% is very possible w/ this rest interval.

Advanced- at this stage of training, the program can be more complex; therefore, more “Ingenuity” is required.  Two Important Required Factors:

  1.  If you want to increase arm size, you must be on a weight gain program, the body will NOT grow the arms, if you are not gaining any body weight.
  2. More development can be gained in building the arms by increasing the weight in upper body exercises such as the bench/incline press/s (get stronger) training intensity of 80-90% of a max and high rep Pull ups ( I perform up to 100 pull ups per workout).


(NOTE: if you have consistently been using a bicep exercise for more than 3-4 weeks then change the bicep exercise to another basic one for another cycle of 3-4 weeks w/ these protocols):):

Exercises- Standing Dumbbell Curls – 6-8 sets of 25 reps


(Note- if you are following a heavy bench press routine of 5-6 sets you will only need 1 tricep exercise of 4-6 sets).

Perform 6-8 sets with 15-20 Reps each set, if you are training your arms in a split routine.

Frequency 2-3 times a week

Exercises- Reverse Triceps Dips – 3-4 sets of 15-20 reps (One of my personal favorites)

(If you are unable to perform this exercise, then I would recommend you do bench dips)

Lying Dumbbell Tricep Extension – 3-4 sets of 15-20 reps

I know a lot of you will still question whether or not these ““higher rep routines” will develop the arms.  Keep this in mind:

3sets x 8rep each set (95lb) bicep curls= 24 reps x 95 lbs= 2,280 lbs “total work load” vs

A high rep set of 3 sets x 25 reps (65lb) = 75 reps x 65 lbs= 4,875 lbs “total work load”

This is almost 2,600 lbs of greater workload using the higher rep set, now do you get my point! You’re Growing Bigger Guns Faster!

I’ll give you a good testimony of strength using the high rep method, since I have been doing these ‘high rep’ exercises for arms most of my career. I have been challenged in the gym a couple of times.  Someone once bet me I could not curl the 65lb dumbbells- I accepted the challenge and curled the 65’s for 6 reps.  In another challenge, I curled the 75 lb dumbbells for 6 reps.  Honestly, I surprised myself of having this strength (I could not have performed this heavy weight consistently for 6 reps without having trained using this “High Rep” System.)  And, just in case you were wondering…in the off season, my arms measure out naturally at 18”.  Yours can to – so get to it!

In summary, when it comes to building the arms don’t limit your workouts with doing the same old reps.  Reach out of your comfort zone and go for the High Reps!  You will feel your arms BURN and get a major PUMP.  I am not the first person to offer this rep range, Jeff Everson former editor of Muscle & Fitness has written articles offering higher reps for the arms especially for bicep training.   Good Luck with your workouts.

About the Author:  Ramsey Rodriguez is a Sports Fitness Consultant with 25 years of professional experience in fitness training, sports nutrition and natural alternatives for health and wellness.  He has also created sport-specific training and nutrition programs for various professional and collegiate athletes in the areas of football, sprinting, swimming, weightlifting and powerlifting.  His

Mission Statement:  I am 100% committed to the passion and pursuit of improving human performance.

Ramsey Rodriguez was born and raised in Texas, earned his Bachelor of Science degree in Physical Education and a minor in Health from The University of Texas at San Antonio.  He is a nationally certified sports trainer credentialed as a Certified Strength and Conditioning Specialist (CSCS) through the National Strength and Conditioning Association (NSCA).  He also carries a CISSN certification from the International Society of Sports Nutrition.  Ramsey is a disciple of Dr. Angel Spassov ( a world-renowned Bulgarian strength and conditioning specialist and former 7 time Olympic Coach), who taught him Periodization Training methods based on Eastern Bloc theory and whose inspiration led to the creation and development of  “Tribustol” some years later.  In 1994, Ramsey, alongside several other notable names in the sports industry, conducted the first Creatine Monohydrate studies for weightlifters.  Over the past 15 years, Ramsey Rodriguez has made appearances on several televised sports/fitness programs, including, “The Larry North Fitness Show”.  He has also published articles for various health and fitness magazines and has collaborated with and been featured in several internet articles by Jon Benson, including the popular book, “Fit Over 40”.

In addition to his accomplishments, Ramsey founded two successful companies:  Pinnicle Fitness, Inc. and Nutritional Ergogenic Systems (NES).  NES is dedicated to developing safe and effective nutritional supplements designed as an alternative to anabolic steroids.  NES was formed around the creation and development of “Tribustol”- an all natural proprietary blend that is solely intended to enhance performance, build lean muscle mass, improve strength and quicken recovery time.

Currently, Ramsey resides in Dallas, Texas.  He is a competitive natural bodybuilder and former NPC Bodybuilding Judge.  He also takes an active interest in powerlifting via his affiliation with 100% RAW Powerlifting.

Ramsey Rodriguez  is the Founder of the Nutritional Ergogenic Systems Inc.; www.tribustol.com


Interview – Tony Ricci MS FISSN CNS

Tony is a Fellow of the ISSN and ISSN Certified Sports Nutritionist.  He sat down with SNI to chat about training and the fight sports!

SNI:  The majority of your career is dedicated to sports nutrition. However your focus in S & C is exclusively to combat sports, why just this particular sports discipline? And besides, MMA is one of my favorite sports to watch! (Jose Antonio).

First, because I have a lifetime of practice dedicated to multiple disciplines within the combat sports. Secondly, I love the challenge of conditioning the biomotor abilities in combat sports. I enjoy balancing the delicate art and science of training protocols for these athletes. The fact that linear periodization models for strength, power and speed, can rarely be applied due to a host of variables, really makes S&C for elite level fighters as much of an art as a science. Your protocols can put a fighter in rehabilitation for 3 – 6 months, or potentially contribute to a world championship/title performance. And, then there is the psychological aspect of conditioning a fighter that I love most. You are not just training their biomotor abilities, you are training their mind. You are further instilling a belief within them that they are a champion, and no matter what happens on the mat, in the ring, or the octagon, they have been there many times over in their training, and then cannot be broken mentally as a result.

SNI: What is your first line of strategy in program design for fighters?

Oh boy, first the balancing acts. That is, balancing the egos and concerns of every coach, manager and promoter. You find most of the people you deal with in the combats sports are themselves well-balanced, as they have a chip on each shoulder. After that, I collaborate extensively with the coaches from all disciplines. I need to know what they want out of their fighter and how they want to dictate the fight. Once this is done I gather an extensive background on the fighters past training disciplines so immediately I will know how they have been conditioned previously and where they may lag as a result. I will review all the available data and film of my fighter as well that of their opponent. Once I have this information I know how each fighter wins or loses, submission, knockout, decision, and how long it takes them to do so. Have they won early and never gone 3 five minute rounds, or have they historically taken it to the bell? With this data I can now start formulating my program to my fighter’s strengths and weaknesses, conditioning them to ensure a  rough night for his/her opponent.

SNI: After consultation with trainers, coaches, and aggregating data, what is an example of how you may design protocols specifically for a fighter?

Once we establish peace and consistency amongst trainers, managers, etc, I will design the program with two things in mind first, their previous conditioning experience and the conditioning necessary to dictate the fight. For example, if I have a wrestler with supreme systemic cardio conditioning and the ability to fight endlessly on the ground, when transitioning to MMA, we will do extensive conditioning on strike specific exercises, both for punching and kicking, as they may have to further enhance their localized endurance and buffering capacity in the extremities to ensure high striking volume if needed. For the experienced Jiu Jitsu competitor moving to MMA we emphasize a lot of explosive level- changes. This sport occurs with the body horizontal to the ground most of the match, so standing them up to improve striking ability and endurance on their feet is vital as they already have an established conditioning base for ground fighting. And for the boxer or kickboxer going MMA, they will now need absolute power and strength not used as much in a stand-up game, so we’ll emphasize grip strength and endurance, full body isometric strengthening, and movements enhancing the biomotor abilities for take down defense and surviving on the ground.

SNI:  Is developing S & C programs for the combat athletes distinctly different than other sports?

Yes! Of course all elite level athletes have enormous training volume, but the pro fighter may supersede that of any athlete with the exception of some Olympic athletes. There are so many interdisciplinary training practices and coaches involved that you really have to carefully adjust your program based upon total training volume, or be sure to be scolded by everyone, including a pilates coach who once took it to me for my training protocols as she insisted her discipline took greater precedent over mine in fight specific preparation. Nevertheless, remember, you win these sports by knocking out or hurting your opponent more than they hurt you, so the fighter will go through a camp with multiple minor and major injuries, so your best calculated plans and periodization models are likely to be incessantly interrupted. And while true of all elite athletes, more often than not you will have to pull your fighter away from training and force them to rest as opposed to telling them to turn it up.

SNI: Is there a significant difference in training the stand-up fighter, for example, as opposed to wrestler or mma ground fighting specialist.

Definitely! I emphasize relative power, speed and strength more with the stand up fighter, power to bodyweight ratio. That is, the ability to relocate their body at high speeds. I have always said fighting is like real estate, in which they say all that matters is – location, location, location! Fighting too is location, location, location, particularly for the boxer and kickboxer if they wish to hit with maximum power or avoid being hit by maximum power. I do extensive footwork and lateral plyometric work with my stand up fighters. The MMA fighter will tie up, hold, grab and literally lift their opponents at times, so there is a much greater emphasis on absolute power, speed and strength. The MMA protocol will include a lot more loads in various exercises to assist in manipulating their opponent’s bodyweight. Additionally, the differences may be most evident in their cardio conditioning, as a stand up fighter may require some road/distance work, whereas the cardiovascular protocols of the MMA fighter generally emphasize sprinting/interval training. There is course interdisciplinary carry over in training, but these are some possible differences.

SNI: The art and science of S & C for combat sports seems to be progressing rapidly, nevertheless, where do you think improvement is needed.

In short, assessing the needs of each fighter is imperative. I understand the difficulty in individualizing programming when working with multiple fighters or a large camp, but conditioning is best when specific to the aforementioned variables for each fighter. A training program that may improve the performance and fighting style of one athlete can truly impede the performance of another. I have said the same about nutrition, while it is necessary and beneficial to scale dietary practices, is it also at times a travesty to attempt to do so.

SNI: Which training camp are you affiliated with now? Bellmore Kickboxing http://www.bellmorekickboxingacademy.com/  and Long Island MMA http://www.limixedmartialarts.com/index.html

A shout out to my business partners @ http://mycompetitivelife.com/   Chris Algieri, fellow CISSN and Dr Michael Camp who always further my knowledge in fight science. Thanks to good friend Doug Balzarini from whom I have learned much and JC Santana for pioneering S&C for combat sports. 

Contact Tony @ 917-520-7819 or tony@mycompetitivelife.com