Author Archives: Jose Antonio

Hierarchy of Evidence is Wrong


By Jose Antonio PhD FNSCA FISSN.

A pithy summary

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

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

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

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

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

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

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

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

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

Androgens – Roid Rage Nonsense

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

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

Creatine – The Tipping Point

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

Caffeine – thank Dr. David Costill for this one

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

The Big Picture

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

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

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

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

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


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


1.         ACSM Position Stand on Anabolic Steroids:

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

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

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


New Ways to Treat


By Livia Ly MS RD LDN and Melza van Roijen MS. We are in a new health care era. One marked by treatment integration. Many health care professionals have begun treating their patients and clients as people rather than mere numbers on a chart. Patients today are looking for holistic preventive approaches to optimize their health and well-being. Preventive medicine doctors already exist and have the goal to promote and maintain health and well-being and to prevent disease. However, we need more than apple

Have you heard of integrative medicine? It is a great concept; designed to follow a whole-person approach that treats the person and not just the disease. Well, let me introduce myself, I am a dietitian trained both in São Paulo, Brazil and in Chicago, U.S. I believe that nutritional caretakers should not only consider the diagnosis, but also decode the hidden messages expressed by the client. I consider the entirety of the human being since the human body is unique with structured organs and systems that are interdependent.

I moved to the U.S. in 2008 and quickly learned how different the methods of treatment are in these two countries. The primary focus of conventional health treatments in the U.S. is often the disease, and not the patient. In Brazil there is a larger emphasis on prevention. For example, when I lived in Brazil, I underwent multiple medical exams every year to proactively check my health. Those same exams are typically only performed in the U.S. to reactively diagnose a symptom. Also, our Brazilian Dietary Guidelines were in the American headlines last year and well-known public health advocates, like Marion Nestle and Michael Pollan, praised them for being food-based.

The American government and the private sector are now realizing that prevention will save a lot of money. The U.S. is facing a severe healthcare cost crisis that is mainly due to the increasing number of chronic illnesses in the population. There is hope, however, if we focus more on prevention and not just the treatment of illness. The key is a lifestyle change that incorporates both nutrition and exercise! But, we need more than that.


Here are the ten Brazilian guidelines:

1. Make natural or minimally processed foods the basis of your diet

2. Use oils, fats, salt, and sugar in small amounts when seasoning and cooking natural or minimally processed foods and to create culinary preparations

3. Limit consumption of processed foods

4. Avoid consumption of ultra-processed foods

5. Eat regularly and carefully in appropriate environments and, whenever possible, in company

6. Shop in places that offer a variety of natural or minimally processed foods

7. Develop, exercise and share cooking skills

8. Plan your time to make food and eating important in your life

9. Out of home, prefer places that serve freshly made meals

10. Be wary of food advertising and marketing

In addition to the Brazilian guidelines, I also recommend to my clients functional foods and nutraceuticals: foods or ingredients that produce beneficial health effects beyond their basic nutritional functions. Various health conditions can be managed with functional foods and nutraceuticals, including prevention of hair loss or weak nails, decrease in the progression of aging skin, improvement of muscle growth, control of hypothyroidism or migraines, and help to promote lasting weight loss in a healthy manner. I also believe that individualized recommendations will promote greater and longer lasting results. We are unique and therefore need personalized strategies. Finally, I believe that listening to client stories and looking at interactions among genetic, food sensitivity, environmental, cultural, and lifestyle factors can positively influence long-term health.

Livia LyAbout Author: Livia Ly, MS, RD, LDN is a registered dietitian and nutritionist trained both in Brazil and in the United States. She is the founder of Nutrily, LLC a nutrition consultancy company that follows a holistic approach.



Melza van RoijenAbout Editor: Melza van Roijen, MS is a volunteer at Nutrily, LLC. “I completed my B.S. in psychology at the College of Charleston in 2010 and my M.S. in behavioral neuroscience at Tulane University in 2014. I have worked in many different research labs over the years and have investigated topics such as drugs of addiction, traumatic brain injury, neuroendocrinology and spatial cognition.”


In Defense of Cortisol

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

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

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

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

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

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

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

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

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

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

Science References For All You Nerds

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

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

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

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

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

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

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

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

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

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

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

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

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

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


Train Not Just The Booty But The Brain


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

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

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

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

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

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

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

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

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

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

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

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

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

About the AuthorSONY DSC


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


What a Pain in the…Back


By Aimee Polgar DC-s, CISSN – Approximately 80% of people experience low back pain (LBP) in their life time, and low back pain does not discriminate- men and women are equally affected, with children and adolescents also reporting pain and an increasing number of athletes suffering as well. It is commonly perceived that low back pain only affects the older, overweight, inactive population but the number of collegiate athletes that experience low back pain ranges from 1% to greater than 30% (1, 6, 7)- So what gives?

The majority of acute low back pain is mechanical in nature, meaning that there is a disruption in the way the components of the back (the spine, muscle, intervertebral discs, and nerves) fit together and move (4). Many of these findings however are not visible on conventional radiographs and therefore present a challenge for physicians, physical therapists and athletic trainers when recommending treatment and rehab for athletes with low back pain.

So where do we go from here?

For patients and athletes with no organic cause to their back pain, the initial focus should be on pain management for the acute bout of low back pain and strengthening and rehab for preventative measures. Pain management should focus on decreasing inflammation with an Low-Back-Painanti-inflammatory diet, ice and modalities such as interferential current. NSAIDs that are naproxen based (such as Aleve) also have positive outcomes in the acute stage for pain.

From there it is crucial to keep the athlete moving! Old school methods of management for acute low back pain were bed rest, but it is now known that that is exactly the opposite of what we want to do because intervertebral discs rely on the motion of the spine for nutrition as well as clearance of waste buildup through a process called imbibition. A 2011 study by Dufek et al. showed that backward walking had positive outcomes on pain and general function in athletes with low back pain. The study showed that during backward walking, the typical heel-strike associated with ground contact is eliminated because the toe contacts the ground first. The kinematic difference has the potential to manifest itself in a more anteriorly aligned pelvis which may open up the facet joints in the vertebral column, therefore, help in alleviating the pressure and associated low back pain (3). Results of the study concluded that all LBP subjects reduced self-reported pain and over half significantly increased their low back range of motion. Both groups (pain reporting athletes and non) increased velocity, stride parameters, and low back ROM following 3 weeks of backward walking exercise. It appears that the presence of LBP did not interfere with the ability of participants to adapt to the actions of backward walking. Both groups achieved greater walking velocity with a greater percent increase in stride length versus stride rate.

Adding specific spinal stabilizing exercises is crucial to increase strength in the supportive muscles that we often overlook when training larger muscle groups because support and stability to the low back arises from muscles. Interestingly, it is not strength but coordination between agonist and synergist muscles which plays a pivotal role in resisting injury. Sparto et al., report that spinal loading forces increased during a fatiguing isometric trunk extension effort without a loss of torque output (5). Torque output remained constant because as the erector spinae fatigued, substitution by secondary extensors such as the internal oblique and latissimus dorsi muscles occurred.

Agonist-antagonist muscle coactivation is an important mechanism in preventing spine injury, as well. Cholewicki et al., examined the theory that antagonistic trunk muscle coactivation is necessary to provide mechanical stability to the lumbar spine around a neutral posture (2). The authors found that antagonistic muscle coactivation increased in response to increased axial load on the spine.

Nutritionally it is important to prevent excessive weight gain (which usually is not an issue for athletes but may be for the average individual) as well as maintain a diet sufficient in protein, calcium, phosphorus and vitamin D to maintain healthy bone growth and repair. Hydration status is also largely important to help maintain proper intervertebral disc height, as discs are made approximately of 80% water! And yes, it is true that you may lose up to ¼ – ½” in height by the end of the day due to dehydrated discs!

So what is the take away message here?

Don’t be surprised if athletes and even children report low back pain- it is become more and more common due to the increased stress we put on our spines, but in a healthy individual, it is easily managed and does not need to become a chronic issue. Rule number one, cut back on activity but DO NOT tell your athlete to stop moving. Rule two: manage pain and inflammation primarily and then stabilize the spine with agonist (spinal erectors) and antagonists (abdominals) exercises. And finally, the golden rule: whatever you do all day, stretch the opposite way (and try walking backwards)!!!


  1. Bono CM. Low-back pain in athletes. J Bone Joint Surg Amer 2004;86:382-396.
  2. Cholewicki J, Panjabi MM, Khachatryan A. Stabilizing function of the trunk flexor-extensor muscles around a neutral spine posture. Spine 1997;19:2207-2212.
  3. Janet Dufek, et al. “Backward Walking: A Possible Active Exercise for Low Back Pain Reduction and Enhanced Function in Athletes.” Journal of Exercise Physiology 2011; Vol14:2
  4. “Low Back Pain Fact Sheet,” NINDS. Publication date December 2014. NIH Publication No. 15-5161
  5. Sparto PJ, Paarnianpour M, Massa WS, Granata KP, Reinsel TE, Simon S. Neuromuscular trunk performance and spinal loading during a fatiguing isometric trunk extension with varying torque requirements. Spine 1997;10:145-156.
  6. Spencer CW, Jackson DW. Back injuries in the athlete. Clin Sports Med 1983;2:191-215.
  7. Watkins RG, Dillin WH. Lumbar spine injury in the athlete. Clin Sports Med 1990;9:419-448.

You’re Lovin’ It!


By Jose Antonio PhD FNSCA FISSN. 

Bite-Sized McNuggets For You To Chew On:

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

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

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

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

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

Check out what they ate!

Check out what they ate!

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

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

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

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

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


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

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

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

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

To wit:

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

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

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

I Dare You to Read These Studies on McDs and Coke

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

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


Cardio Makes You Fat and Apples Will Rise


By Jose Antonio PhD FNSCA FISSN 

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

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

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

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

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

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

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

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

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


President Clinton should have done more cardio and less McDonalds.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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


% Fat in 1973 % Fat in 1988


8.0 12.5


20.1 22.1

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

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


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

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

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

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

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

The moral of the story:

Pooks running

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

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

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

Read This All You Cardio Haters

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Protein Popcorn


Popcorn is loved across the UK. Market analyst Mintel reports in 2013 the UK popcorn market as a whole was worth £53 million with sales having increased nationally by 10% in 2012 alone. But parallel to this growth is also the emergence of the discerning, health conscious consumer group who don’t want their popcorn dripping in toffee and other unhealthy additives. In 2010 market research firm Datamonitor identified this group as a ‘lifestyle user’ and it’s believed this particular customer is key to the development of the sports nutrition sector.Naked-Protein-Popcorn

Understanding this dual-demand better than anyone else is multi-award winning sports nutrition brand THE PROTEIN WORKS™. Launching the world’s first protein popcorn they’ve kept the high levels of polyphenols and antioxidants that occur naturally in popcorn and enhanced them whey protein, organic coconut oil and sweetened them with stevia extract to make a completely natural and healthy alternative known as Naked Protein Popcorn™.

Talking about this recent innovation to leave TPW™ Towers is Co-Founder Nick Smith who says, “The popcorn has been a huge success and took social media by storm. We sold out in a matter of hours as the hashtag #ProteinPopcorn went viral around Twitter. We’re overwhelmed by the response and are so glad people share our passion for unique and healthy snacks.”

Nick also hints that this could be the first of many protein innovations saying, “We’ve had a great first year but we feel the best is yet to come. We’ve a pipeline of totally unique products and are joining forces with experts outside the sector to combine expertise in what will be some pretty exciting collaborations, so watch this space!”

TO get your popcorn readyAnd it seems their optimism is rightly placed. As the sports nutrition and ‘protein’ sector grows Senior Consumer Analyst, Richard Parker, states it’s the ‘lifestyle users’ driving it. These are not necessarily athletes but are choosing to consume sports nutritional products as an initial building block to a healthier lifestyle. These customers now play a critical role in the growth of the sector which market intelligence firm Euromonitor claim, despite the VAT increase that hit the sports nutrition sector in the UK in 2012, grew by 16% and has now reached value sales of £301 million.

About THE PROTEIN WORKS™ is the most innovative and forward thinking sports nutrition brand in the market today. Established in late 2012, TPW™ has grown rapidly with a passion for sports nutrition and a vision to raise the bar in terms of product quality and level of service for sports nutrition customers.  Using only the finest quality raw ingredients, innovative production processes and an unwavering commitment to all natural colours and flavours, THE PROTEIN WORKS™ offer unparalleled quality and value for money.

Contact details – For further information or for images call Ross Edgley on 01928 571 677/ 07841 749 167 or email

Sweet Surprise

by Dr. Chantal Isabela Charo.  Oh no! Artificial sweeteners are destroying my gut microbiota!! Wait, what’s a microbiota??Gut health 2

Before you blindly cast your verdict on artificial sweeteners read my article below. I explain everything you need to know about artificial sweeteners, your gut health, the study that went viral and what you need to do to keep your gut healthy without having to give up your diet coke.

Every month or two, we watch the emergence of a new health trend that goes viral, whether it’s the gluten free diet hype, oil pulling, Chia seeds, Detox diets, the list goes on and on. Feeling out of date? Log on Instagram or Facebook and look at some model’s profile, you’ll find the latest pseudo-scientific findings guaranteed to catch your attention and sell you their product. You know what I am talking about; we have all been guilty of following a health fad for one reason or another. This is one of my biggest frustrations as a research scientist, also involved in the clinic with patients.  Some diet trends are a “cute” way to keep us motivated when we feel like we are about to fall off the diet wagon. There are the diet trends that people follow when they want to find an excuse to why they are not losing weight or reaching their fitness goals, “ I am bloated after eating a huge bowl of pasta, cheese preceded by Olive Garden’s bread basket, darn it! It’s the gluten. I am going to go on a gluten free diet tomorrow”. Whilst the majority of diet trends simply don’t work. Trendy diets are just a trend, I try to remind my patients and friends that all the time. Now, this last category of diet trends is my biggest pet peeve. It’s the type of trend Dr. Mercola and his ilk spread like soft butter on hot French bread.

Can you believe that Mercola’s latest posts are that artificial sweeteners are doing more harm than sugar to diabetics? Now that makes about as much sense as putting lipstick on a pig and having the little oinker enter a beauty contest. These falsehoods gives a patient the false hope that by radically changing what has been medically shown for years to work, and replacing it with a hypothesis that has no scientific data, they are cured. That, I cannot deal with. This can cause serious health issues including death.

This month’s latest health trend is a scientific study by Dr. Eran Elinav’s research group, published in a top tier journal called Nature. The study suggested a correlation between artificial sweeteners and gut health. They found that mice who were fed a diet high in artificial sweeteners such as Splenda and sweet n’ low were more likely to suffer from a disequilibrium in intestinal flora. Did you know? There are about 100 trillion bacteria in our intestines. Some are good bacteria, aiding in our digestive health and metabolism, while others are bad bacteria secreting harmful metabolite. The ratio of good gut bacteria to bad gut bacteria is very important to our digestive health; however, there is no definite connection between gut health and diabetes. Sadly, the media over extrapolated the results of this scientific study to generate inaccurate exaggerated and catchy titles in a desperate attempt to get your attention.healthy-gut

Here’s what you need to know about artificial sweeteners, Dr. Eran Elinav’s Study, your gut bacteria and diabetes. First, let me break down the results of the study. What the Weitzmann group actually did was as follows;  they studied the effect of a diet rich in sucralose (Splenda), aspartame, saccharin (Sweet n’ Low) and glucose on metabolic abnormalities on microbiota and the resultant effects on glucose metabolism. They found that artificial sweetener consumption alters the good to bad bacteria balance and the effect caused by saccharin (sweet n’ low) was the most pronounced. Data was generated over a period of 10 weeks. I would like to emphasize this point. They measured the effect of a normal, FDA approved dose of a diet that contains artificial sweeteners, such as Splenda and sweet n’ low, over a short period of 10 weeks, and found a correlation between glucose intolerance, gut bacteria balance and diabetes. Based on their study, the majority of the population that has consumed artificial sweeteners over a period of 10 weeks or more should have glucose intolerance, a lack of good bacteria, or worse diabetes, which is not quite the case. Without looking at the paper or having any science background, simply stop for a second and think. How well do those scientific lab findings coming a from a top notch lab apply to real life? Note that preliminary findings done in mice are important.  But we ultimately need confirmation in well done human clinical trials.

Please read this over and over. This study does not prove that if you are adding artificial or zero calorie sweeteners to your diet you will get diabetes. There are thousands of studies done over decades and decades clearly showing that too much sugar, lack of exercise, and a corpulent lifestyle contributes mightily to diabetes. There are thousands of studies who have shown the beneficial effects of substituting sugar with artificial sweeteners. Diabetics are now able to add to their diet foods that are artificially sweetened and enjoy the sweet taste of foods they couldn’t before. The problem we are facing with obese and overweight patients is not consumption of Splenda or sweet n’ low, or even diet coke. The problem we are facing is gluttony. The “oh, it’s only 0 calories? Then, Let me have 10 diet cokes today, and a whole jar of sugar free jam” syndrome.  The “I want everything I can have and more” syndrome. The “I am fat because something is going on inside of me and not because I overeat”. This is what we need to work on curing first, food overconsumption, before jumping to the conclusion that to get rid of obesity we need to replace diet coke with a regular coke.

Are you worried about your intestinal health? The good thing is that you can reset your gut bacteria, without giving up artificial sweeteners.

Here are some of my tips to improve your gut health

1-     Eat food based probiotics.  They increase the number of good bacteria.

2-     Add dairy to your diet. Milk and yogurt are rich in bifidobacteria , a type of bacteria that releases acidic substances, bad bacteria cannot survive in.

3-     Eat food based prebiotics. Those foods contain non digestible carbohydrates such as asparagus, leeks, onions, garlic and whole grains.

4-     Reduce fatty food consumption. Fatty foods can damage gut lining which allows harmful metabolites secreted by bad gut bacteria to be leaked into the blood stream and cause inflammation.

5-     Get rid of stress. Stress increases inflammation and reduces your immunity making your body more prone to foreign invasion by bacteria and viruses.

6-     Beware of antibiotics. Antibiotics kill good and bad bacteria. When good bacteria are killed, you risk having yeast infections, skin rashes and allergic reactions. So if you are taking an antibiotic course, add a live probiotic supplement after consulting with your physician.

Biography – Dr. Chantal Charo is a metabolism expert and sports nutritionist based in ChantalMiami, FL.  She received her PhD from the prestigious University of Texas Houston Health Science Center and has spent years researching metabolic disturbances and inflammation at the MD Anderson Cancer Center. Dr. Charo did her post-doctoral studies on the metabolic functions of estrogen receptor and adipose tissue regulation. And is an assistant professor who teaches undergraduate and graduate medical physiology and anatomy courses. Aside from being actively involved in both research and academics, Dr. Chantal Charo has dedicated herself to promoting scientific nutrition and fitness by being a full time writer and a clinical sports nutritionist. As a clinical sports nutritionist, Dr. Chantal Charo has worked with numerous celebrities and athletes ranging from NBA players, body building competitors and casual individuals wanting to lose weight and get healthy. Dr. Chantal Charo has also launched, a virtual online sports nutrition clinic with a team of highly trained nutritionists, celebrity trainers and chefs to answer all your diet, fitness and supplement questions.

Skeletal Muscle Hypertrophy: Science of Size


By Sérgio Fontinhas.  Each muscle fiber is a single, multinucleated cell, made up of smaller units called myofibrils. Myofibrils have a repeating pattern called a sarcomere, which is the basic functional unit of muscles. The myofibril is made up of even smaller structures called myofilaments, which are long chains of proteins actin and myosin. Another set of proteins regulate the interaction between actin and myosin. In the actin thin filament there’s a binding site that a myosin head can reach and grab, but the binding sites are covered. Calcium causes configurational changes and uncovers the binding sites for myosin. This calcium is stored in muscle cells in the sarcoplasmic reticulum distributed around the myofibrils.  Strength training can result in localized muscle tissue damage. When a certain threshold is exceeded, sarcomeres break. (It is assumed that optimum sarcomere length is 2.5 μm). This damages contractile elements or myofibrillar structures, disrupts the sarcolemma and sarcoplasmic reticular, causes damage to supportive connective tissue and injuries in the cytoskeleton (1). This damage may generate a hypertrophic response (2, 3). Muscle damage is a frequent response after unaccustomed exercise, or when performing high intensity exercise. A trainee may experience stiffness and delayed-onset muscle soreness (aka DOMS).  Other metabolic consequences are increases in creatine kinase, muscle troponin I, myoglobin and heavy myosin chain (4).Cat wt lifting

Eccentric actions – The best way to induce micro tears is by emphasizing eccentric training. The eccentric contraction has been proven through countless studies to cause the most damage, which has been shown to mediate a hypertrophic response (5,6), causing myofibrillar remodeling (7,8).  The distribution of sarcomeres on each myofibril is nonuniform, the weakest sarcomeres are located at different regions. This nonuniform lengthening causes a shearing of myofibrils and deforms membranes(4).  The presence of disrupted sarcomeres in myofibrils and damage to the excitation–contraction (E–C) coupling system are signs of damage in a muscle from eccentric exercise (9). During active stretch of a muscle, most of the length change will be taken up by the weakest sarcomeres (10) in myofibrils (the weakest half-sarcomeres). These sarcomeres become progressively weaker and then lengthen rapidly, uncontrollably, to a point of no myofilament overlap. Then overstretched sarcomeres are distributed at random along muscle fibers. When the muscle relaxes, some myofilaments in the majority of overstretched sarcomeres become disrupted (11).  During repeated eccentric contractions it is postulated that the number of disrupted sarcomeres grows, until a point is reached where membrane damage occurs. It is at this point that damage to elements of the E–C coupling machinery becomes apparent. Subsequently the fiber may die (Fig. 1).damagefromeccentricexercise

(12) Membrane damage begins with tearing of t-tubules followed by damage to the sarcoplasmic reticulum, uncontrolled Ca2+ release. If the damage is extensive enough, parts of the fiber, or the whole fiber, may die. Breakdown products of dead and dying cells would lead to a local inflammatory response associated with tissue oedema and soreness (12). Although it’s not clear, the first step in the damage process can be t-tubule rupture, leading to inactivation of some sarcomeres, but the reverse sequence beginning with sarcomere disruptions can also lead to t-tubule damage (12).  There are also observations of abnormal t-tubular arrangements after eccentric exercise (13).

Eccentric actions and force generation – Muscles achieve higher absolute forces when contracting eccentrically (14–16). Heavy negatives, or supramaximal eccentric actions involve eccentric contractions at a weight greater than concentric 1RM. It has been shown that eccentric strength is approximately 20–50% greater than the concentric strength (17) and even predicted to be up to 64% greater (52). Eccentric contractions could stimulate greater adaptations (18), because increases strength are thought to be proportional to the magnitude of force developed (19).  Eccentric training is more effective at increasing total and eccentric strength than concentric training, and appears to be more effective at increasing muscle mass than concentric training, possibly because of the higher forces developed. Adaptations after eccentric training are highly specific to the velocity and type of contraction (20). Eccentric exercise preferentially recruit fast twitch muscle fibers (53,21,22,23) and perhaps recruitment of previously inactive MUs (21,24). This results in an increased mechanical tension in type II fibers, which have the greatest potential for muscle (53,25,26,27).  Compared with concentric contractions, eccentric contractions also produce less fatigue and are more efficient at metabolic level. Unaccustomed eccentric contractions produce transient muscle damage, soreness and force impairments.arnold-big-arms

Eccentric actions and protein synthesis – Passive muscular tension develops because of lengthening of extra myofibrillar elements, especially collagen (28). This increases the active tension enhancing the hypertrophic response.  Eccentric contractions elicits greater gains in lean muscle compared with concentric and isometric contractions (29,30,31,32). Maximal muscle hypertrophy can only be attained if eccentric muscle actions are performed (33).  When lifting the same weight concentrically and eccentrically no significant difference between the two contractions is observed, if volume is equalized. However in a few studies there’s was a slight advantage for the concentric actions (34,54). Eccentric actions are best done supramaximal, above 1RM concentric load. Lengthening the muscle increase protein synthesis more than a concentric contraction (34), in part by releasing phosphatidic acid, which encourages protein synthesis (35). Another pathway is through the activation of satellite cells located on the outside of muscles. Satellite cells move to the damaged area and fuse to muscle, becoming a part of it (36), increasing muscle fiber size by the addition of the satellite cell’s nucleus to the muscle.  The more nuclei, the greater the growth potential. Plateau happens when we can’t adequately activate satellite cells (37,38), therefore maximize eccentric loading may be very beneficial.

Other increases have also been observed, such as a faster rise in protein synthesis (39), greater increases in IGF-1 messenger RNA (mRNA) expression (40), and more pronounced elevations in p70S6k (41), when compared with other types of contractions.

As for the tempo, faster speed eccentric contractions release more growth factors, more satellite cells, and greater protein synthesis than slow speed eccentric contractions (42,43). A 2- to 3-second tempo is hypothesized to be ideal for maximizing a hypertrophic response (43).  Eccentric training is also associated with an increased metabolic stress. Higher eccentric intensities elevate lactate buildup and spike anabolic hormonal levels (44).

Muscle swelling and soreness – In human subjects, the initial fall in tension after eccentric exercise is followed by a slow rise over 2–4 h, presumably recovery from metabolic exhaustion. Then 24 h later there’s a second fall in tension (45).  Eccentric exercise is followed by sensations of stiffness and soreness the next day (46), transient muscle damage, soreness and force impairments (47).  Because of eccentric exercise the contracting muscle is forcibly lengthened. Delayed muscle soreness sets in at about 6–8 h after the exercise and peaks at about 48 h (45,48). A second bout of eccentric exercise, a week after the first, leaves us much less stiff and sore.   The injury triggers a local inflammatory response that is accompanied by some oedema. The breakdown products of injured tissues sensitize nociceptors (12,45,49). These nociceptors respond to stimuli that are normally non-noxious, leaving the muscle tender to local palpation, stretch and contraction. A component of the delayed soreness from eccentric exercise may involves large-fiber mechanoreceptors (50,51).  The repair mechanism involves the addition of sarcomeres to regenerating muscle fiber, as shown by animal experiments.   Neutrophils migrate to the area of micro trauma. Damaged fibers release several agents that attract macrophages and lymphocytes to the injury site. The purpose of macrophages is to remove cellular debris and to produce cytokines that activate myoblasts, macrophages and lymphocytes. This response triggers the release of various growth factors that regulate satellite cell proliferation and differentiation (44).Girls-Lift-Weights

Stretch overload, hypertrophy and hyperplasia – Hypertrophy involves the enlargement of contractile elements (55). Hyperplasia on the other hand results in an increase in the number of fibers.  Increasing muscular density is very painful. However if significant damage is inflicted the number of fibers can actually increase. As noted, eccentric actions cause the most damage, but there’s another method such as stretch overload.

Stretch induced overload is when a certain load stretches a muscle, either intermittently, progressively, or chronically. These methods typically produce more sarcomeres in series (elongation). It’s also strongly associated with hyperplasia (56,57,58,59). This is usually studied in animal models.

1. Intermittent stretch – The intermittent stretch consists of stretching the muscle with the same weight. Stretch periods lasted for 24h in animal models, with 2 or 3 days or rest days in between for recovery. This method produce muscle fiber hypertrophy without fiber hyperplasia (60).  Part of the mass increase is due to increases in muscle length. In one study muscle length increased 26.1% in intermittently stretched muscle (60).

2. Progressive stretch overload  – Progressive stretch overload of skeletal muscle results in hypertrophy before hyperplasia (61,62). In progressive overload the load is increased every workout, with 2 to 3 days of rest days in between for recovery (61). Again, stretch periods of 24h each. The adaptive response to progressive stretch overload involve an initial fiber hypertrophy – that is increase and peak in cross sectional area and length – followed by hyperplasia (61). Muscle fibers may attain a critical size before the onset of fiber hyperplasia. If fibers enlarge to a critical size and are subjected to further stress they undergo a splitting process, the parent fiber gives rise to two or more daughter fibers (61).  This method produced 142% increase in cross-sectional area (in 16 days of stretch muscles); 50% increase in muscle length; 318% increase in muscle mass (after 28 days of stretch). All of these results exceed any reported in the literature.

3. Chronic stretch – Chronic stretch overload results in hyperplasia before hypertrophy (63). Chronic stretch does not allow for a recovery or rest interval and therefore results in significant muscle fiber injury (60,64). Hence, the initial fiber hyperplasia in the chronically stretched model may be an injury-related phenomenon (60).

Training strategies

Intensity – Intensity refers to the load lifted, the closer the load is to 1RM the greater the intensity. Higher intensity is related with low repetition due to the high percentage of load. It’s argue to be the most important variable for growth (44,66), at least to target the fast-twitch fibers. Intensity is customarily expressed as a percentage of 1RM and equates to the number of repetitions that can be performed with a given weight. For this purposed training at high intensity is suggested, as well as intensity of effort (intention of lifting the weight explosively even though it won’t go fast).

Rest interval – Different rest periods have distinct effects on strength capacity and metabolite buildup, thereby impacting the hypertrophic response (44,67). Long rest intervals afford full recovery of strength, maximizing mechanical tension (at the expense of metabolic stress). Most of the strength capacity is recovered within the first minute (44,68). A rest interval of 90-120s may be optimal for maximizing mechanical stress.

Repetitions – A repetition range of 1-5 is considered to be low, 6-12 is considered moderate, and above 15 is considered high. Low repetitions with long rest intervals maximize mechanical tension, due to the higher load one can lift. Therefore low repetition schemes are suggested to maximize muscle damage.


1. Heavy negatives – Heavy negatives (supramaximal loaded eccentric actions) is the performance of eccentric contractions at a weight greater than concentric 1RM. This technique usually requires a spotter to help raise the weight. A muscle is not fully fatigued during concentric training (65), therefore the use of heavy negatives is recommended for an additional hypertrophic stimulus.

2. Assisted Negatives – This technique involves performing regular repetitions while a spotter applies pressure on the negative portion of the rep. Using a load above 1RM isn’t always necessary, the point is doing more total eccentric work than concentric, for any number of reps, for example 70% concentric RM and 90% eccentric.

3. Emphasizing the Negative – Taking 3-5 seconds to lower the weight may allow a lifter to induce a maximum amount of damage. Emphasizing the negative may increase the micro tears in your muscles and release more satellite cells.

4. Forced Negatives – After concentric failure there’s still more work, failure is not achieved eccentrically. After concentric failure a spotter can assist on the positive rep while finishing eccentric reps until failure.

5. Loaded stretches – Putting the muscle at the most stretched position and using a load to stretch. This should be with a moderate weight for at least 30s, perhaps at the end of a set. Several approaches are possible: using one stretch after failure in every set, intraset-stretches (instead of rest interval), descending or ascending. Note that the stretching protocol eliciting more gains was the progressive stretch, in which the weight is increased every workout, but can also be increased every set.


Eccentrics, especially supramaximal eccentric contractions produce:

1. The most muscle damage

2. More protein synthesis

3. More hypertrophy

4. More strength

5. More growth factors

6. More satellite cells

Should be performed above with a load above 1RM, with a tempo between 1-3 seconds, and must be used in moderation (risk of muscle fiber death).


1. Hill, M and Goldspink, G. Expression and splicing of the insulin-like growth factor gene in rodent muscle is associated with muscle satellite (stem) cell activation following local tissue damage. J Physiol 549: 409–418, 2003.

2. Izquierdo, M, Ibanez, J, Gonzalez-Badillo, JJ,Hakkinen, K, Ratamess, NA, Kraemer, WJ, French, DN, Eslava, J, Altadill, A,Asiain, X, and Gorostiaga, EM. Differential effects of strength training leading to failure versus not to failure on hormonal responses, strength and muscle power increases. J Appl Physiol 100: 1647–1656, 2006.

3. Evans, WJ. Effects of exercise on senescent muscle. Clin Orthopaed Rel Res 403(Suppl.): S211–S220, 2002.

4. Tee JC, Bosch AN, Lambert MI (2007). Metabolic consequences of exercise induced muscle damage. Sports Med 37: 827-836.

5. Evans WJ. Effects of exercise on senescent muscle. Clin Orthop Relat Res 403(Suppl): S211–S220, 2002.

6. Hill M and Goldspink G. Expression and splicing of the insulin-like growth factor gene in rodent muscle is associated with muscle satellite (stem) cell activation following local tissue damage. J Physiol 549:409–418, 2003.

7. Crameri RM, Langberg H, Magnusson P, Jensen CH,Schroder HD, Olesen JL, and Kjaer M. Changes in satellite cells in human skeletal muscle after a single bout of high intensity exercise. J Physiol 558:333–340, 2004.

8. Yu JG and Thornell LE. Desmin and actin alterations in human muscles affected by delayed onset muscle soreness: A high resolution immunocy to chemical study. Histochem Cell Biol 118: 171–179, 2002.

9. Warren,G. L. Ingalls, C.P. Lowe, D.A. Armstrong, R.B. (2001). Excitation-contraction uncoupling: major role in contraction-induced muscle injury. Exercise and Sport Sciences Reviews 29, 82–87.

10. Morgan, D. L. (1990). New insights into the behavior of muscle during active lengthening. Biophysics Journal 57,209–221.

11. Talbot, J. A. & Morgan, D. L. (1996). Quantitative analysis of sarcomere non-uniformities in active muscle following a stretch. Journal of Muscle Research and Cell Motility 17,261–268.

12. U. Proske D. L. Morgan. Muscle damage from eccentric exercise: mechanism, mechanical signs,adaptation and clinical applications. Journal of Physiology (2001),537.2, pp.333–345

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Some Underutilized Supplements That Rock, Part 2

by George L. Redmon PhD ND.

For the great majority of us are satisfied with appearance as though it serves as reality and  more than often, these seemingly things influence more so than those that are. Niccolo Machiavelli, 1527

When you review the quote above by one of histories most influential management and political theorist they imply that in many cases individuals of a specific society or company become comfortable with the ways things are versus making changes that represent what they need to be. When you put these comments in the context of moving the body from its present state to that of an elite body builder, the message resonates loudly in reference to the unintended state of complacency some individual resistance training enthusiasts fall into.  For example, while whey protein, creatine,  and arginine may serve as solid foundations to any sound body building supplemental program,  what other products are needed to support recovery, growth hormone production, insulin modulation, reduction of pain and inflammation, generation of energy, reduction of body fat, protein synthesis, nitric oxide production, detoxification to the reduction of exercise induced cortisol levels?

Solving This Anabolic Puzzle Diversely  

When you review this short list of anabolic parameters and add in the complexity of managing and sustaining the physical and emotional stamina necessary to reach your goals, general appearances can begin to influence versus individual needs.  However, the reality versus the appearance of the best approach to take here is to take advantage of a complement of past, present and emerging products across various supplemental categories versus limiting your choices to products that appear to only fit the general body building mold. Forward thinking sports medicine researchers today have adopted this attitude as more products once considered to be strictly medicinal in nature have been found to offer an array of benefits to resistance training individuals. The goal of this report is to outline a few of these globally researched and unfortunately underutilized supplements that definitively do the job as advertised, despite appearing to be second best and or a non-categorized resistance training supplement. Incidentally, this list is extensive and can’t be covered in one article two or three for that matter. Correspondingly, this report is divided into two parts.

However, the goal here is to reinforce and establish the need to search and find the right combination of products that meet your individual needs.                      

Some Atypical and Typical Ergogenic Products 

Section: IV: Protein


For some time beef protein had all but disappeared from the body building landscape. It is however making a strong comeback. In fact, researchers at McMasters University in Canada recently reported that subjects eating a six ounce serving equaling 170g of 85% lean ground beef resulted in significant changes in the rate of protein synthesis (creation of new muscle) following exercise. Furthermore, beef contains varying amounts of amino acids that promote growth and a host of other nutrients. While there is concern about the fat content in beef, many sports nutritional researchers insist that beef 2 to 3 times a week to augment proteins like whey and casein would greatly benefit growth efforts.

Section V: Insulin Mimickers

As cited by the well-known sports medicine researcher Dr. Eric Serrano, despite being one of the body’s most anabolic hormones, insulin has a Dr. Jekyll/ Mr. Hyde side effect on the body. Despite its ability to quickly drive nutrients into muscle cells to promote growth, un-regulated insulin spikes can cause large deposits of body fat. For this reason, the usage of specific ergogenics that keep insulin stabilized are highly sought after. While there are many the 2 below are excellent.

Alpha Lipoic Acid (ALA)

ALA is known for its antioxidant capabilities and its ability to naturally stabilize blood glucose levels by mimicking (imitating) the physiological actions of insulin. For example, in a study appearing in Free Radical Biology and Medicine,  seventy-four patients were divided into four groups (placebo, and 600mg ALA once, twice, or three daily) for a 4-week trial to examine its effects on insulin sensitivity, using a measurement called the Metabolic Clearance of Glucose (MCR). ALA treatment led to significant improvement in MCR. Another trial found improvements in insulin resistance and fasting glucose after 300mg of oral ALA daily for eight weeks.

Suggested Dose: 600 mg/d

Vanadyl Sulfate

Vanadly Sulfate is derived from the trace mineral vanadium and plays a major role in regulating blood sugar by increasing the rate at which carbohydrate and protein enter muscle cells. This helps to swell muscle fibers, increasing both size and vascularity.  Vanadyl also diverts sugar away from storage in fat cells, supports protein synthesis, increases muscle pumps and hardness similarly to nitric oxide. As you know, when competing bodybuilders ensure that they have increased vascularity on the day of a contest, so that muscles look more prominent and visible. This look adds to the interest and to the uniqueness of that individual’s physique.
Suggested Dose: 60 mg before workouts.

Section VI: Nitric Oxide Boosters


L- Citrulline is found abundantly in watermelon and is linked to arginine production, the precursor to nitric oxide. Ironically, citrulline elevates levels of arginine more effectively than supplemental arginine itself. In fact, a study appearing in Circulation AHA Scientific Sessions revealed that an oral dose of 3.8 grams of citrulline resulted in a 227% peak increase in arginine levels after 4 hours, compared with a 90% peak increase with the same dose of arginine. Researchers have discovered the reason for this anomaly occurs because citrulline bypasses metabolism in the liver and gastrointestinal tract and is formed in the urea cycle when the liver and kidneys get rid of ammonia and lactic acid,

finally being synthesized in the intestines , where it is converted into arginine. Furthermore, L-citrulline assists in constructing and increasing the supply of molecular elements the body needs to form proteins.

Suggested Dose: 6 grams/d before workouts.


Pycnogenolis an extract of French maritime pine tree bark that grows along the coast of southwest France. That special pine contains natural antioxidants called anthocyanins. Current data indicates that Pycnogenol is absorbed into the bloodstream in about 20 minutes and once absorbed, its maximum protective effects appear to lasts about 72 hours. Recently, scientist at the Hiroshima University Graduate School of Biomedical Sciences in Japan reported that pycnogenol enhances nitric oxide (NO) production. Conversely, emerging research has demonstrated that the combination of Pycnogenol / Arginine heightens NO release at a greater rate. For example, once arginine is absorbed by the intestines, it travels into the bloodstream where it is converted into NO. However, this chemical reaction requires an enzyme known as nitric oxide synthase (NOS). Unfortunately, NOS limits the amount of arginine that can be converted into NO. However, the researchers above discovered that 180mg of pycnogenol for two weeks increased the activity and amount of NOS available to catalyze this conversion process by 42%.

Suggested Dose: 50-100mg/d

Section VII: Testosterone Production

 Zinc and Magnesium Aspartate (ZMA)

Zinc plays a key role in the production of natural testosterone by inhibiting it’s conversion into estrogen and in the process converts estrogen into testosterone. On the other hand studies indicate that magnesium increases free and total testosterone levels in both sedentary individuals and in athletes. Conversely, early studies by Dr. Lorrie Brilla, PhD, a sports performance researcher at Western Washington University reported that ZMA significantly increase free testosterone levels and muscle strength. In fact, 30mg of zinc and 450mg of magnesium per day elevated testosterone levels by 30%  with a 4% increase in IGF( insulin growth factor) levels, an anabolic hormone that decreases during aging, while those who took a placebo had a 10% decrease in testosterone and a 22% decrease in IGF-1.

Dr. Brilla, reported that subjects in this study lasting 8 weeks study had 2.5 times greater muscle strength gains than a placebo group. Pre and post leg strength measurements were made. The strength of the ZMA group increased by 11.6% compared to only a 4.6% increase in the placebo group. As an added bonus here ZMA enhanced growth hormone production when taken before bedtime. More importantly, ZMA is not a pro-hormone or hormone precursor and will not suppress your own natural production of testosterone.

Suggested Dose: 30mg zinc/450mg magnesium/d.

Some Other Accessory Nutrients That Deliver

While this report can’t cover the large body of under-utilized supplements you have at your disposal, the list below represents a few other products that definitively deliver. This list isn’t all inclusive but includes: Carnitine{ fat-burning}, Chromium{insulin stabilization} , CLA (conjugated linoleic acid){fat-reduction},  Dehydroepiandrosterone (DHEA){stress reduction/testosterone production},  D-ribose{energy}, Enzymes{anti-inflammatory/nutrient metabolism}, Forskolin{thermogenic} , HMB (Beta-hydroxly-beta-methylbutyrate),{ lean muscle mass and strength gains},Medium Chain Triglycerides (MCT’s){energy/fat burner}, NAC (N-acetyl –cysteine) {detoxification/muscle preservation}, Rhodiola Rosea {ATP regeneration/stress reduction/mental clarity} , Synephrine{ephedra alternative without the jitters } Taurine {building block of other amino acids}, Tribulus Terrestris{ testosterone production} , Tyrosine {mood elevation}and 7 Keto DHEA{cortisol and fat reduction}.

Conclusions – Dr. Jeffery Bland, Ph.D. a well-known Professor of Nutritional Biochemistry states that amino acids are generally considered non-essential for most individuals. However on the basis of an individual’s unique genetic nature these non-essential compounds may become an essential auxiliary nutrient to meet the person’s individual pharmacological need. This nutritional concept of individualized need is now referred to as the justification theory. Conversely, how well you organize and utilize your supplement choices will have a great impact on your growth efforts. Diversity and sound research based on your individual need should be your guiding light.


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Bloomer R.J., Smith W.A., Glycine propionyl-L-carnitine increases plasma nitrate/nitrite in resistance-trained men. Journal of International Society of Sports Nutrition. 2007 Dec;4:22.

Brilla, L.R., Conte, V. Effects of zinc-magnesium (ZMA) supplementation on muscle attributes of football players. Medical and Science in Sports and Exercise. 1999 May; 31(5): 627-759.

Burke, E, Fahey, J., Phosphatidyserine (PS): Promise For Athletic Performance. New Cannan CT: Keats Publishing, 1998.

Cavagnini, F.,  Invvitt, C.,,. Effect of acute and repeated administration of gamma aminobutyric acid ( GABA) on growth hormone and prolactin secretion in man. Acta. Endocrinology( Copenh) .1980; 93(2): 149-154.

Carkoudian, N. Skin blood flow in adult human thermoregulation: how it works, when it does not and why. Mayo Clinic Proceedings. 2003 May; 78(5): 603-612.

Cohen, N, Halberstam, M. Oral vanadyl sulfate improves hepatic and peripheral insulin sensitivity in patients with non-insulin-dependent diabetes mellitus. Journal of Clinical Investigation. 1995; 95: 2501-2509

Cynober L. Pharmacokinetics of arginine and related amino acids. Journal of Nutrition. 2007 Jun;137(6 Suppl 2):1646S-1649S.

Fahey, T.D., Pearl, M.S. The hormonal and perceptive effects of phosphatidylserine administration during two weeks of resistive exercise-induced overtraining. Biolology and Sport. 1998;15:135-144.

Goldwater, I, Gefel, D,  Insulin-like effects of vanadium: basic and clinical implications. Journal of Inorganic Biochemistry. 2000;80: 21-25.

Hickner R,C, Tanner C, J. et al. L-citrulline reduces time to exhaustion and insulin response to a graded exercise test. Medical Science Sports and Exercise. 2006;38:660-666.

Jacob, S., Ruus P. et al. Oral administration of RAC-alpha-lipoic acid modulates insulin sensitivity in patients with type-2 diabetes mellitus: a placebo-controlled pilot trial. Free Radical Biology and Medicine. 1999 Aug; 27(3-4):309-314.

Jay, A. Management and Machiavelli. Holt Reinehart and Winston: New York, 1967.

Kon, M., Effect of Coenzyme Q10 supplementation on exercise-induced muscular injury of rats. Exercise Immunology Review. 2007;13; 76-88.

George L. Redmon, Ph.D. – Dr. Redmon 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 nation’s 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.

Why Not Fat?

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

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

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

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

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

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


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