Tag Archives: ISSN

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.

References

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.

 

 

 

Energy Drinks and McDonalds

By Jose Antonio PhD FISSN.  Let’s face it.  Energy drinks are as much a part of our culture as tailgating, barbequing on the weekends, cheering for the underdog, and overeating during the Thanksgiving holiday.  With folks in a mad dash to accomplish umpteen things during the day, it’s no wonder that energy drinks are as ubiquitous as chopsticks in a Chinese restaurant. In fact, the US energy drink category is expected to hit an amazing 19.7 billion dollars in 2013.  Now that my friends is a bunch of money.  So it should come as no surprise when Monster Energy Drink gets sued vis a vis the death of a 14-year old girl.  It’s like going to a buffet and realizing that all the food is gone.  Who do you blame?  Oh yeah, the fat man in the corner with plates stacked from floor to ceiling. 

If that flew over your head, my point is folks want to blame somebody or something.  And who better to blame (and make money) than a large company with a big fat wallet.  That’s the easy way.  And apparently what they teach in law school (this of course doesn’t apply to my legal friends). :-)

So the story goes like this: “A complaint filed by Wendy Crossland and Richard Fournier, of Maryland, states that their daughter, Anais Fournier, went into cardiac arrest after consuming the drinks.  Monster Beverage Corp. is based in Riverside County, Calif., which is where the case was filed. Fournier was “unconscious when emergency personnel arrived at her home,” according to the complaint. Doctors at Johns Hopkins Hospital induced a coma in an attempt to reduce brain swelling, but after several days, “the decision was made to terminate life support,” the complaint said.  The opinion of the Maryland medical examiner’s office is that Fournier died of cardiac arrhythmia due to caffeine toxicity that impeded her heart’s ability to pump blood.  The autopsy report also concluded that Fournier suffered from Ehlers-Danlos syndrome — an inherited disorder that can make connective tissues, like skin and blood vessel walls, flexible and weak.”  (Original source: KTLA.com)

Now certainly, the loss of a child is perhaps the most devastating event that could happen in anyone’s life.  There is no recovering from it.  Ever.   However, what is just blatantly incorrect is to blame an energy drink (and in particular caffeine) when it is clear that there are warning labels plastered on these drinks that are as obvious as those ugly billboards up and down Interstate 95. 

Keep in mind, the primary ingredient in these drinks is caffeine.  And coffee is THE original energy drink.  What’s next, Starbucks getting sued because someone decides to down 10 Frappaccinos?  Fournier apparently consumed two 24-ounce Monster drinks within 24 hours.  With roughly 240 mg of caffeine in a 24 ounce can, that makes for a total of 480 mg of caffeine.  That interestingly enough is really not a high dose.   On the surface, there is just so much that seems out of kilter with this lawsuit.  Blaming an energy drink for this is like blaming McDonald’s for obesity. 

Science Says

Rather than giving you my personal opinion, here’s an edification on the science.  I will admit however that caffeine is one of my favorite supplements/drugs of all time.  The first thing I do in the morning is head straight to the coffee maker and brew up some super strong java.  This stuff is great; it works very well and it has a safety record longer than the Great Wall of China.

Besides an energy boost, endurance enhancer, and a brain stimulator, there’s evidence that caffeine can alter improve performance in tasks of strength and speed.  For instance, maximal anaerobic power increases significantly after ingesting 250 mg of caffeine.  According to a recent study published in the British Journal of Sports Medicine, “caffeine can favourably affect some strength parameters in highly resistance-trained males.1”  Furthemore, a “caffeine-containing supplement may be an effective supplement for increasing upper-body strength.” 2  So even the strongest of the strong can benefit from caffeine supplementation.

Also, caffeine ingestion resulted in a blood lactate level that was higher versus the placebo.  Meaning, caffeine allows you to work a lot harder (hence, the greater lactic acid build up!).  So you think those guys competing for the yellow jersey in the land of wine and the Eiffel tower are the only ones to use caffeine?3  (Okay, they use other stuff, but that’s for another article on another day).

A Pain No More

Ever wondered why many over the counter pain medications have caffeine added to them?  Adding caffeine to both aspirin or acetaminophen makes them relieve headache pain about 40% better than they do without caffeine. Caffeine also helps your body absorb these medications, allowing you to get back to your daily life faster.4 In a study of low caffeine consuming college-aged males, they took one of two doses of caffeine (5 or 10 mg of caffeine per kg body weight) or placebo and 1 hour later completed 30 minutes of moderate intensity cycling exercise (60% VO2peak).

Caffeine increased resting systolic pressure in a dose-dependent fashion but these blood pressure effects were not maintained during exercise. Caffeine had a significant linear effect on leg muscle pain ratings meaning the higher the dose, the better pain relief provided by caffeine. The average pain intensity scores during exercise after ingesting 10 mg caffeine per kg body weight, 5 mg per kg, and placebo were 2.1, 2.6, and 3.5, respectively (the lower the number, the more pain relief).  According to the authors, “the results support the conclusion that caffeine ingestion has a dose-response effect on reducing leg muscle pain during exercise and that these effects do not depend on caffeine-induced increases in systolic blood pressure during exercise.”5,6

Now you probably have noticed that a dose of 10 mg per kg body weight of caffeine is equal to 681 mg for a 150 lb individual. 

The International Society of Sports Nutrition published a Position Stand on caffeine which can be summarized by the following seven points:

1.)    Caffeine is effective for enhancing sport performance in trained athletes when consumed in low-to-moderate dosages (~3-6 mg/kg) and overall does not result in further enhancement in performance when consumed in higher dosages (≥ 9 mg/kg).

2.)     Caffeine exerts a greater ergogenic effect when consumed in an anhydrous state as compared to coffee.

3.)    It has been shown that caffeine can enhance vigilance during bouts of extended exhaustive exercise, as well as periods of sustained sleep deprivation.

4.)     Caffeine is ergogenic for sustained maximal endurance exercise, and has been shown to be highly effective for time-trial performance.

5.)      Caffeine supplementation is beneficial for high-intensity exercise, including team sports such as soccer and rugby, both of which are categorized by intermittent activity within a period of prolonged duration.

6.)    The literature is equivocal when considering the effects of caffeine supplementation on strength-power performance, and additional research in this area is warranted.

7.)     The scientific literature does not support caffeine-induced diuresis during exercise, or any harmful change in fluid balance that would negatively affect performance.7

Bottom line: when used properly, caffeine (and hence energy drinks) are clearly quite safe.

SIDE BAR – Special Sugar – Ribose

Caffeine is clearly the ‘king’ of energy.  However, other ingredients are worth looking at as well. For instance, the carbohydrate category is intriguing.  Remember, sugars do provide energy and are an important fuel for intense anaerobic exercise.  Do you think you’ve got a handle on carbohydrates?  You’ve got complex carbs, simple sugars, low, high, and medium glycemic sugars and carbs.  One of the lesser known sugars is something called ribose.

Ribose chemistry – First let’s start with a little biochemistry to help you understand what exactly ribose is.  At our most basic level, we need to synthesize adenosine triphospate (ATP) in order for us to generate energy for muscle contraction (as well as all energy-requiring processes).  The adenosine part of ATP is made up of adenine and ribose; attached to that are three phosphate molecules (hence, TRIphosphate).  See, this is as simple as 8th grade biology.  In order for your body to produce energy, one of those phosphate molecules is cut off from ATP thus forming ADP (adenosine DIphosphate).  Now we’re left with adenine, ribose, plus 2 phosphates. I’m going to skip a few steps (yawn…biochemistry can be boring) to get to the point. Ribose can help via a couple ways.  One way is called the “salvage pathway.”  Basically, your body tries to get the breakdown products from energy metabolism and recycle them such that you replenish your ATP supplies.  Ribose helps promote this salvage pathway such that your ATP stores are replenished.  But if you’re short on ribose, your body has to create ATP from scratch.  This happens if your body excretes too much of the metabolic byproducts of metabolism.  And for the creation of “new” ATP, ribose is also needed.  Interestingly, glucose can also do the job; but it’s a much slower process.  If you’re someone who exercises intensely, supplemental ribose may be helpful.  Here’s one study that shows an ergogenic effect of ribose.

In a study published in Current Therapeutic Research, scientists gave healthy, male recreational bodybuilders (18 to 35 years) either placebo (dextrose) or ribose (10 g/d in powder formulation). The ribose-supplemented group experienced a significant before and after increase in the total work performed, whereas the placebo group did not change significantly. Also, the ribose-supplemented group experienced a significant increase in 1-RM bench press strength, whereas the placebo group did not change significantly.  Furthermore, ribose has been shown to have the following effects as well.  Perhaps its antioxidant effects are the most intriguing.

  1. The combination of D-ribose with reducing antioxidants may provide a more optimal state of cellular protection during and following times of oxidative stress.1
  2. Ribose demonstrated a beneficial trend in lower MDA and reduced glutathione levels during hypoxic stress.2
  3. Ribose may both serve as an energy source and enhance the de novo synthesis of purine nucleotides.3
  4. Ribose, a naturally occurring pentose sugar, has been shown to enhance the recovery of myocardial or skeletal muscle ATP and TAN levels following ischemia or high-intensity exercise.4

Bottom line:  in addition to caffeine, ribose may be a ‘energy’ supplement that’s good for your cells.

References – Ribose

1.             Addis P, Shecterle LM, St Cyr JA. Cellular protection during oxidative stress: a potential role for D-ribose and antioxidants. Journal of dietary supplements 2012;9:178-82.

2.             Seifert JG, Subudhi AW, Fu MX, et al. The role of ribose on oxidative stress during hypoxic exercise: a pilot study. Journal of medicinal food 2009;12:690-3.

3.             Wagner DR, Gresser U, Zollner N. Effects of oral ribose on muscle metabolism during bicycle ergometer in AMPD-deficient patients. Annals of nutrition & metabolism 1991;35:297-302.

4.             Dodd SL, Johnson CA, Fernholz K, St Cyr JA. The role of ribose in human skeletal muscle metabolism. Medical hypotheses 2004;62:819-24.

References – Caffeine

1.            Jacobson BH, Weber MD, Claypool L, Hunt LE. Effect of caffeine on maximal strength and power in elite male athletes. British journal of sports medicine 1992;26:276-80.

2.            Beck TW, Housh TJ, Schmidt RJ, et al. The acute effects of a caffeine-containing supplement on strength, muscular endurance, and anaerobic capabilities. Journal of strength and conditioning research / National Strength & Conditioning Association 2006;20:506-10.

3.            Anselme F, Collomp K, Mercier B, Ahmaidi S, Prefaut C. Caffeine increases maximal anaerobic power and blood lactate concentration. Eur J Appl Physiol Occup Physiol 1992;65:188-91.

4.            Strong FC, 3rd. It may be the caffeine in Extra Strength Excedrin that is effective for migraine. The Journal of pharmacy and pharmacology 1997;49:1260.

5.            O’Connor PJ, Motl RW, Broglio SP, Ely MR. Dose-dependent effect of caffeine on reducing leg muscle pain during cycling exercise is unrelated to systolic blood pressure. Pain 2004;109:291-8.

6.            Motl RW, O’Connor PJ, Dishman RK. Effect of caffeine on perceptions of leg muscle pain during moderate intensity cycling exercise. J Pain 2003;4:316-21.

7.            Goldstein ER, Ziegenfuss T, Kalman D, et al. International society of sports nutrition position stand: caffeine and performance. Journal of the International Society of Sports Nutrition 2010;7:5.

Paddling and Corenography

coreby Jose Antonio PhD FISSN. Not to be confused with Pornography, Corenography instead refers to the proliferation of books, websites, and blogs dedicated to ‘Core Training.’ Nevertheless, do a search on Amazon.com and faster than you can download that goofya$$ video of the fake Kardashian wedding video, you’ll find scores of fitness books dedicated to training the ‘Core.’  Sort of like the ‘core’ of an apple, you can define ‘core training’ as training the muscles attached to your torso (i.e. the abdominal muscles and lower back).  This includes all the abdominal muscles (rectus abdominus, internal and external obliques, transverse abdominus and intercostals), the spine (the erector spinae group) and the hip flexors (iliacus and psoas, together known as the iliopsoas).  Basically these muscles stabilize and move the center or core of your body.  All this anatomy talk is making me sleepy.  Back to my point.  Apparently core training can do lots of things.  If you look at various book titles, you have “The Complete Book of Core Training: The Definitive Resource for Shaping and Strengthening the “Core” — the Muscles of the Abdomen, Butt, Hips, and Lower Back.”  That pretty much explains it.   But then you have a ‘revolutionary’ type of program (sort of like the American or French Revolution I guess) in “The Core Performance: The Revolutionary Workout Program to Transform Your Body & Your Life.”  And of course, if your IQ doesn’t exceed a banana, then “The Complete Idiot’s Guide to Core Conditioning Illustrated” is for you.You’d think with a plethora of books on core training that nobody figured out before that training your abs, back, and hip flexors/extensors was important.  But as with many things in exercise, it’s basically a ‘different way’ of looking at the same thing.  If you do a full squat, you are training the core.  If you do heavy curls using an EZ curl bar, believe me, you’re training the ‘core.’  Heck, doing a friggin’ push-up trains the ‘core.’  But if you’re tired of the gym and doing silly exercises on Swiss Balls, BOSU, and assorted plastic contraptions, why not do ‘core’ work that also serves to increase muscle strength and endurance.  And it’s a helluva lot more fun that balancing on a stinkin’ Swiss ball.  What is it? Outrigger paddling my friends.  What exactly is outrigger paddling?  Well way back when, ole Captain Cook arrived in Kealakekua Bay in the year 1779, he reported seeing at least 1500 canoes. Purportedly, Hawaii must have numbered between 6,000 and 12,000 canoes for a population of 175,000 to 225,000. (http://www.coffeetimes.com/july97.htm) Here was a culture that was dependent on the ocean and used ancient canoes to get from the beach to 7-11.  Okay, maybe not 7-11, but when you’re in need of coconut water, the island next door might be your best bet. Polynesians actually have used the outrigger canoe as a mode of travel dating back thousands of years.  Paddling, specifically outrigger canoe paddling, utilize all the core muscles, as well as the muscles surrounding the shoulder joint.  The rotation, flexion, and extension of the torso while paddling is a much better core workout than all the latest fad of the day exercises that you see at your local gym.  In fact, the paddling sports are unique as a strength-endurance sport in that you train your cardiovascular system intensely but in addition, you can gain quite a bit of muscle mass, especially in the back and shoulders.  Think of each paddling stroke as weight training using water as resistance.  For instance, an ‘easy’ workout would consist of a one hour paddle in which your stroke cadence is 60 per minute (15 strokes left then right, alternating); if you do a rep count, that’s 1,800 reps on the left and right side respectively.  That to me, is a helluva lot better than getting on some newfangled plastic ball and doing an exercise that you’ll never encounter in real life.  But that’s just me.

So do yourself a favor, take a break from the gym and workout on the water.  There are paddling clubs all over the world.  Check out http://www.y2kanu.com/ (the pictures here are courtesy of them), www.kanaluimiami.com and www.ocpaddler.com. Believe me; It is more fun getting a hard workout on the open ocean doing strength-endurance work for the upper body and ‘core’ while working the lower extremity muscles as stabilizers.  And besides, how often can you workout and see dolphins all at the same time?

 

 

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

Fish Oil For Fat Loss

Fish oil is most known for its beneficial cardiovascular and cardiac health effects, and continues to top the list of health promoting supplements. In 2004 FDA approved a prescription fish oil preparation for treatment of high blood triglycerides (hypertriglyceridemia) (1). Recently several studies have shown that fish oil also has other beneficial effects, which might appeal more to the younger crowd, and especially to fitness and bodybuilding enthusiasts. One of these effects is fat loss.

Fish Oil Induced Fat Loss

In the 80s early 90s, several animal studies showed that fish oil reduces body fat (2-5) and weight gain (6-9), and limits adipose tissue expansion (10-12). These effects have been seen during both a decreased (3, 7), constant (5) or even increased energy intakes (6). This indicates that the fatty acids in fish oil, notably EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid), have an effect on the partitioning of fat between oxidation (fat burning) and storage in the body.

Mechanism – how does it work?

In search for the mechanisms behind fish oil induced fat loss, it has been found that fish oil exerts favorable metabolic effects by modulating gene expression (which is the process by which the information encoded in a gene is converted into protein)(2, 13-26). While we inherit our genes (or blueprints) from our parents, what determines the way in which our blueprints are interpreted is largely dictated by a collection of environmental factors. The nutrients we consume are among the most influential of these environmental factors (27, 28). One dietary constituent that has a strong influence on our genetic makeup is dietary fat (2, 13, 14, 16-19, 21-23, 25, 29). Fatty acids from dietary fat not only influences hormonal signaling events, but also have a very strong direct influence on the molecular events that govern gene expression.

More specifically, it has been shown that the fatty acids EPA and DHA from fish oil (by affecting gene expression) inhibit the activities of fat synthesizing (lipogenic) enzymes (30-37), while at the same time stimulating the activities of key enzymes that govern fat oxidation (fat burning) (2, 38-46).

Fish oil also has been shown to increase levels of adiponectin and decrease levels of cortisol (47, 48). Adiponectin is a novel adipose tissue-specific protein that circulates in human plasma at high levels (49). It is one of the physiologically active polypeptides secreted by adipose tissue, whose multiple functions have started to be understood in the last few years. Some of its beneficial effects are enhanced insulin sensitivity, and lowered plasma glucose (blood sugar) and triglyceride levels (49, 50). A reduction in adiponectin expression is associated with insulin resistance (49), and adiponectin levels are inversely related to the degree of adiposity (50). The activity of adiponectin has also been associated with steroid and thyroid hormones, glucocorticoids, and nitric oxide, and has anti-atherogenic and anti-inflammatory properties (50). Thus, it is plausible that fish oil induces some of its effect by affecting adiponectin levels.

While the functions of adiponectin are just starting to emerge, it is likely to become a target for therapeutic applications in the future.

It is interesting that fish oil lowers cortisol. While the exact role of cortisol in obesity isn’t fully elucidated (51, 52), it is known that excessive cortisol levels result in substantial fat mass gain (53, 54). Thus, the reduction in cortisol levels after fish oil supplementation could contribute at least partly to the fat loss observed with fish oil supplementation. In another article I’m covering the anti-catabolic/muscle growth effects of fish oil in more detail.

Fish Oil for Muscle Growth

Does it work in humans – what’s in it for me?

At this point you might be thinking “ok, that all sounds nice, but I’m not a rat. Does it work in humans”?

Yes! Read on…

Non-dieting

Recently several studies have shown that fish oil also can help people to get in shape. In a landmark study in healthy young non-obese males, 6 g of fat from butter, olive oil, sunflower oil and peanut oil was replaced with 6 g fish oil (corresponding to 1,100 mg EPA and 700 mg DHA) per day (55). After 3 weeks the researchers noted a significantly increased resting fat burning (fat oxidation) and a 1.94 lb (0.88 kg) decrease in body fat (measured by the golden standard method DEXA). There was no change in body weight. This fat loss was seen despite that subjects were told not to change their usual exercise and food habits.

Other studies have confirmed the fat loss effects of fish oil when added to people’s usual lifestyle habits.

One study gave healthy men and women (mean age 33 yrs), who were told to maintain their current food and exercise practices 4 g fish oil, providing 1,600 mg EPA and 800 mg DHA (48). After 6 weeks, the placebo group, which was given 4 g of safflower oil, showed a tendency towards fat gain. In contrast, the fish oil group experienced a significant reduction in fat mass of 1.1 lb (0.5 kg) and increase in fat-free mass of 1.1 lb (0.5 kg) (measured by air displacement plethysmography), with no change in body weight.

A 1.1 lb reduction in fat mass combined with a 1.1 lb increase in fat-free mass, without changes in subject’s typical food and exercise habits is pretty remarkable body composition improvement. It also underscores the importance of investigating fat mass and lean mass separately, since just measuring body weight will not tell anything about potential body composition changes, which after all is what is interesting from both a health, esthetic and physical performance viewpoint. For more into on the anti-catabolic and lean mass gaining effects of fish oil, see Fish Oil for Muscle Growth

Another study, also against a background of constant food and exercise routines, gave obese type 2 diabetic female subjects 1,080 mg EPA and 720 mg DHA for 2 months, or placebo paraffin oil (56). Even though there was no change in body weight, the fish oil group demonstrated a significant reduction in fat mass by 3.6 lb (1,614 kg). This fat mass reduction was mainly due to a decrease in trunk (belly) fat. In addition, fish oil group experienced a reduction in fat cell size by 6.3 % (56).

It has also been found that supplementing with fish oil for 3 weeks (1,100 g EPA and 700 g DHA daily) significantly decreases insulin levels and increases fat burning after consumption of carbohydrate rich meals (57). Supplementation with fish oil providing 2,400 mg EPA and 1,600 mg DHA for 3 weeks also boosts fat burning during jogging exercise (58).

Combined with exercise

Fish oil seems to be even more effective when combined with exercise. In obese men and women, the effects of the addition of 6 g of fish oil daily (providing 360 mg EPA and 1,560 mg DHA) in combination with regular aerobic activity (walking 45 min three times per week at an intensity of 75% of age-predicted maximal heart rate) for 12 weeks, was investigated (59). The results showed that the combination of fish oil and regular aerobic activity not only improved several risk factors for cardiovascular disease, but also significantly reduced body fat mass with 4.4 lb (2 kg) (59). The finding that

body weight and body fat percentage didn’t change in the placebo group (which was put on the same exercise program but received 6 g sunflower oil instead of the fish oil)  underscores the efficacy of fish oil for fat loss.

It is interesting that the fat loss seen in the fish oil – exercise group occurred even though the subjects did not change their usual food habits; they just added the fish oil supplement and exercise program to their regimen. This indicates the great potential benefits of fish oil combined with regular physical activity for improving body composition and cardiovascular health.

In this study, no fat loss was seen in fish oil only group (which didn’t exercise). This is probably due to the very low dose of EPA. Most studies showing that fish oil increases fat loss have use fish oil products that provide 1.5-2 times more EPA than DHA, like Lean Lipid Complex does.

Combined with a calorie restricted diet

Fish oil supplementation can boost calorie restricted diets as well. This was found in a study that investigated the effect of including fish oil as part of an energy-restricted diet, on weight loss (60). Young obese adults were put on a calorie restricted diet (30 % less calories than their usual intake, about 600 calorie deficit), supplemented with 6 g fish oil providing 1,500 mg EPA + DHA, or placebo (sunflower oil capsules). It was found that the fish oil enriched diet resulted in 2.2 lb (1 kg) more weight loss and greater reductions in waist circumference after only 4 weeks, than the same diet without fish oil (60).

Combined with a calorie restricted diet and exercise program

In a study that tested the effect of adding 2,800 mg/day fish oil (EPA:DHA ratio 2:1) to a low-calorie diet combined with an exercise program, severely obese women (61). After 3 weeks the fish oil group lost 3.3 lb (1.5 kg) more weight and slashed almost 1 inch (2.3 cm) more fat from their hips, than the non-supplemented group.

While body fat changes were not reported, the researchers did find a greater increase in blood beta-hydroxybutyrate (a ketone body) in the fish oil supplemented group compared with control group, and interpreted this as providing evidence of greater fat oxidation in the fish oil group (61). These findings indicate that the addition of fish oil to a relatively short (3 week) weight loss program comprising severe caloric restriction and exercise, may increase fat oxidation and lead to greater improvement in body composition.

Perspective on fish oil and fat loss

In contrast to the positive studies, there are a few that didn’t show any fat loss with fish oil supplementation (62-65). This could be due to differences in subject characteristics (age, initial body fat mass, baseline physical activity), methodological differences, and differences in fish oil preparations.

As outlined above, several high quality studies have shown that fish oil supplementation has a significant fat loss effect in addition to all its other health promoting effects. The majority of evidence thus supports fish oil’s ability to shift fat metabolism away from storage towards burning of body fat, even in humans.

It’s getting better – fat loss combined with lean mass (muscle) gain

In one of the most recent studies on fish oil’s fat loss effect, men and women (mean age 33 yrs) where given 4 g of fish oil corresponding to 1600 mg EPA and 800 mg DHA (48). After 6 weeks, the placebo group, which was given 4 g of safflower oil, showed a tendency towards fat gain. The fish oil group instead had lost 0.5 kg of fat mass and gained 0.5 kg of lean mass, with no change in body weight.

This is a very beneficial body composition effect and underscores the importance of investigating fat mass and lean mass separately, since just measuring body weight will not tell anything about changes in body composition. After all, it’s not weight loss per see, but fat loss and muscle gain that’s interesting from both a health, esthetic and physical performance viewpoint. I cover the muscle growth stimulating and anti-catabolic effect of fish oil in another article

Fish Oil for Muscle Growth

Bottom Line

Whether you are on a diet or not, adding a fish oil supplement to your regimen can effectively help you get in shape. The additional calories from the fish oil will not get stored (66); quite to the contrary, fish oil will help you get rid of calories you already have stored in your body fat. What’s interesting is that fish oil supplementation seems to reduce body fat and waist circumference despite unchanged exercise and/or other dietary practices.

Aim for a daily fish oil intake that provides you with at least 1600 mg EPA and 800 mg DHA, but a higher dose, 2400 mg EPA and 1600 mg DHA (a total of 4 g EPA and DHA total), might result in a larger fat loss. To achieve this high intake of EPA and DHA it is advisable to take a fish oil concentrate. In an upcoming article I will go into more detail about fish oil concentrates, different ratios of EPA to DHA in fish oil preparations, their relative effectiveness, safety aspects of high dose fish oil supplementation, and sort through the myriad of fish oil supplements currently available on the market, to help you find a good fish oil supplement that will give you the best bang and effectiveness for your buck.

References:

1.           Mason CM, Long J, Conroy C 2011 Prescription Omega-3s: An Overview for Nurse Practitioners. The Journal of cardiovascular nursing 26:290-297

2.           Baillie RA, Takada R, Nakamura M, Clarke SD 1999 Coordinate induction of peroxisomal acyl-CoA oxidase and UCP-3 by dietary fish oil: a mechanism for decreased body fat deposition. Prostaglandins, leukotrienes, and essential fatty acids 60:351-356

3.           Hill JO, Peters JC, Lin D, Yakubu F, Greene H, Swift L 1993 Lipid accumulation and body fat distribution is influenced by type of dietary fat fed to rats. International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity 17:223-236

4.           Ikemoto S, Takahashi M, Tsunoda N, Maruyama K, Itakura H, Ezaki O 1996 High-fat diet-induced hyperglycemia and obesity in mice: differential effects of dietary oils. Metabolism: clinical and experimental 45:1539-1546

5.           Su W, Jones PJ 1993 Dietary fatty acid composition influences energy accretion in rats. The Journal of nutrition 123:2109-2114

6.           Cunnane SC, McAdoo KR, Horrobin DF 1986 n-3 Essential fatty acids decrease weight gain in genetically obese mice. The British journal of nutrition 56:87-95

7.           LeBoeuf RC, Veldee MS 1993 Genetically determined body weight loss in mice fed diets containing salmon oil. The Journal of nutrition 123:547-558

8.           Mori T, Kondo H, Hase T, Tokimitsu I, Murase T 2007 Dietary fish oil upregulates intestinal lipid metabolism and reduces body weight gain in C57BL/6J mice. The Journal of nutrition 137:2629-2634

9.           Pan DA, Storlien LH 1993 Dietary lipid profile is a determinant of tissue phospholipid fatty acid composition and rate of weight gain in rats. The Journal of nutrition 123:512-519

10.         Belzung F, Raclot T, Groscolas R 1993 Fish oil n-3 fatty acids selectively limit the hypertrophy of abdominal fat depots in growing rats fed high-fat diets. The American journal of physiology 264:R1111-1118

11.         Parrish CC, Pathy DA, Angel A 1990 Dietary fish oils limit adipose tissue hypertrophy in rats. Metabolism: clinical and experimental 39:217-219

12.         Ruzickova J, Rossmeisl M, Prazak T, Flachs P, Sponarova J, Veck M, Tvrzicka E, Bryhn M, Kopecky J 2004 Omega-3 PUFA of marine origin limit diet-induced obesity in mice by reducing cellularity of adipose tissue. Lipids 39:1177-1185

13.         Clarke SD 2000 Polyunsaturated fatty acid regulation of gene transcription: a mechanism to improve energy balance and insulin resistance. The British journal of nutrition 83 Suppl 1:S59-66

14.         Clarke SD 2001 Polyunsaturated fatty acid regulation of gene transcription: a molecular mechanism to improve the metabolic syndrome. The Journal of nutrition 131:1129-1132

15.         Clarke SD 2004 The multi-dimensional regulation of gene expression by fatty acids: polyunsaturated fats as nutrient sensors. Current opinion in lipidology 15:13-18

16.         Clarke SD, Baillie R, Jump DB, Nakamura MT 1997 Fatty acid regulation of gene expression. Its role in fuel partitioning and insulin resistance. Annals of the New York Academy of Sciences 827:178-187

17.         Clarke SD, Gasperikova D, Nelson C, Lapillonne A, Heird WC 2002 Fatty acid regulation of gene expression: a genomic explanation for the benefits of the mediterranean diet. Annals of the New York Academy of Sciences 967:283-298

18.         Clarke SD, Jump DB 1994 Dietary polyunsaturated fatty acid regulation of gene transcription. Annual review of nutrition 14:83-98

19.         Clarke SD, Thuillier P, Baillie RA, Sha X 1999 Peroxisome proliferator-activated receptors: a family of lipid-activated transcription factors. The American journal of clinical nutrition 70:566-571

20.         Davidson MH 2006 Mechanisms for the hypotriglyceridemic effect of marine omega-3 fatty acids. The American journal of cardiology 98:27i-33i

21.         Jump DB, Clarke SD, Thelen A, Liimatta M, Ren B, Badin M 1996 Dietary polyunsaturated fatty acid regulation of gene transcription. Progress in lipid research 35:227-241

22.         Jump DB, Clarke SD, Thelen A, Liimatta M, Ren B, Badin MV 1997 Dietary fat, genes, and human health. Advances in experimental medicine and biology 422:167-176

23.         Nakamura MT, Cho HP, Xu J, Tang Z, Clarke SD 2001 Metabolism and functions of highly unsaturated fatty acids: an update. Lipids 36:961-964

24.         Ntambi JM, Bene H 2001 Polyunsaturated fatty acid regulation of gene expression. Journal of molecular neuroscience : MN 16:273-278; discussion 279-284

25.         Price PT, Nelson CM, Clarke SD 2000 Omega-3 polyunsaturated fatty acid regulation of gene expression. Current opinion in lipidology 11:3-7

26.         Raclot T, Oudart H 1999 Selectivity of fatty acids on lipid metabolism and gene expression. The Proceedings of the Nutrition Society 58:633-646

27.         Moustaid-Moussa N, Berdanier CD 2001 Nutrient-Gene Interactions in Health and Disease. 2nd ed ed: CRC Press

28.         Berdanier CD, Moustaid-Moussa N 2004 Genomics and Proteomics in Nutrition. 1st ed ed: CRC Press

29.         Lapillonne A, Clarke SD, Heird WC 2004 Polyunsaturated fatty acids and gene expression. Current opinion in clinical nutrition and metabolic care 7:151-156

30.         Hannah VC, Ou J, Luong A, Goldstein JL, Brown MS 2001 Unsaturated fatty acids down-regulate srebp isoforms 1a and 1c by two mechanisms in HEK-293 cells. The Journal of biological chemistry 276:4365-4372

31.         Kim HJ, Takahashi M, Ezaki O 1999 Fish oil feeding decreases mature sterol regulatory element-binding protein 1 (SREBP-1) by down-regulation of SREBP-1c mRNA in mouse liver. A possible mechanism for down-regulation of lipogenic enzyme mRNAs. The Journal of biological chemistry 274:25892-25898

32.         Mater MK, Thelen AP, Pan DA, Jump DB 1999 Sterol response element-binding protein 1c (SREBP1c) is involved in the polyunsaturated fatty acid suppression of hepatic S14 gene transcription. The Journal of biological chemistry 274:32725-32732

33.         Nakatani T, Kim HJ, Kaburagi Y, Yasuda K, Ezaki O 2003 A low fish oil inhibits SREBP-1 proteolytic cascade, while a high-fish-oil feeding decreases SREBP-1 mRNA in mice liver: relationship to anti-obesity. Journal of lipid research 44:369-379

34.         Shimano H, Yahagi N, Amemiya-Kudo M, Hasty AH, Osuga J, Tamura Y, Shionoiri F, Iizuka Y, Ohashi K, Harada K, Gotoda T, Ishibashi S, Yamada N 1999 Sterol regulatory element-binding protein-1 as a key transcription factor for nutritional induction of lipogenic enzyme genes. The Journal of biological chemistry 274:35832-35839

35.         Worgall TS, Sturley SL, Seo T, Osborne TF, Deckelbaum RJ 1998 Polyunsaturated fatty acids decrease expression of promoters with sterol regulatory elements by decreasing levels of mature sterol regulatory element-binding protein. The Journal of biological chemistry 273:25537-25540

36.         Xu J, Nakamura MT, Cho HP, Clarke SD 1999 Sterol regulatory element binding protein-1 expression is suppressed by dietary polyunsaturated fatty acids. A mechanism for the coordinate suppression of lipogenic genes by polyunsaturated fats. The Journal of biological chemistry 274:23577-23583

37.         Yahagi N, Shimano H, Hasty AH, Amemiya-Kudo M, Okazaki H, Tamura Y, Iizuka Y, Shionoiri F, Ohashi K, Osuga J, Harada K, Gotoda T, Nagai R, Ishibashi S, Yamada N 1999 A crucial role of sterol regulatory element-binding protein-1 in the regulation of lipogenic gene expression by polyunsaturated fatty acids. The Journal of biological chemistry 274:35840-35844

38.         Desvergne B, Wahli W 1999 Peroxisome proliferator-activated receptors: nuclear control of metabolism. Endocrine reviews 20:649-688

39.         Kersten S, Desvergne B, Wahli W 2000 Roles of PPARs in health and disease. Nature 405:421-424

40.         Latruffe N, Vamecq J 1997 Peroxisome proliferators and peroxisome proliferator activated receptors (PPARs) as regulators of lipid metabolism. Biochimie 79:81-94

41.         Minnich A, Tian N, Byan L, Bilder G 2001 A potent PPARalpha agonist stimulates mitochondrial fatty acid beta-oxidation in liver and skeletal muscle. American journal of physiology Endocrinology and metabolism 280:E270-279

42.         Nakatani T, Tsuboyama-Kasaoka N, Takahashi M, Miura S, Ezaki O 2002 Mechanism for peroxisome proliferator-activated receptor-alpha activator-induced up-regulation of UCP2 mRNA in rodent hepatocytes. The Journal of biological chemistry 277:9562-9569

43.         Power GW, Newsholme EA 1997 Dietary fatty acids influence the activity and metabolic control of mitochondrial carnitine palmitoyltransferase I in rat heart and skeletal muscle. The Journal of nutrition 127:2142-2150

44.         Schoonjans K, Staels B, Auwerx J 1996 The peroxisome proliferator activated receptors (PPARS) and their effects on lipid metabolism and adipocyte differentiation. Biochimica et biophysica acta 1302:93-109

45.         Krey G, Braissant O, L’Horset F, Kalkhoven E, Perroud M, Parker MG, Wahli W 1997 Fatty acids, eicosanoids, and hypolipidemic agents identified as ligands of peroxisome proliferator-activated receptors by coactivator-dependent receptor ligand assay. Mol Endocrinol 11:779-791

46.         Reddy JK, Mannaerts GP 1994 Peroxisomal lipid metabolism. Annual review of nutrition 14:343-370

47.         Delarue J, Matzinger O, Binnert C, Schneiter P, Chiolero R, Tappy L 2003 Fish oil prevents the adrenal activation elicited by mental stress in healthy men. Diabetes & metabolism 29:289-295

48.         Noreen EE, Sass MJ, Crowe ML, Pabon VA, Brandauer J, Averill LK 2010 Effects of supplemental fish oil on resting metabolic rate, body composition, and salivary cortisol in healthy adults. Journal of the International Society of Sports Nutrition 7:31

49.         Diez JJ, Iglesias P 2003 The role of the novel adipocyte-derived hormone adiponectin in human disease. European journal of endocrinology / European Federation of Endocrine Societies 148:293-300

50.         Nedvidkova J, Smitka K, Kopsky V, Hainer V 2005 Adiponectin, an adipocyte-derived protein. Physiological research / Academia Scientiarum Bohemoslovaca 54:133-140

51.         Walker BR 2001 Activation of the hypothalamic-pituitary-adrenal axis in obesity: cause or consequence? Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society 11 Suppl A:S91-95

52.         Salehi M, Ferenczi A, Zumoff B 2005 Obesity and cortisol status. Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme 37:193-197

53.         Bjorntorp P, Rosmond R 2000 Obesity and cortisol. Nutrition 16:924-936

54.         Pasquali R, Vicennati V, Cacciari M, Pagotto U 2006 The hypothalamic-pituitary-adrenal axis activity in obesity and the metabolic syndrome. Annals of the New York Academy of Sciences 1083:111-128

55.         Couet C, Delarue J, Ritz P, Antoine JM, Lamisse F 1997 Effect of dietary fish oil on body fat mass and basal fat oxidation in healthy adults. International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity 21:637-643

56.         Kabir M, Skurnik G, Naour N, Pechtner V, Meugnier E, Rome S, Quignard-Boulange A, Vidal H, Slama G, Clement K, Guerre-Millo M, Rizkalla SW 2007 Treatment for 2 mo with n 3 polyunsaturated fatty acids reduces adiposity and some atherogenic factors but does not improve insulin sensitivity in women with type 2 diabetes: a randomized controlled study. The American journal of clinical nutrition 86:1670-1679

57.         Delarue J, Couet C, Cohen R, Brechot JF, Antoine JM, Lamisse F 1996 Effects of fish oil on metabolic responses to oral fructose and glucose loads in healthy humans. The American journal of physiology 270:E353-362

58.         Huffman DM, Michaelson JL, Thomas T, R. 2004 Chronic supplementation with fish oil increases fat oxidation during exercise in young men. . JEPonline 7:48-56

59.         Hill AM, Buckley JD, Murphy KJ, Howe PR 2007 Combining fish-oil supplements with regular aerobic exercise improves body composition and cardiovascular disease risk factors. The American journal of clinical nutrition 85:1267-1274

60.         Thorsdottir I, Tomasson H, Gunnarsdottir I, Gisladottir E, Kiely M, Parra MD, Bandarra NM, Schaafsma G, Martinez JA 2007 Randomized trial of weight-loss-diets for young adults varying in fish and fish oil content. Int J Obes (Lond) 31:1560-1566

61.         Kunesova M, Braunerova R, Hlavaty P, Tvrzicka E, Stankova B, Skrha J, Hilgertova J, Hill M, Kopecky J, Wagenknecht M, Hainer V, Matoulek M, Parizkova J, Zak A, Svacina S 2006 The influence of n-3 polyunsaturated fatty acids and very low calorie diet during a short-term weight reducing regimen on weight loss and serum fatty acid composition in severely obese women. Physiological research / Academia Scientiarum Bohemoslovaca 55:63-72

62.         Brilla LR, Landerholm TE 1990 Effect of fish oil supplementation and exercise on serum lipids and aerobic fitness. The Journal of sports medicine and physical fitness 30:173-180

63.         Warner JG, Jr., Ullrich IH, Albrink MJ, Yeater RA 1989 Combined effects of aerobic exercise and omega-3 fatty acids in hyperlipidemic persons. Medicine and science in sports and exercise 21:498-505

64.         Krebs JD, Browning LM, McLean NK, Rothwell JL, Mishra GD, Moore CS, Jebb SA 2006 Additive benefits of long-chain n-3 polyunsaturated fatty acids and weight-loss in the management of cardiovascular disease risk in overweight hyperinsulinaemic women. Int J Obes (Lond) 30:1535-1544

65.         DeFina LF, Marcoux LG, Devers SM, Cleaver JP, Willis BL 2011 Effects of omega-3 supplementation in combination with diet and exercise on weight loss and body composition. The American journal of clinical nutrition 93:455-462

66.         Bays HE, Maki KC, Doyle RT, Stein E 2009 The effect of prescription omega-3 fatty acids on body weight after 8 to 16 weeks of treatment for very high triglyceride levels. Postgraduate medicine 121:145-150

About Monica Mollica > www.trainergize.com

Monica Mollica has a Bachelor and Master degree in Nutrition from the University of Stockholm / Karolinska Institue, Sweden. She has also done PhD level course work at renowned Baylor University, TX. Today Monica works as diet/health counselor, medical writer, health journalist, and website developer. She is also a fitness model.

As a young athlete, Monica realized the importance of nutrition for maximal performance, and went for a major in Nutrition at the University of Stockholm. During her years at the University she was a regular contributor to Swedish fitness and bodybuilding magazines. She has written a book (in Swedish) for health professionals, “Functional Foods for Health and Energy Control” with over 700 scientific research citations, and authored several book chapters in Swedish popular press publications.

After having earned her Bachelor and Master degree in Nutrition, she completed one semester at the PhD-program “Exercise, Nutrition and Preventive Health” at Baylor University Texas, Department of Health Human Performance and Recreation.

Having lost her father in a lifestyle induced heart attack at an age of 49, she is specializing in cardiovascular health, and primordial/primary prevention. She is a strong advocate of early intervention in adolescence and young adulthood, and the importance of lifestyle habits for health promotion at all ages.

Today, Monica is sharing her solid academic knowledge, real-life hands on experience and passion by offering diet/nutrition/exercise/health consultation services, and working as a health journalist and medical writer, specializing in fitness, health promotion and anti-aging.

 

Brown rice protein: for your digestive and athletic needs

By Scarlett Blandon, MS RDN.  Unless you were a vegan (or a yogi…or maybe a protein powder junky) the chances of you knowing about brown rice protein are slim to none.  Rice protein is a novel source of protein derived from the entire rice grain (including bran layer), and is available as brown-rice-jara concentrate or isolate just like other protein powders.  It offers several benefits that other protein powders do not, but chances are those merits have been drowned out by:  (1) the negative stereotypes surrounding rice protein’s  plant-based origin; (2) the popularity and media-hype of whey protein.  Sure, rice protein might not have all the looks and attractive qualities that whey does, but it’s those unique differences that make it an outstanding alternate protein source for athletes and sports enthusiasts alike.  Here are a few reasons why you might consider brown rice protein:

Easy on the stomach—and the immune system.

Dairy- and soy-derived protein supplements might be wonderful for X number of reasons, but unfortunately, not everyone can digest these proteins, and some might even be highly allergic to them.  The Food Allergy Research & Education organization states that about 15 million Americans have food allergies and this number appears to be on the rise1.  Milk and soy happen to be two of eight foods accounting for 90% of all food allergies1. Aside from dairy allergies, 30-50 million Americans are lactose intolerant2.  And despite lactose-free claims on dairy-derived protein supplements, many still anecdotally experience GI distress which can negatively interfere with training or performance (or number of friends :-) ).

Gluten is another, increasingly common immune-system offender. Some commercial protein supplements may contain ingredients derived from or made with gluten. This can be detrimental to the 3 lowcarb_riceoatsmillion Americans diagnosed with Celiac disease and many more who remain undiagnosed3.  What’s worse is that damage to the microvilli from gluten can actually cause a person to develop lactose-intolerance, rendering them doubly restricted from those food groups4.

On the other hand, brown rice protein is derived from rice, a well-known hypoallergenic food source.  As a staple food in many cultures (for thousands of years!), rice is highly unlikely to elicit an allergic reaction (or intolerance) and is not surprisingly recommended as a first food for babies.  As such, rice protein is expectedly gentle on the GI tract and may offer greater benefit to those athletes or exercise enthusiasts with food allergies, intolerances or sensitivities.

Aids in recovery and builds muscle, much like whey.

Up until recently, nothing was truly known about the ability of rice protein as a sports nutrition supplement.  Despite this, rice protein withheld much criticism from the athletic and scientific community given previous literature on the generally inferior quality of plant-based proteins and other data showing that low doses of plant-based proteins (mainly soy- and wheat-derived) do not increase muscle protein synthesis compared to animal-based proteins5,6.

Yes, rice and thus rice protein is limited in lysine and apparently less digestible than dairy proteins. But do these apparent “weaknesses” in rice protein make it unsuitable for sports nutrition? One study to date, says no.

The study, published in Nutrition Journal in June 2013, found that 24 collegiate athletes were able to obtain significant gains in muscle, power and strength whether they were taking a 48g rice protein or whey protein supplement following resistance training for 8 weeks7. They also experienced similar increases in acute recovery. Despite differences in amino acid profile, digestibility and digestion rate of the proteins, there were no statistical differences between groups.  The authors assert that protein type or composition is of less significance, when key nutrients are adequately provided. In this case, one key nutrient: leucine.  The leucine levels provided by the brown rice protein supplement appeared to be within or above the 2-3g threshold needed to maximize muscle protein synthesis8-11.

Although more research is needed in this arena for rice protein, these results indicate that at 48g, rice protein can serve as a substitute for whey protein for building muscle and strength.  This would be especially beneficial for those athletes who follow a vegan/vegetarian lifestyle, are unable to digest dairy-based proteins and/or are looking for an alternate protein source.

Suits vegan or other plant-based lifestyles.

Almost 16 million people consider themselves vegetarian and another 6 million consider themselves vegan in the US alone according to one 2012 survey12.  Motives behind these plant-based lifestyles might include views on animal welfare, religious and cultural beliefs and/or environmental concerns.  However, 47% of vegans indicate that their major reason for following this diet is actually health, followed by animal welfare (40%)13.  While exercise is a health-related activity, it is not unreasonable to consider the inclusion of some athletes or sports enthusiasts in this population.

Although vegans & vegetarians are able to consume all essential nutrients from plant-based foods alone, it can be a challenge for athletes when certain nutrients like protein are needed in higher quantities.  Supplements like rice protein offer a convenient and concentrated source of protein to help meet their needs. Unlike soy, rice protein does not contain phytoestrogens which can potentially interfere with hormones.

Rice protein is also an excellent option for those trending on natural or other plant-based lifestyles.  Unlike many dairy- or soy-based protein supplements, rice proteins are predominantly processed using only water and natural enzymes rather than toxic solvents like hexane. Certain rice proteins may also offer value over other protein sources since it is not from a genetically modified source, does not come from an animal known to be treated with growth hormones (rbST/bGH), anabolic steroids (AAS), estrogens and other hormones, antibiotics or other chemicals known to, suspected of, to affect or have an impact upon human health.

Whether you are looking to rotate your protein source, give your stomach a break, trend on a novel and natural product all while building muscle and gaining strength, rice protein might be the choice for you.

About the Author: Scarlett Blandon is the in-house nutrition scientist for Axiom Foods, the worlds’ leading manufacturer of hexane-free rice protein among other plant proteins, and for Growing Naturals, a consumer brand specializing in hypoallergenic plant proteins and natural lifestyle products. At Axiom and GN she oversees all research-related ventures and nutrition communications. Having worked closely with renowned researchers in the past, she is dedicated to expanding the literature on rice- and other plant proteins while cultivating the knowledge of consumers and manufacturers alike.

REFERENCES

  1. Facts and statistics. Food Allergy Research and Education. Available at:  http://www.foodallergy.org/facts-and-stats
  2. Lactose intolerance. Wexner Medical Center, Ohio State University. Available at: http://medicalcenter.osu.edu/patientcare/healthcare_services/digestive_disorders/lactose_intolerance/Pages/index.aspx
  3. Case S. Celiac disease, gluten sensitivity and the gluten-free diet. July 2011. Available at: http://www.nutrition411.com/component/k2/item/28313-celiac-disease-gluten-sensitivity-and-the-gluten-free-diet
  4. Lactose intolerance and celiac disease. Celiac Disease Foundation. Available at: http://www.celiac.org/images/stories/PDF/lactose-intolerance.pdf
  5. Wilkinson SB, Tarnopolsky MA, Macdonald MJ, et al. Consumption of fluid skim milk promotes greater muscle protein accretion after resistance exercise than does consumption of an isonitrogenous and isoenergetic soy-protein beverage. Am J Clin Nutr. 2007; 85: 1031-1040.
  6. Norton LE, Layman DK, Bunpo P, et al. The leucine content of a complete meal directs peak activation but not duration of skeletal muscle protein synthesis and mammalian target of rapamycin signaling in rats. J Nutr. 2009; 139: 1103-1109.
  7. Joy J, Lowery RP, Wilson JM, et al. The effects of 8 weeks of whey or rice protein supplementation on body composition and exercise performance. Nutrition J. 2013; 12:86
  8. Norton LE, Layman DK. Leucine Regulates Translation Initiation of Protein Synthesis in Skeletal Muscle after Exercise. J Nutr. 2006; 136(2): 533S-537S.
  9. Norton L, Wilson GJ. Optimal protein intake to maximize muscle protein synthesis. Agro Food industry hi-tech. 2009; 20: 54-57.
  10. Paddon-Jones D, Sheffield-Moore M, Zhang XJ, et al. Amino acid ingestion improves muscle protein synthesis in the young and elderly. Am J Physiol Endocrinol Metab. 2004; 286: E321-E328.
  11. Tipton KD, Ferrando AA, Phillips SM, et al. Postexercise net protein synthesis in human muscle from orally administered amino acids. Am J Physiol. 1999; 276: E628-E634.
  12. Newport F. In the US, 5% consider themselves vegetarian. Gallup Wellbeing. 2012. Available at: http://www.gallup.com/poll/156215/consider-themselves-vegetarians.aspx

 

Choosing the right “Cardio Modality” for pre and post workouts?

By Chris and Eric Martinez, CISSN, CPT, BA.  The lovely world of cardio, we have to love it right? Cardio has countless benefits for the human body, so it must be good for us, right? How else do you think all the celebrities stay so skinny and “toned?”cardio-on-empty-stomach1

How many times have you seen people get to the gym and hop on a cardio machine and just gas themselves, and not to mention go do some resistance training right after. Or what about when someone gets done from an intense lifting session, then goes off and does an intense cardio session?

We know you’ve seen this before and we are not going to get into the psychology of why people do this because that could be a whole other article itself. We are more focused on is it optimal to perform cardio pre and post workout? With a specific focus on which cardio modality (type of cardio you do) is the best to perform to avoid the interference effect of strength, power, and hypertrophy gains? But before we give you the answer, it’s vital that we always have to take people’s goals, activity level, overall health, and training experience into consideration before anything. So please read this with an open mind and a non-black and white answer, all or nothing approach.

What’s This Interference Effect Thing?

When we refer to the interference effect, we are talking about the interference of strength, power, and hypertrophy gains (muscle growth) when doing cardio pre or post workout. This topic of discussion has been floating around for quite some time now, whether concurrent training is optimal or not.

We all have our biased opinions, but what is the correct cardio modality to do pre and post workout and should we even be doing cardio pre or post workouts? That is the million dollar question that many of us would like to know.

Why continue to keep robbing your hard earned gains and progress if you don’t need to. Instead, why not continue to maximize your overall potential the correct way instead of shooting yourself in the foot? As always, we bring scientific based evidence to the table to get to the bottom of these popular topics, because the research doesn’t lie folks.

Before we delve into the research, we want to quote what Brad Schoenfeld said:

“There is no one cookie-cutter recommendation I can provide that will be ideal for everyone. People have varying responses to exercise programs. Large inter-individual differences are seen in any research protocol. Thus, in giving advice on a topic such as this, I can only provide general recommendations that must be individualized based on a variety of genetic and environmental factors. This is the essence of evidence-based practice, which should form the basis of every fitness professional’s decision making process.” (1)

We can’t agree more with this statement and we truly feel this statement is a legitimate and valid way of viewing such a topic like this one.

Cardio Modalities

We are certain we can all agree that there are numerous different cardio modalities out there today. To name a few modalities that have more ground-reaction force with higher impact are:

Pretty much all the badass cardio workouts that we look forward to doing.

Cardio modalities that minimize ground-reaction forces are:

  • Cycling bikes
  • Treadmillscardio-gym2
  • Ellipticals
  • Various machine based equipment

The stuff we like to watch TV on or read magazines 😉

These are all great choices whether you use them in the form of HIIT or LISS, but which modality is more optimal to prevent the interference effect and when should you do these you ask? Let’s delve into some research shall we.

Should you do cardio pre or post workout?

Layne Norton and Jacob Wilson claim that when you choose a cardio modality such as running or sprinting after a resistance training bout, the ground-reaction force (think sprints) and distance causes more muscle damage as opposed to a modality with less impact such as cycling instead. Cycling seems to be more similar to hip and knee flexion as opposed to running because it’s biomechanically interfering with squat and leg press patterns. This muscle damage seems to be coming from the eccentric components when running and sprinting (2).

Norton and Wilson make a valid point in the essence that if you are going to do cardio post workout, make sure you do it in the form of an opposing muscle group. Let’s say you did a grueling lower body workout, you would then want to do cardio in the form of using your upper body, something like rope slams because otherwise if you go and run or do sprints you are going to get a complete interference effect and possibly get injured.

After resistance training you have mTOR (cell growth) being ramped up and protein synthesis (making of new proteins) being turned on and when you do cardio after resistance training you get such high drastic rises in AMP kinase (signaling cascade for ATP production) that it ends up shutting off protein synthesis. In easier terms, cardio after weights interferes with the muscle growth phase and a good analogy is after training you turn the faucet on for muscle growth and when too much cardio is being done or after training, it shuts the faucet off.

As for pre workout cardio, this tends to be a little trickier than post workout cardio and we say this because it really depends on a lot of factors such as: What muscle groups are you training that day? What form of cardio are you doing pre workout (low, moderate, or high intensity)? What modality will you use? Are you in a low calorie and glycogen depleted state?

A Study in the Medicine and Science in Sports and Exercise shows 30 minutes of jogging pre workout decreases volume of spinal discs and leads to a reduction in the amount of weight you can load on your back (3). For example, if you did a moderate-high intensity cardio bout such as jogging before squats it’s probably not a good idea because it will lead to decrements in strength and negatively affect your squats. Jogging shows to have a lot of muscle damage in the quads, hams, and glutes, so this will definitely affect your squat game.

A 2012 study in the International Journal of Sports Nutrition showed extended periods of moderate volume concurrent strength, power, and endurance training interferes with explosive strength development (4). This is not something you want if you’re trying to increase your 1 rep max on squats and deadlifts.

The data is pretty clear that performing moderate-high intensity cardio pre workout will lead to decrements in strength and power with your resistance training. Perhaps doing cardio earlier in the day and performing resistance training later in the day will not have a negative impact on either the performance or the measured markers of the exercise induced growth stimulus the resistance training session will have. However, we highly encourage doing resistance training and cardio on separate days as this would be the most optimal route to go.

Is there really an interference effect?

            In a study by Wilson et al. a large body of research indicates that combining aerobic and resistance exercise (concurrent training) has a negative effect on gains in muscular strength and size (5). There is credence to the underlying concept that catabolic processes predominate to a greater extent in aerobic training, and concurrent exercise therefore has the potential to impair muscular gains. There is even evidence that cardio can blunt the satellite cell response (helps with muscle growth) to a bout of resistance exercise and therefore potentially impair the protein-producing capacity of muscle (6). With that said, why are people still considering doing cardio pre or post workout if clearly the evidence indicates that it can potentially inhibit muscular gains, strength, and power?

What if you could avoid the interference effect?

            Burn more calories, increase muscle, and acutely increase your metabolic rate, sounds good, right? This is where the famous HIIT cardio would come into play. When you think of HIIT, high intensity and high stress should be taken into consideration. What we have to keep in mind is that stress has to be recovered from, just like the stress from weight training. Last time we checked HIIT cardio is done during the week along with resistance training. If you are still recovering from a HIIT cardio session to the point that it affects your ability to lift weights, then it can be detrimental to your gains. If there is a significant eccentric component (sprinting and running), or high level of impact, HIIT can cause problems in your overall training and potentially lead to chronic overuse injuries. You have to be cautious and smart when incorporating HIIT into your training protocol because it seems that the work to rest ratios in HIIT intervals are very similar to resistance training sets and your number one focus should be on progressive resistance training.

Here are some ways to avoid the interference effect.

  • Schedule your cardio around your resistance training, especially HIIT cardio
  • If your number one priority is resistance training, then perform cardio modalities that minimize ground-reaction forces
  • Perform a cardio modality that is opposite of the muscle group your training. For example, if you do train legs then do an upper body dominate form of cardio and vice versa
  • If you absolutely have to do cardio the same day as your resistance training and you can’t find a cardio modality opposite of the body part you trained then make sure to keep the intensity to low-moderate

Wrapping this up

We believe that the research is pretty clear here when it comes to this particular topic. Clearly there is no black and white answer, sorry to disappoint, but at least we have a great indication of what to do and when not to do it. It’s tough to predict that anyone can avoid any interference effect when it comes to aerobic or anaerobic training. Just like anything else you have to compensate something. We are not all built like machines and able to handle the same workload as others. Genetics always play a vital role in how someone responds to training. Other factors such as nutrition, stress, sleep, occupational activity, ect. All must be taken into account. Refer back to Brad Schoenfeld’s quote if needed, it pretty much tells you there are only general recommendations that can be given here. The best thing to do is choose the correct cardio modality that suits your training and goals. Always train hard, think logically, and but most importantly train smart.

References:

(1)  Schoenfeld, AARR Research Review. Cardio Roundtable Discussion. February and March 2013.

(2)  Norton, L & Wilson J. Muscle college radio with Dr. Layne Norton & Dr. Jake Wilson. http://www.rxmuscle.com/2013-01-11-01-57-36/muscle-college/7694-muscle-college-3-12-13.html

(3)   Kingsley, MI., et al., Moderate-Intensity Running Causes Intervertebral Disc Compression in young adults. Med Sci Sports Exerc, 2012.

(4)  Mikkola, et al., Neuromuscular and cardiovascular adaptations during concurrent strength and endurance training in untrained men. Int J Sports Med. 2012.

(5)  Babcock, L, Escano, M, D’Lugos, A, Todd, K, Murach, K, and Luden, N. Concurrent aerobic exercise interferes with the satellite cell response to acute resistance exercise. Am. J. Physiol. Regul. Integr. Comp. Physiol. 302: 2012.

(6)  Wilson, J.M., et al., Concurrent Training: A Meta Analysis Examining Interference if Aerobic and Resistance Exercise. J Strength Cond Res, 2011.

About The Authors:

Chris and Eric Martinez, CISSN, CPT, BA, also known as the “Dynamic Duo” operate a world class personal training and online training business “Dynamic Duo Training,” They’re also fitness and nutrition writers, fitness models, and coaches that love helping people reach their goals. Their philosophy is “No excuses, only solutions.”

Visit them at:

Dynamic Duo Training

Blogsite

FaceBook Page

Twitter

YouTube Channel 

Phosphatidic Acid: The Next Anabolic Breakthrough?

By Richard Choueiri.  Over the past few decades, several non-hormonal compounds have gained popularity as a result of their anabolic effects on the human body. Among these compounds are creatine, arachidonic acid and, of course, the branched-chain amino acid leucine. Thanks to the ongoing research in the field of sports nutrition, scientists might have just discovered the next anabolic breakthrough: phosphatidic acid (PA).

imgf000004_0001PA, chemical structure 1,2-diacyl-sn-glycero-3-phosphate, is a type of phospholipid integral to the structure of cell membranes. In addition, it is a key metabolite in the biosynthesis of several phospholipids and triacylglycerols, which are more commonly referred to as triglycerides. Furthermore, PA acts as a signaler to proteins and this is where things get exciting.

One of the proteins PA signals is the mammalian target of rapamycin (mTOR), a serine- and threonine-specific kinase that regulates cell growth, such as muscle cell hypertrophy. It is well established in the field of sports nutrition that a roughly three-gram bolus dose of leucine is required for turning on the mTOR pathway, thus activating protein synthesis. This fact leads to an important question: can mTOR signaling be further enhanced to maximize protein synthesis?

Researchers at the Human Performance Laboratory in Orlando, Florida, conducted a study using PA to gain more insight on its effects mTOR. The researchers randomly assigned 16 resistance-trained young men to one of two groups. One group was given 750mg of PA and the other group was provided with a placebo, 750mg of rice flour. The subjects were assigned to a one-rep max attempt on the bench press and the squat, two fundamental compound lifts. The researchers obtained body composition data and ultrasonography of the subjects during the first testing session to establish baselines. An ultrasonography is a type of ultrasound imaging technique for muscles, tendons and joints.

resistance-training2After an eight week trial of PA-supplementation, in which the subjects were asked perform a four-day per week resistance training protocol comprised of exercises using 70% of their one-rep max, researchers conducted a second body composition and ultrasonography test. The subjects were also asked to perform a second one-rep max attempt on the bench press and the squat. Both groups increased their squatting strength, the PA-supplementing group more so than the placebo group at 12.7% and 9.3%, respectively. As for body composition changes, the PA group achieved a 2.6% increase in lean body mass, while placebo group only gained 0.1%. These findings suggest that PA has an anabolic effect on resistance trained men, in addition to increasing lower body strength, when combined with a resistance training protocol consisting of exercises performed at 70% of one-rep max.

It is possible that the anabolic effect of PA documented in the study may have been due to an enhancement of mTOR via PA’s signaling ability. Research by the Pennsylvania State University College of Medicine has suggested that PA binds to mTOR and enhances mTORC1 activity, so this could very well be the mechanism of action that leads to PA’s anabolic effect. mTORC1 is one of two multi-protein complexes that make-up mTOR, the other complex being mTORC2.

Although the research on phosphatidic acid and its potential non-hormonal anabolic effects is still in the preliminary stages, this compound looks very promising. Don’t be surprised if PA begins to pop up on supplement ingredients lists in the near future. The next anabolic breakthrough may have just arrived.

References:

Fang, Y., et al. (2001). Phosphatidic acid-mediated mitogenic activation of mTOR signaling. Science. 294:1942-1945.

Hanahan, D.J., et al. (1984). Phospholipids as dynamic participants in biological processes. Journal of Lipid Research. 25:1528-1535.

Hoffman, J.R., et al. (2012). Efficacy of phosphatidic acid ingestion on lean body mass, muscle thickness and strength gains in resistance-trained men. Journal of the International Society of Sports Nutrition. 9:47.

Rasmussen B. (2009). Phosphatidic acid: a novel mechanical mechanism for how resistance exercise activates mTORC1 signaling. Journal of Physiology. 587:3415-4316.

Winter, J.N., et al. (2010). Phosphatidic acid mediates activation of mTORC1 through the ERK signaling pathway. American Journal of Physiology: Cell Physiology. 299:C335-C344.

Xiaochun B., et al. (2009). Key factors in mTOR regulation. Cell and Molecular Life Sciences. 67:239-253.

You, J.S., et al. (2012). Mechanical stimulation induces mTOR signaling via an ERK-independent mechanism: implications for a direct activation of mTOR by phosphatidic acid. The Public Library of Science ONE. 7(10): e47258. doi:10.1371/journal.pone.0047258.

Bio – Richard Choueiri

Richard Choueiri is a professional writer specializing in fitness, nutrition and health. His work has been featured on over 10 major online and print publications. He is the author of The Human Statue Workout: Your 365 Day-a-Year Guide to Transforming Your Body Into a Masterpiece. Richard double majored in exercise science and nutritional science at Rutgers University. He holds a personal trainer certification through the American College of Sports Medicine.  Richard has over a decade of training experience.

Long-Chain Omega-3 Fatty Acids: Friend or Foe to Prostate?

Long-Chain Omega-3 Fatty Acids: Friend or Foe to Prostate?

There’s more than meets the eye regarding the recent controversy over omega-3 levels and prostate cancer risk — Lets take a closer look.  Hector Lopez, MD, CSCS, FAAPMR.  A large-scale prospective case-cohort study evaluating plasma fatty acid levels and prostate cancer risk, published in JNCI (Journal of the National Cancer Institute) online ahead of print on July 10th, 2013 has created quite the stir amongst media, health care professionals, nutrition researchers, and the dietary supplement industry…Again! To quote the great Yogi Berra, “It’s like déjà vu, all over again.” 

ms-diet-omega-3-6-575x262

This recent study was led by Drs. Alan Kristal from the Fred Hutchinson Cancer Research Center, and Theodore Brasky of The Ohio State University Comprehensive Cancer Center in the USA as a follow up to their 2011 study.  This new study analyzed data and blood plasma phospholipid status from men who participated in the SELECT (Selenium and Vitamin E Cancer Prevention Trial) trial from 427 participating sites across Europe, USA, Canada and Puerto Rico. Blood was analyzed for 834 “cases” diagnosed with prostate cancer (156 of which were high-grade), and an age-matched subcohort, comparison group of 1,393 all of which were selected from the 35,533 participants.

Without going into an in-depth review of the study (beyond the scope or goal of this post), the men with the highest blood plasma levels of the long-chain omega-3 PUFAs (EPA, DPA, and DHA) were associated with increased risk for low-grade, high-grade and total prostate cancer (44%, 71% and 43% increased risk, respectively).  Intriguingly, a higher omega-6 level (Linoleic acid) was associated with reduced risk of low-grade and total prostate cancer, but there was no dose response relationship. prostatecancercompare

A few salient points to consider here:

1) Within the prostate cancer cases, their plasma phospholipid fatty acid profile was divided into quartiles. The lowest risk group had < 3.68% tissue levels (plasma phospholipids) VS. highest prostate CA risk group being at > 5.3%. This is quite a narrow range of plasma phospholipid fatty acid concentration to draw conclusions from.  Moreover, the mean EPA + DPA + DPA fatty acid % in plasma phospholipids was only 4.48% in controls (non-cancer group), and 4.66% in the total cancer case group. Again, an even narrower range–caution must be taken before drawing sweeping or extreme conclusions and interpretation of this data. So, what does that mean for individuals who are supplementing actively with fish oil and simultaneously keeping vegetable oil LA (omega-6) intake down that typically walk around at 7-15% (who incidentally have lowest sudden cardiac death risk and lowest 25-year mortality rates)?

It is possible, that some biochemical scenario plays out where, with respect to prostate CA, you are better off either being real low (at which point your risk for cardiovascular morbidity & mortality goes up), or at the higher goal range of >8%?  There is some interesting preclinical, mechanistic data showing that high levels of DHA increases expression of SDC-1 (a transmembrane proteoglycan) in prostate tissue.  SDC-1 may help with mediating apoptosis (programmed cell death) of prostate cancer cells, by suppressing proto-oncogene (a normal gene that when mutated can cause cancer by deranging cell growth and differentiation mechanisms) signaling.

2) This is NOT a (RDBCT)…it isn’t even an open label “intervention-based” trial. Simply an epidemiologic, nested case-cohort based association.  The SELECT study was not designed specifically to look at omega-3 fatty acid associations, a priori (from earlier knowledge). That simply means the original SELECT randomized, placebo-cotrolled clinical trial was not originally set up to answer the question of whether “Increased intake of long-chain omega-3 polyunsaturated fatty acids lead to increased rates of prostate cancer development.”  Hence, that limits the “robustness” and “strength of causality assessment” of the data. Further, there was no mention in the study of dietary fish intake or fish oil supplementation.  Is it possible that the sicker individuals began taking fish oil or increasing their fish intake in an attempt to improve their health? Again, it does not allow us to discern whether the “association” exists with fish oil supplementation vs. fish from food sources vs. particular type of fish [Salmon vs. Mackerel vs. Sardine vs. Cooked (Grilled, Baked or Fried) or Raw as in Sushi]. Could there be some xenobiotic or persistent organic pollutants acting as a carcinogen in one of these sources?  After all, it is well established that certain heavy metals (e.g., cadmium, mercury), dioxins and PCBs are mutagenic and carcinogenic.

A few things stand out about the methods used to evaluate fatty acid status.  First, the plasma phospholipid fatty acid assay is considered to be more representative of ACUTE and dynamic biomarker of omega-3 fatty acid intake by many experts in the biochemical analysis of fatty acids.  Short-term factors such as a single meal or supplemental fish oil dose can increase plasma phospholipid omega-3 levels by over 2-fold within 6-10 hours. That is because this assay includes lipids found in the lipoprotein fraction of blood (such as chylomicrons, LDL subtypes, VLDL, etc.), not just in cell plasma membranes such as the omega-3 index (% of omega-3 fatty acids in RBC membrane).  Erythrocyte (or Red Blood Cell) membrane fatty acid analysis is a more reliable biomarker of SUBACUTE omega-3 fatty acid intake, with stable values reflecting dietary intake over a 2-3 month period.

Let’s admit that this study utilized data mined from a very large, prospective study, with a large number of prostate cancer cases—this is a strength. The SELECT trial that this study was based on had a very good follow up and small amount of attrition.  This minimizes the potential for a phenomenon we observe in research known as attrition bias (a kind of selection bias, where the subjects who dropout are discounted, effectively changing the characteristics of one comparison group vs. another that may lead to drawing inappropriate conclusions from the data/results).

3) Then, we do need to consider the question of whether there is “fire at the heart of this smoke” that could be attributable to some as yet undetermined mechanism?  After all, there are at least 3 more large studies that support the findings of this study.  However, there are also at least 3 other studies that conflicts with the current study showing an inverse relationship between long-chain n-3 PUFA tissue levels and prostate cancer risk.  Keep in mind that cancer biology is incredibly complex with, not only many factors that contribute to risk, progression, etc., but also many of these very factors interact to create even more layers of complexity.

Having said that,  I have a few theories, including:

** In the case of prostate biology, immune “surveillance” of cellular oncoproteins play a much larger role in identifying and creating cytotoxicity and apoptosis (programmed cell death pathways) to keep these precancerous cells at bay.

** At certain levels of tissue n-3 concentration, there may be a physiologic/molecular environment whereby mitogenic/ oncogenic and cellular proliferative pathways are driven forward and, while tumor suppressive and differentiation pathways are inhibited. This scenario could promote tumorigenesis/ carcinogensis, especially in a scenario where there is just enough immune suppression to allow for this cellular activity to spiral out of control, without the typical safety mechanism and breaks that would limit DNA mutagenesis & damage.

** Lipid peroxides generated at the local prostatic tissue level may, in certain individuals, overwhelm their capacity to neutralize this oxidative stress.  This scenario could theoretically lead to increased DNA damage, that increases potential to outpace DNA repair mechanisms and transform cells to loose cell growth/proliferation regulation.

** Could there be certain genotypes (nutrigenetic & epigenetic mechanisms) that increase susceptibility to the above theories? Given what we have learned from genome wide association studies (GWAS) in the last decade, this is certainly a possibility.

4) Interestingly, this association appears to be tissue specific. As opposite association (inverse relationships) exist for omega-3 status and other cancers, e.g., breast, colon, and possibly pancreatic.

5) There is interesting data that demonstrates what I would refer to as a “metabolic dissonance” in energy metabolism of prostate cancer cells.  In stark contrast to cancers of other tissues, where metabolism becomes more heavily glycolytic (strong preference to using glucose for fuel during energy metabolism), prostate adenocarcinoma cells appear to switch toward greater beta-oxidation of fatty acids to drive its bioenergetic needs! This “metabolic dissonance” with respect to the unique physiology of prostate cancer could very well be a major factor leading to the observed association between long-chain omega-3 PUFA and prostate tumorigenesis in Brasky et al study.

6) Prostate cancer detection has increased dramatically over the last 10-15 years, not only due to the prevalence of PSA screening, but also lower threshold to biopsy has lead to increased diagnosis.  This is particularly the case with detection of microfoci of prostate malignant cells in smaller (lower volume) prostates…Hence, there is a greater probability of sampling malignant microfoci in smaller prostates.  This is an aspect that was not controlled for (Hazard ratios in the study were not adjusted for this variable) in the Brasky et al study.

7) There is also robust evidence that contradicts and opposes the conclusions and interpretation of the Brasky et al data.  For example, the work of Chua et al. (2013), Sorongon-Legaspi et al. (2013), Torfadottir et al. (2013), Chavarro et al (2008), Terry et al. (2001), Harvei et al (1997), and others show a protective effect of higher levels of tissue omega-3 fatty acid status, with lower prostate cancer risk and prostate cancer mortality.

8) It is also imperative to try adding context and maintaining perspective whenever faced with new information that may change behavior; or in this case, information that may change clinical management and dietary advice.  Lets keep the following numbers in mind to add some more perspective, color and light to this data from a public health, and risk assessment standpoint. (from National Cancer Institute-Surveillance Epidemiology and End Results, and National Heart, Blood and Lung Institute-NIH):

Prostate Cancer- U.S. :

  • Age-adjusted incidence rates (for all races) from 2006-2010: ~152/ per 100,000 men
  • Age-adjusted death rates (for all races) from 2006-2010:  ~23/ per 100,000 men
  • Prevalence of prostate cancer diagnosis: ~2.6 million men on January 1, 2010
  • Direct cost burden from prostate cancer in U.S. in 2010:  ~$14 Billion

Cardiovascular Disease- U.S.

  • Age-adjusted death rates (for all races) from in 2008:  ~244/ per 100,000 population (both men and women)
  • Prevalence of cardiovascular disease diagnosis: ~82.6 million men in 2006
  • Direct cost burden from CVD in U.S. in 2008: ~$218 Billion

9) Although the jury is still not out with respect to the relationship long-chain omega-3 PUFAs found in fatty fish and fish oil and prostate cancer risk, progression or severity, I believe the sheer numbers tell us what the lowest hanging fruit is relative to public health focus and resources.  I do agree with the authors that prostate health history should be taken at least be taken into consideration, when weighing potential risk to benefit ratio of increasing long-chain n-3 PUFA intake.

10) As with so much in science, medicine, health and nutrition, the more data we have access to, the more questions arise.  One burning question this study raises that is of interest to consumers, industry and health care providers—How would these findings change when evaluating specific dietary sources of long-chain n-3 PUFA (e.g., concentrated fish oil supplements vs. Sushi vs. Baked, Grilled or Fried fish)?

Overall, the benefits of increasing omega-3 status (and decreasing omega-6 overabudnance) for most people FAR outweigh potential risks.  Stay tuned…but as always keep a cool head and try to avoid being drawn into dramatic, emotionally-charged and sensational headlines. These observational, case-control cohort studies may be useful for generating hypotheses to test in well-controlled prospective clinical trials, but far from establishing causality. So, what am I doing with this information you ask?  Well…I’m still taking my fish oil, eating a variety of fish while we await for stronger evidence (which I seriously doubt we’ll ever see :)). Oh, and by the way, NO…I am not going to intentionally increase my omega-6 vegetable oil intake—despite the fact that this study revealed that elevated plasma omega-6 fatty acid levels were associated with decreased risk of low-grade and total prostate cancer. Remember to take your fish oil and call me in the morning! J

BIO – Hector Lopez, MD, CSCS, FAAPMR

Dr. Lopez is a board-certified specialist in physical medicine and rehabilitation, with a concentration in spine, sports and musculoskeletal medicine. He also has post-graduate training in nutritional biochemistry. An active researcher, speaker, author, and clinician, he is recognized for uniquely integrating the best available methods in the fields of musculoskeletal medicine, endocrinology and metabolism, regenerative medicine, exercise and nutritional science. Dr. Lopez has been a founding partner and director of several integrative orthopedic, spine, and sports medicine facilities, and he is a principal and chief medical officer of the Center for Applied Health Sciences (CAHS), a leading multidisciplinary clinical research institute. Dr. Lopez is also co-founder of Supplement Safety Solutions (SSS), a NutravigilanceTM, quality assurance, medical monitoring, and regulatory consulting company. In addition, he is a consultant to professional athletes and to the nutritional supplement industry as product developer, research advocate, and safety and regulatory expert.

References

  • Brasky T, Darke A, Song X, Tangen C, Goodman P, Thompson I, Meyskens F, Goodman G, Minasian L, Parnes H, Klein E, Kristal AR. Plasma Phospholipid Fatty Acids and Prostate Cancer Risk in the SELECT Trial. J Natl Cancer Inst. 2013 Jul 10 [Epub ahead of print].
  • Chua ME, Sio MC, Sorongon MC, Morales ML Jr. The relevance of serum levels of long chain omega-3 polyunsaturated fatty acids and prostate cancer risk: A meta-analysis. Can Urol Assoc J. 2013 May;7(5-6):E333-43.
  • Harris WS, Pottala JV, Varvel SA, Borowski JJ, Ward JN, McConnell JP. Erythrocyte omega-3 fatty acids increase and linoleic acid decreases with age: observations from 160,000 patients. Prostaglandins Leukot Essent Fatty Acids. 2013 Apr;88(4):257-63.
  • Harris WS, Thomas RM. Biological variability of blood omega-3 biomarkers. Clin Biochem. 2010 Feb;43(3):338-40.
  • Harvei S, Bjerve KS, Tretli S, et al. Prediagnostic level of fatty acids in serum phospholipids: omega-3 and omega-6 fatty acids and the risk of prostate cancer. Int J Cancer. 1997;71(4):545–551.
  • Howlader N, Noone AM, Krapcho M, Garshell J, Neyman N, Altekruse SF, Kosary CL, Yu M, Ruhl J, Tatalovich Z, Cho H, Mariotto A, Lewis DR, Chen HS, Feuer EJ, Cronin KA (eds). SEER Cancer Statistics Review, 1975-2010, National Cancer Institute. Bethesda, MD, http://seer.cancer.gov/csr/1975_2010/, based on November 2012 SEER data submission, posted to the SEER web site, 2013.
  • Hu Y, Sun H, Owens RT, Gu Z, Wu J, Chen YQ, O’Flaherty JT, Edwards IJ. Syndecan-1-dependent suppression of PDK1/Akt/bad signaling by docosahexaenoic acid induces apoptosis in prostate cancer. Neoplasia. 2010 Oct;12(10):826-36.
  • Liu Y. Fatty acid oxidation is a dominant bioenergetic pathway in prostate cancer. Prostate Cancer Prostatic Dis. 2006;9(3):230-4.
  • National Heart, Lung, and Blood Institute. Unpublished Tabulations of the National Health Interview Survey, 2010. Available at: http://www.cdc.gov/nchs/nhis/nhis_2010_data_release.htm.
  • O’Flaherty JT, Hu Y, Wooten RE, Horita DA, Samuel MP, Thomas MJ, Sun H, Edwards IJ. 15-lipoxygenase metabolites of docosahexaenoic acid inhibit prostate cancer cell proliferation and survival. PLoS One. 2012;7(9):e45480.
  • Sorongon-Legaspi MK, Chua M, Sio MC, Morales M Jr. Blood level omega-3 Fatty acids as risk determinant molecular biomarker for prostate cancer. Prostate Cancer. 2013;2013:875615.
  • Terry P, Lichtenstein P, Feychting M, Ahlbom A, Wolk A. Fatty fish consumption and risk of prostate cancer. Lancet. 2001 Jun 2;357(9270):1764-6.
  • Torfadottir JE, Valdimarsdottir UA, Mucci LA, Kasperzyk JL, Fall K,Tryggvadottir L, Aspelund T, Olafsson O, Harris TB, Jonsson E, Tulinius H, Gudnason V, Adami HO, Stampfer M, Steingrimsdottir L. Consumption of fish products across the lifespan and prostate cancer risk. PLoS One. 2013 Apr 17;8(4):e59799.
  • Zha S, Ferdinandusse S, Hicks JL, Denis S, Dunn TA, Wanders RJ, Luo J, De Marzo AM, Isaacs WB. Peroxisomal branched chain fatty acid beta-oxidation pathway is upregulated in prostate cancer. Prostate. 2005 Jun 1;63(4):316-23.

 

Nutritional Counseling and Free Speech Update

By Rick Collins, JD, FISSN

Does nutritional advice raise an issue of Free Speech?  A recent Fourth Circuit case from North Carolina should be of interest to the nutrition community as it moves forward through the court system [Cooksey v. Futrell, et al, http://www.ij.org/images/pdf_folder/first_amendment/paleo/paleo-4th-opinion.pdf].  The relevant facts and Court’s holding follow.

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In 2009, Steve Cooksey was rushed to the hospital in a diabetic coma.  Diagnosed with Type II diabetes, he was advised by licensed dietitians to eat a diet high in carbohydrates and low in fat.  Instead, he adopted a “Paleolithic diet” high in fat and low in carbohydrates.  On this regimen, he purportedly dropped 78 pounds, ceased need for medications, and regained his health.  The following year, he launched a website now called “Diabetes Warrior.”   The site contained a disclaimer that Cooksey was not a licensed medical professional and did not have any formal medical education or special dietary qualifications.  The site promoted the high fat/low carbohydrate diet and Paleo lifestyle to combat obesity and diabetes.

Cooksey’s website had three relevant components: (1) a free advice column of visitor questions and his answers; (2) a free “Personal Dietary Mentoring” section, in which visitors would post questions or share stories and he would respond; and (3) a fee-based diabetes coaching service, in which Cooksey provided individualized advice on the Paleo diet.

Cooksey came to the attention of the North Carolina Board of Dietetics/Nutrition when he attended a nutritional seminar on diabetes and expressed dissenting opinions during the question-and-answer segment of the seminar.  Someone present at the seminar reported Cooksey to the Board, which is charged with administering North Carolina’s Dietetics/Nutrition Practice Act, claiming that Cooksey was engaging in the unlicensed practice of dietetics – a Class 1 misdemeanor.  The Executive Director of the Board called Cooksey and told him that “he and his website were under investigation.”  He was told to take down the fee-based portion of his website and make other changes.  Cooksey reluctantly complied “because he feared civil and criminal action against him . . . .”  The State Board subsequently sent Cooksey documents with a red-pen review of his site, noting areas of “concern” with large red “X’s.”  He was told not to address “specific questions” or give specific advice (e.g., suggesting to a site visitor to introduce “whipping cream” into her diet).  He was told that having a meal plan on the site was permissible, but that “recommending it directly to people you speak to or who write you” requires a license.   Cooksey did not contact the Board further, but instead altered his website and “ceased expressing opinions in the form of personal dietary advice based on his fear of civil and criminal action against him by the State of North Carolina.”

Cooksey thereafter filed suit in the Western District of North Carolina, alleging the Board violated his First Amendment rights.  He claimed that restricting his speech in the advice freedomofspeechcolumn, personal dietary mentoring, and the fee-based coaching sections of his site was an unconstitutional restriction and “chilling” of free speech.  The American Civil Liberties Union of North Carolina filed a friend-of-the-court brief in Cooksey’s support.  The Board filed a motion to dismiss for lack of standing and ripeness, and for failure to state a First Amendment claim.  Essentially, they argued that because they had issued no formal decision and Cooksey had voluntarily taken down the relevant sections of his site, Cooksey had suffered no actual injury – that he had no standing to raise a First Amendment claim and that such claim was premature.  The district court agreed and dismissed the complaint.

However, the three-judge appellate panel, which included retired Supreme Court Justice Sandra O’Connor, held that the district court erred in not analyzing Cooksey’s claims under the First Amendment standing framework.  The appellate court held that Cooksey had sufficiently satisfied the First Amendment injury requirement by showing that the State Board’s actions had an “objectively reasonable chilling effect on the advice and commentary he posted on his website.”   Thus, the district court’s order dismissing Cooksey’s complaint was vacated and the case was sent back to be considered on the merits.

What happens from here forward could have big implications not only for the nutritional community but for millions of other people who give free or paid advice over the Internet, as the court will now need to decide the case on First Amendment grounds.  How far can a licensing board or other government authority go in regulating or censoring speech?  And what is the proper balance between protecting the public and ensuring protected free speech?  Stay tuned for further proceedings in Cooksey’s case…

[© Rick Collins, 2013.  All rights reserved.  For informational purposes only, not to be construed as legal or medical advice. Rick Collins is Legal Counsel to the ISSN; visit Rick at www.rickcollins.com.]

BIO – Rick Collins, Esq., FISSN is a popular personality in the bodybuilding, health, fitness and nutrition communities. A successful lawyer, author, lecturer and magazine columnist, he is a partner in the law firm of Collins, McDonald & Gann, PC, in Mineola, New York. He was formerly a criminal prosecutor, personal trainer and film actor. As an attorney, he has been awarded the highest accolades for legal abilities and ethical standards (AV-rating) from the prestigious Martindale-Hubbell directory of lawyers, and he is listed in the Bar Register of Preeminent Lawyers.  Rick serves on the Advisory Board of the ISSN, www.theissn.org.

Out-Muscling Neurological Disorders with Creatine

By Chantal Isabela Charo, Ph.D.  Creatine is one of the most popular ergogenic aids in sports nutrition, used by athletes, bodybuilders, the military or anyone participating in a physical activity involving short bursts of high intensity exercise.  One of the mechanisms in which creatine improves exercise capacity is via an increase in the stored phosphagens (e.g. ATP and PCr).   In the human body, creatine exists in both the free and phosphorylated form (phosphocreatine or PCr) and more than 95% is contained within skeletal muscle.  Creatine is mostly known as a performance enhancer in sports nutrition; however, it has become more evident that creatine plays a role in in the central nervous system which will be reviewed in this article.  Several studies have shown a similar pattern of impaired creatine metabolism in psychiatric patients with neurological diseases such as Huntington and Parkinson’s which lead scientists and clinicians to question the therapeutic role of creatine in treating and/or preventing mental illnesses. Although many of the molecular mechanisms are not well understood, exogenous creatine supplementation has been proposed and/or proven to improve the outcome of neurodegenerative diseases such as Alzheimer’s, Parkinson’s, ALS, and Huntington’s.  Although the detailed mechanisms of the creatine-induced neuroprotection for each disease is different, the basic overall hypothesis is that creatine supplementation is improves the overall bioenergetics and/or mitochondrial deficits associated with each particular neurodegenerative disease.  A study done by Watanabe’s group in 2002, showed that creatine supplementation improved mental concentration, memory and learning in normal healthy subjects and early stage Alzheimer’s Disease patients. creatine_monohydrate_1_1Another group, conducted a study on Lou Gehring patients (another neurological disease caused by the degeneration of neurons in the central nervous system), showed  that buffering cellular energy with exogenous creatine might have a neuroprotective effect (Hervias etal, 2006). Strong support for exogenous creatine supplementation to be an effective neuroprotective agent comes from studies done on Huntington Disease (characterized by abnormal “dance like” body movements and lack of muscular coordination) which may ultimately improve and/or extend the quality of life for individuals afflicted with HD. Studies showed improved motor performance, extended survival, attenuated the loss in body weight and brain weight, reduced neuron atrophy, upon creatine supplementation (Ferrante et al. 2000; Andreassen et al. 2001; Dedeoglu et al. 2003). Additionally, some studies have found an association between creatine metabolism and cognitive function in schizophrenia, generating much interest in the role creatine plays in the pathogenesis of the disorder. In addition to its neuroprotective roles, research suggests that creatine might not only enhance physical performance. there has been a significant amount of research done on creatine supplementation as an enhancer of cognitive performance and brain function. Another study by Watanabe’s group showed that creatine supplementation reduced mental fatigue (Watanabe et al.,2002). Interestingly, recent emphasis has been on the role of creatine supplementation and depression in women. Studies from the University of Utah, brain institute, have shown that patients who combine creatine with an antidepressant respond to their medications faster and better than patients who take antidepressants alone. The eight-week study included 52 women with depression taking the antidepressant Lexapro. Researchers observed dramatic improvements in women’s brain chemistry after combining only 5 grams of creatine with their daily doses of antidepressant medications.

For those who don’t respond well to antidepressants, creatine could become an inexpensive way to improve treatment outcomes. Furthermore, exogenous creatine was shown to improve working memory and intelligence scores in human subjects with diminished phosphocreatine levels due to limited meat intake (Rae et al., 2003).
Creatine supplementation has been generally regarded as safe and has been used for extended periods of times by athletes with few reported side effects. Creatine is a constituent of a normal diet of protein-based foods, such as milk, meat, and nuts. It is not considered an essential nutrient because the kidneys, liver, pancreas, and possibly brain cells are able to synthesize about half of the body’s requirements of creatine from the amino acids arginine, glycine, and methionine (Andres et al., 2008; Béard and Braissant, 2010; Wyss and Kaddurah-Daouk, 2000).

Bottom line – Creatine is not only good for your muscles, but it’s pretty darn good for the brain.

BIO  –  Dr. Chantal Charo is an Asst. Professor of Physiology, a Sports Nutritionist and a Medical Writer from Miami, FL.  Her research particularly focuses on undestanding hormonal imbalances and sugar metabolism in pancreatic diseases. Dr. Charo is also involved in numerous clinical trial in her field and has most recently completed a trial on NSAIDs and pancreatic diseases. Chantal earned her Ph.Ds. in Biomedical Sciences and Cancer Biology from the prestigious University of Texas Houston and the UT MD Anderson Cancer Center. As a sports nutritionist Dr. Charo collaborated with leading supplement companies across the United States by researching ways to target insulin resistance and hormonal imbalance in women, as well as the Euthyroid Sick syndrome and the female athlete using functional nutrition and biomedicine. Chantal hosts a medical segment on a local daily talk show which aims at promoting awareness to women and combating health illiteracy. In support of her research, Chantal has received fellowships from National Cancer Institute, the National Institute of Health and more. She is a Fellow of the American Association of Cancer Researchers, the American Pancreatic Association and the American Breast Cancer Association, and was the recipient for many outstanding scientist awards. The link to Dr. Charo’s Sports and Functional Nutrition Clinic is www.facebook.com/sportsnutritionclinic

Manipulating Night-Time Anabolic/Catabolic Cycles

For years we sports nutritionist missed the boat when it came to maximizing muscle mass because we ignored the night time decrease in muscle growth caused by post-absorptive muscle catabolism. We now know that the body is primed for growth and repair during sleep. What we must do is give the body the necessary materials it needs to do its job.  Dr. Mauro Di Pasquale, M.D.431147-bigthumbnail

When you review the comments above by the renowned sports nutritional physiologist Dr. Mauro Di Pasquale, they imply that for some time researchers may have considered night-time catabolism’s impact on growth to be negligible and didn’t warrant attention. Those comments also imply that this reasoning may have stemmed from the fact that the problems with the body’s ability to absorb and utilize nutrients during sleep couldn’t be altered or minimized as the body simply breaks down existing muscle tissue to supply the energy needed to keep its metabolic activities going. Despite this innate back-up process, it is a process that occurs for an 8 to 9 hour time frame. The fact is that every night becomes a catabolic night of biblical proportions the minute you lay down to sleep. Catabolic processes begin there assault with a pre-programmed set of muscle destroying instructions. So precise and destructive is this catabolic activity that it naturally occurs via cyclical up-regulation of various catabolic compounds or hormones during normal sleep cycles, hence its reference to as the post absorptive muscle catabolic syndrome.

When It Rains It Pours

As a point of reference here a syndrome is defined as a set of general symptoms all occurring at the same time that collectively indicate or characterize being in a morbid (unhealthy) state. Scientifically,  this internal network or place were all this muscle breakdown occurs and is converted to energy is referred to as the ubiquitin-proteasome or UPP pathway. It is here where cortisol the stress and muscle wasting hormone production is increased and accelerated as a direct result of exercise induced stress. Contrary to popular belief, the sleep cycle isn’t just a rest, repair and detoxification phase. In practical terms here, sleep becomes a survival and catabolic period to the body because of a lack of nutrients it has to work with. However, researchers now know that by the time you switch this catabolic switch off, that you have lost substantial amounts of lean muscle tissue. The other part of this axiom is the fact that you are consistently playing catch-up to promote growth. The question then becomes how can the nutrients the body needs be proved or maintained over the course of a normal sleep cycle to combat this impending catabolic syndrome before bedtime?

Understanding Post-Absorptive Physiology

Based on Dr. Pasquale’s comments above, the body is primed for growth and repair during sleep and that there are ways to counter-balance this catabolic cycle. The fact is the body has some built in mechanisms to protect itself via the release of certain hormones to minimize the impending catabolism. This could be somewhat compared to bears getting set for hibernation, when no new nutrients will be coming in for a period of time. For example, testosterone, growth hormone, and IGF-1(insulin growth factor) and insulin tend to remain elevated during sleep. These hormones guard against muscle wasting by reducing the production of cortisol and other catabolic hormones to help maintain protein synthesis. Other compounds the body calls upon include circulating glucose, fatty acids, liver and muscle glycogen (stored glucose), branch chained amino acids, glutamine and other amino acids. These sources can supply up to 1200 needed calories to slow down catabolic activity for about 12 hours. The bottom line here, maintaining your scheduled intake of nutrients throughout the day can impact night-time catabolism, especially your amino acid intake. Additionally, your carbohydrate intake replenishes lost glycogen that is stored within the liver and muscle tissue that serve as backup fuel when blood glucose levels fall. Conversely, the body uses part of your internal amino acid pool to fuel metabolic activity during sleep. If that pool is low, the body will breakdown your existing muscle tissue to support its nutritional needs.

Please Note: as a point of clarification here, to replenish glycogen stores lost during the day, they are replenished via carb intake, not protein. To replenish diminished glycogen researchers recommend a daily intake of 3 to 5 grams of carbohydrate for every pound of your body weight across the day, divided evenly with your feedings. Additionally, if you are taking a few individual amino acids like glutamine and arginine I strongly suggest that you also take a full pre-digested amino acid formula following a workout and right before bedtime.

Know Your Anabolic Hormones

As stated there are a number of hormones the body secretes to counter-act night-time muscle loss. Make no mistake about it, how adept you are at sustaining the balance and symmetry between the repeated cascade of your anabolic and catabolic hormones has a direct impact on Endocrine_growth_regulation-244x300your ability to preserve muscle tissue during sleep. Having a working knowledge of the anabolic / catabolic aspects of these hormones is just prudent.  For example, you have the ability to help the body accelerate the secretion of growth hormone during sleep via the intake of various amino acids (arginine, glutamine, ornithine) and other supplements. The following synopsis outlines a few of these anabolic hormones that focus on minimizing night-time muscle catabolism, as well as its acceleration.

The Anabolic Hormones

Androgens – this class of hormones are considered male dominate hormones with testosterone being the most well-known. Androgens have a dramatic impact on muscle development. They are drawn to tiny receptors found in muscle tissue that appear to signal muscle cells to accelerate protein synthesis via a process known as androgen receptor complex binding.  This process appears to turn on muscle cell DNA while also inhibiting the up-regulation of glucocorticoids like cortisol that cause muscle wasting.  Androgens like testosterone also help stimulate the production of other anabolic hormones like insulin growth factor ( IGF) and growth hormone. Resistance training itself causes natural spikes in testosterone, however, lack of sleep, overtraining, stress, and sugary drinks and snacks can inhibit testosterone secretion at night. In fact data indicates that a small glucose drink can reduce testosterone production by 25%. Additionally, deficiencies of vitamin D definitively lower testosterone levels. As cited by Lee Meyer, author of Low Testosterone: By The Numbers vitamin D biologically acts more like a hormone than a vitamin, despite being referred to as the muscle vitamin. Studies have shown that when muscle receptor cells levels of vitamin D fall, decreased muscle strength and performance follow, as a direct result of its positive impact on testosterone production. Conversely, intense physical and mental stress lowers testosterone as a direct result of its down-regulation of the enzyme 11BHSD-1 located in the Leydig cells of the testes.

Stress: An Androgens Worst Nightmare

It is important to remember your body is a network of multiple deeply interconnected systems, all of which get impacted to various degrees by heavy training. Recovering from this ordeal is about more than just not lifting. It’s about giving your muscles and joints the space to heal and super-compensate, letting your nervous system calm down, and getting adequate rest. In general terms here, some researchers, especially Russian physiologist, recommend the use of adaptogens before bed and or following workout to restore order to these interconnected systems. This in essence primes the body for growth as cited above by Dr. Pasquale.Some well- known anti-stress supplements you may want to consider here include, vitamin B- complex, DHEA (dehydroepiandrosterone) , siberian ginseng and rhodiola rosea. Rhodiola has been used extensively by Russian power lifters. Research shows that this herb actually primes the system to deal with the heavier aftershocks of stress that disrupt normal metabolic processes when exercised induced stress begins to sound the alarm to internal body systems. When this occurs to help the body secretes more cortisol, which accelerates muscle tissue breakdown. It is here where rhodiola steps in to neutralize this mishap, and restore order, much like paratroopers dropped into a war zone, hence it tag as a adaptogen ( a substance that restores balance).

Please Note: to help your body maintain the anabolic potential testosterone affords, some of the most widely used supplements that stimulate testosterone production in the bodybuilding industry are: arginine, aromataste inhibitors( substances which block estrogen production) like chrysin, DHEA, long jack root. maca root, muira puama, tribulus and ZMA( zinc maganesium aspartate).

Growth Hormone (GH) – this hormone is composed of many different amino acids linked together known as peptides. Growth hormone improves the efficiency of muscle cells to take in amino acids, thus enhancing protein synthesis, muscle growth and repair. GH also regulates carbohydrate and fat metabolism, encouraging increased fat burning while preserving carbohydrates. This can have a positive impact on replenishment and maintenance of glycogen (stored glucose). Growth hormone secretions occur during  exercise, however larger spikes occur during sleep, which can be improved via intake of amino acid combinations like arginine/ornithine/ lysine as well as single doses of Gaba and glutamine, about ½ hr before bedtime. Also many amino acids like arginine inhibit the actions of the catabolic hormone somatostatin which inhibits the release of glycogen,  growth hormone and insulin.

Insulin Growth Factor (IGF)- IGF is a peptide hormone and helps prevent protein breakdown and plays a major role with the body’s fat-burning activities. Researchers attribute the increase in new muscle tissue you have been working hard to build to IGF, because it speeds up the activity of cells in the muscle known as satellite cells. Satellite cells appear to down-regulate the activity of the myostatin gene which is known to inhibit muscle growth. Satellite cell  promote hyperplasia (the growth of new muscle tissue).

Protein and the Post Sleep Catabolic Phase

Dr. Deepak Chopra the renowned mind-body researcher reminds us that the world’s greatest chemistry set is the human body. He maintains that the vast array of botanicals studied are done so to mimic the actions of natural chemicals produced by the human body. Based on the examples thus far of the things the body calls upon to protective itself from sleep cycles of catabolism, some protein sources appear to be better suited to help and sustain anabolic activities during sleep. Casein protein and egg protein appear to better suit than whey protein to help nourish the muscles during both the pre-primed and post sleep absorptive phase of protective growth and repair. These proteins tend to break down slowly over the course of a 6 to 8 hour time frame. Whey takes  about 20 minutes  to reach the veins and within forty minutes your system is flooded with amino acids.  Within the hour whey protein has either gone through various metabolic processes and has been synthesized (individual cells constructing various proteins). Simply put, whey can’t help sustain anabolic process during the post-sleep absorptive phase. Studies also indicate that as a direct result of increased oxidation that appears to follow the synthesis of whey protein, this limits its ability to sustain growth and repair for a substantial amount of time.

Please Note: While some oxidation is beneficial this process accelerates muscle protein breakdown during the day and night.  Because of the above it may be a good idea to take a regimen of anti-oxidants (vitamins A, E, C, CoQ10, etc.) to offset this negative aspect of whey protein.

Casein and Egg Proteins Absorptive Physiology

While whey protein may afford more benefits during the course of the day, casein protein is the better choice later in the evening and at night. This due to the fact that casein, a milk protein, curdles in the stomach as it unites with various enzymes.  It generally takes 3 to 4 hours before amino acids hit your blood stream to start the repair of muscle tissue.  In fact in a recent study conducted by researchers in France at the University of Clermont Auvergne comparing whey to casein protein, subjects were given 30 grams of either whey or casein . download (1) After 7 hours researchers found that with casein there was a marked decrease in protein synthesis by 31%.  However, there was 27% less oxidation (degradation) of casein protein vs. whey resulting in a more sustained period of nitrogen retention.  The final and most critical aspect of these numbers was a 34% decrease in muscle protein breakdown.  Bottom line here, this study and countless others confirm why casein should be your protein of choice before bedtime. It helps to create and up-regulate the body’s innate post sleep anti-catabolic environment by enhancing your muscle tissues ability to neutralize the mixture of catabolic chemicals building up a head of steam toward muscle destruction, as you approach the REM stage of sleep. As a point of reference REM stands for rapid eye movement. This stage of sleep is characterized by rapid twitching of the eyes and low-voltage brain wave activity. What is important here is the fact that it is during this time most of the body’s repair cycles occur.

Please Note: Like whey, casein protein is derived from milk.  When you purchase casein protein, make sure it isn’t listed as caseinate or calcium caseinate.  These forms have been extracted before the curdling process and are actually a much lower grade of casein protein.

Egg Protein: A Medium Timed Releasing Protein

Although egg protein has taken a back seat since whey’s introduction to the market place, it is still considered one of nature’s perfect foods. Egg protein contains all of the essential amino acids in the exact proportions needed to promote the growth and maintenance of lean muscle tissue. Egg protein also has a BV of 100 ( biological value) meaning its ability to help muscles maintain nitrogen is excellent. Nitrogen is the amine portion of the amino acid NH2 intimately involved with the growth of lean muscle tissue. Egg protein also has a digestibility ratio of 97% meaning that 97% of it is absorbed as amino acids, major players in the repair process. Current data indicates that egg protein exponentially increases total muscle protein synthesis following a workout. Because of this egg serves as an key pre-priming sleep post-absorptive nutrient. Another key aspect of egg protein’s post absorptive anabolic ability is its high leucine (the key anabolic signaling amino acid) content, its impact on testosterone production and  inhibition of myostatin activity ( a muscle growth inhibiting compound).  For these reasons egg protein is considered a very good post sleep absorptive nutrient that will assist in maintaining your pool of amino acids, thus inhibiting night-time catabolism.

Please Note: Based on the findings presented in this report the suggestion that whey may not be all its hyped up to be, this assumption if made should be quickly down-regulated to inconsequential. Its ability to quickly flood the system with amino acids will quickly initiate muscle repair as you awake from the post sleep catabolic phase. The other aspect here surrounds whey intake before a morning workout and right afterwards. Current data indicates that as little as 10 grams of whey can jumpstart protein synthesis, as well as cited earlier flood your system with needed amino acids within 45 minutes.

Conclusions

It is important to remember that the majority of your growth occurs when you aren’t working out. The biggest mistake you could make in reaching your full anabolic growth potential is not to prepare for natural night time muscle catabolism. Helping to support the body’s attempts to maintain some semblance of its anabolic potential during sleep is the real key to sustaining growth for the long hall.

References

Andersen, L.L., Tufekovic, G., et. al., The effect of resistance training combined with timed ingestion of protein on muscle fiber size and muscle strength, Metabolism, 2005 Feb.; 54(2): 151-156.

Boirie, Y., Dangin, M., et. al., Slow and fast dietary proteins differently modulate postprandial protein accretion, Proceedings of the National Academy of Sciences (USA), 1992; 94: 14930-14935.

Chopra , D. Creating Health. Houghton Mifflin: New York. 1991.

Chromiak, J.A., Antonio, J. Use of amino acids as growth hormone- releasing agents by athletes. Nutrition. 2002 Jul; 187 (7-8): 657-661.

Dangin, M., Bione, Y., et.al., The digestion rate of protein is an independent regulating factor of postprandial protein retention, American Journal of Physiology, Endocrinology, and Metabolism, 2001; 280: E340-E348.

Goto, K., Ishii, N. et.al. The impact of metabolic stress on hormonal responses and muscular adaptations. Medical Science and Sports Exercise. 2005 Jun; 37960; 955-963.

Hackney, A.J., Bruenger, J.T., et.al., Timing protein intake increases energy  expenditure 24 h after resistance training. Medicine and Science in Sports and Exercise. 2010 May; 42 95):998-1003.

Kanaley, J.A. growth hormone, arginine, and exercise, Current Opinion in Clinical Nutrition Metabolism and Care. 2008 Jan; 11 (1):50-54.

Kreider, R., et.al., Effects of whey protein supplementation with casein or bcaa and glutamine on training adaptations 1: Body composition. Medical Science and Sports Exercise. 2003; 2205: 35-5.

Miller, S.L., Tipton, K.K., et. al., Independent and combined effects of amino acids and glucose after resistance exercise, Medicine, Science, Sports and Exercise, 2003; 35(3): 449-455.

Mosoni, L., Mirand, P.P.  Type and timing of protein feeding to optimize anabolism, Current Opinions in Clinical Nutrition and Metabolic Care, 2003; 6(3): 301-306.

Myer, L., Low Testosterone : By The Numbers, Amazon Digital Services: Aug. 2011.

Tang, J.E., Manolakos, J. J.,  et.al., Minimal whey protein with carbohydrate stimulates muscle protein synthesis following resistance exercise in trained young men. Medicine and Science in Sports and Exercise. 2007Dec.;32(60:1132-1138.

Tipton, K. D., Wolfe, R. R., Exercise, protein metabolism and muscle growth. International Journal of Sport Nutrition and Exercise Metabolism.  2001 Mar.;11(1):109-132.

Volek, J.K., Kraemer, W.J., et.al. Testosterone and cortisol in relationship to dietary nutrient and resistance exercise. Journal of Applied Physiology, 1997 Jan; 82(1); 49-54.

Wiegant, F.A., Surinova, S., et.al. Plant adaptogens increase lifespan and stress resistance in C. elegans, Biogerontology. 2009 Feb; 10 (1);27-42.

BIO

George L. Redmon PhD has been associated with the vitamin and health industry for over 25years, having served as The National Product and Education Director for one of the countries largest retailers of nutritional supplements. He has been widely published in many major bodybuilding, fitness and alternative medicine publications. He is the author of Natural Born Fat Burners, Energy for Life and is a member of The National Academy of Sports Medicine and The International Society of Sports Nutrition.