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dr.eddiejo dr.eddiejo

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Eddie Jo, PhD, CSCS*D, CISSN  Professor of Sport and Exercise Physiology Director of the Human Performance Research Lab @ Cal Poly Pomona | NSCA CSCS*D, CPT

Chronic use of over the counter NSAIDs like ibuprofen has been a topic of controversy in sports medicine and training. Many have resorted to mild to high to very high dose NSAID regimens while in training as a means to facilitate muscle recovery regardless of the absence of any chronic inflammatory conditions. Recent scientific literature along with some basic physiology suggests, in opposition, that high to very high dose anti-inflammatory drugs (or perhaps even non-pharmacological agents) may not promote actual muscle tissue recovery and even blunt muscular adaptations to training. For instance in a recent study as presented here, young healthy adults who underwent a high dosage ibuprofen/NSAID regimen during 8 weeks of resistance training experienced attenuated muscular adaptations in strength and hypertrophy compared to a low dose aspirin/NSAID treatment. Although the absence of a non-NSAID control may be a limitation to the study, the authors present justifications in their paper. There are two possible explanations to these findings (at least for now). 1. High dose NSAIDs have shown to inhibit key signaling mechanisms of muscle hypertrophy, and 2. Although not fully substantiated, potent anti-inflammatory agents may inhibit the acute inflammatory response to muscle damage that subsequently signals the regenerative healing process required for actual muscle recovery. This acute inflammatory phase following heavy, muscle damaging exercise is linked to temporary pain/soreness, and therefore high dose NSAIDs may be used to mitigate these effects. However, the question is whether this strategy actually promotes muscle tissue recovery or simply the perception of recovery, i.e. pain management. I speculate the latter being the case more so than the former since this acute inflammatory response essentially signals the subsequent processes of muscle tissue healing. In the absence of chronic inflammation, those engaged in resistance training should not resort to high dose NSAIDs to facilitate muscle recovery as it may inhibit growth signals and processes of tissue repair. Just rest.

What is the interaction among a caloric deficit, resistance training, dietary protein, and muscle protein metabolism? Firstly, an energy deficit promotes a general shift in fuel utilization in that there is an increased reliance on endogenous (stored) fuels such as fat, carbohydrate/glycogen, and amino acids from proteins within various organs in the body including muscle. Thus, during an energy deficit there is a general increase in muscle protein degradation, in turn providing a free amino acid pool to help meet the body's energy needs through their oxidation or serve as a substrate for glucose production (to help maintain blood glucose homeostasis). Also, a lower portion of the free amino acid pool would be reincorporated back into muscle proteins since protein synthesis (or any anabolic process) is energy consuming (not favorable during an energy deficit). Overtime, muscle mass may decrease since the intracellular protein content eventually diminishes. Because an energy deficit exerts these effects on muscle protein metabolism, it is common to experience a loss of lean mass during a caloric deficit diet which at times may reduce the quality of weight loss and exacerbate the normal suppression of resting metabolic rate that accompanies weight loss. The traditional thought is that there is nothing we can do about this. However, an expanding body of recent evidence adequately counters this contention. High volume resistance training together with a higher protein intake (2-3x U.S RDA) has shown to facilitate lean mass retention or growth during a caloric deficit. My recent study showed this was possible even with an extreme ~1000 kcal/day deficit in obese subjects! It appears that increasing dietary protein intake during a caloric deficit provides a greater free amino acid pool to support energy and glucose needs, alleviate the reliance on muscle protein breakdown, and afford the building blocks to synthesize muscle proteins. All one needs now is a stressor to the muscle to stimulate protein synthesis. Here enters resistance training.

A couple weeks I ago I did a similar post on muscle growth and I wanted to share the same perspective as it relates to fat/adipose loss. As we undergo a caloric deficit to drive a loss of adipose mass, we can only assess (at least practically) the efficacy of a program by changes that are observable. And often times we grow impatient when there is a lack of observable change and are quick to label the program ineffective or we simply quit. But when you understand that the reduction of adipose tissue is a process that begins all the way down to the most micro level of the body, the molecular level, you would understand that there is a huge element of time and scale. The size and mass of adipose tissue is really (at least for the most part) composed of the size and mass of all of the associated cells/adipocytes (hundreds of thousands of them). The size and mass of a single adipocytes/adipose cell is determined by the total mass of "stuff" inside each cell. This stuff taking up intracellular space are the various molecules that have specific roles in the cell's functioning. A very large portion of the molecules found in adipose cells are fat/lipid molecules often arranged in a storage form called triglycerides. Caloric deficit is the most potent stimulus for increasing the catabolism/degradation and oxidation of these fat molecules that again make up the size and mass of the adipose cells. So the fundamental point of achieving observable reduction of adipose mass is to consistently drive the catabolism and oxidation of intracellular fats/lipids to eventually atrophy the adipose cell. Even with that, a sufficient amount of cellular atrophy needs to occur to see visual and observable changes in adipose tissue size and mass. As you can see, even a kg reduction in adipose mass requires A LOT of work at the molecular and cellular levels. Persistence and patience is key. Just because you don't see observable changes doesn't mean nothing is happening.

One of the most largely misused data in exercise and muscle physiology are those derived from molecular analysis of key intracellular signaling mechanisms that regulate and initiate muscle protein anabolism/synthesis, i.e. mTOR(C1) pathway. For instance, we have seen data showing increased mTOR activation upon administration of amino acids like leucine, production of high muscle tension, or even simply nutrient supply which implies a positive effect on muscle protein anabolism. These studies are often done in isolated muscle cells, animal tissue, or human muscle biopsies. These data are intended to provide physiological insight into the possible mechanisms underlying any effects that may be seen at the whole body level, e.g. changes in muscle mass and performance. Molecular data, such as those concerning mTOR activation in muscle, are not meant for direct application nor are they to be used as the basis for practical recommendations. A good example of this misuse of molecular data was with studies showing leucine to be stimulatory to the mTOR pathway. This led to a widespread "more leucine = more gains" mindset which was in fact heavily utilized in the marketing of related supplement products like BCAA overly enriched with leucine. This misuse also applies to fitness practitioners who reference these molecular findings as justification for their training program. It's not just about simply using evidence to form training and nutrition practices but rather how you use the evidence.

The seemingly endless debate on low carb vs low fat caloric restriction diets in the context of weight loss is, in my opinion, fueled by 1. mixed anecdotal claims and arguments, 2. psuedoscience, and 3. mixed emprical evidence. As for the latter, key design and methodological limitations such as small sample sizes, heterogenous subject pools, relatively short term treatment periods, or poorly monitored free-living protocols introduce issues that may certainly confound the interpretation of the data and leave us with no real emprical consensus on the topic. Keep in mind however these limitations are quite understandable given the logistics that go into conducting these types of dietary intervention studies. Recently, one of the most comprehensive studies examining this debate was published in JAMA. This study assessed and compared weight loss, RMR, and other measurements in 609 overweight participants undergoing a lower carb or lower fat caloric restriction diet across a whole year. The retention rate for this study was one of the best I've seen in studies of this size and magnitude. The caloric intake was equivalent between the two groups at 3-month time points and results showed that after a year there were no significant differences in total weight loss, body fat %, or RMR suppression between the two diet interventions. These findings suggest, with decently strong evidence, that caloric deficit via caloric restriction is the main driver of weight loss in overweight individuals. It is my opinion that skewing macronutrient composition, at least for dietary carbohydrate and fat, is more practically relevant and perhaps impactful for those already with "healthy" body weight or body composition who are looking to cut a bit more body fat. Next up: are there genetic predispositions to specific diet responsiveness?

In a previous post regarding the false dichotomous view of aerobic and anaerobic integration during exercise, I emphasized the point that your classically termed "anaerobic" exercise is actually very aerobic in the sense that aerobic energy systems are still in fact working on all cylinders even during max effort / sprint type exercise. It's just that a portion of the energy needs cannot be fufilled aerobically and thus this energy void is satisfied anaerobically. The false notion is that during max effort exercise, your muscles switches over to anaerobic metabolism which led to the equally false notion that training in this "anaerobic zone" improves one's conditioning via some enhancement to the anaerobic system (the concept of training specificity misapplied). It is rather due to an improvement in the aerobic systems which involves a host of adaptations from muscle mitochondria to the cardiovascular/respiratory system. This means that the improvement in fitness from, for instance, sprint interval training, is indeed due to aerobic enhancements as measured by improved VO2max and anaerobic threshold. Here's some evidence.

Based on a 2017 meta analysis of 38 sprint interval training trials from across 34 previous studies, there is very strong evidence to suggest that sprint interval training is an effective means of improving ones aerobic capacity by avg. of 7.8% (as measured by change in VO2max). Interestingly, a greater improvement was observed with protocols with less sprint intervals (~2-3 reps) especially compared to the high rep ranges >6. However, the strength of evidence was greatest with protocols using a 4-6 rep range. So to improve aerobic fitness, it may be worthwhile to incorporate SIT into a periodized program consisting of HIIT and mod-high intensity steady state bouts.

The popularity of anti-inflammatory and anti-oxidant modalities among athletes is largely driven by anecdotal and empirical evidence suggesting their efficacy in aiding "recovery" from muscle damage induced by overloading stress. However, this sense of "recovery" should rather and more accurately be described as simply the reduction of soreness which is not directly indicative of healed, i.e recovered, muscle tissue. It is my strongest opinion that the term "muscle recovery" is largely misinterpreted and misused. Many interpret "muscle recovery" as simply the absence of soreness or DOMS (or what I like to call "perceptual recovery") which enables a fallacious view that acute inflammation and free radicals post-exercise is the key therapeutic target for post-exercise muscle recovery. The acute inflammatory and free radical response following muscle damaging exercise is intended to signal the sequential processes of tissue healing. In other words, it is a normal process. Only when in high amounts like after severe damage, inflammatory molecules and free radicals may also trigger surrounding sensory neurons, and the resulting neuroelectrical and chemical signals may translate to pain or soreness. Just like the pain following a sun burn, temporary pain or soreness is a feedback signal to stop perturbing the tissue while it is trying to heal. The absence of soreness does not indicate that muscle tissue has been repaired, so modalities that mitigate acute inflammation are not really muscle recovery aids and may even delay healing, inhibit training adaptations, and reduce structural integrity of muscle with accrued damage. Thus, unless you are an in-season athlete or have an occupation in which performance cannot be limited by soreness, anti-inflammatory and anti-oxidant modalities should be applied with caution.

Some findings from my lab recently accepted for presentation at the 2018 ACSM annual meeting. BCAA supplementation is commonplace in the nutritional programming for athletes and fitness enthusiasts due to it's purported, yet debateable, benefits for muscle growth and recovery from exercise-induced muscle damage. Among the 3 BCAAs, leucine has garnered the most attention as it has shown to be a unique anabolic stimulus to muscle protein metabolism, and thereby becoming the hallmark determinant of dietary protein "quality". Many have theorized that enriching a BCAA supplement with leucine would enhance its effects; in fact, many supplement companies have produced BCAA products on the basis of this theory. Just take a look at the number of obscure BCAA ratios in today's sport supplement market. We've seen up to a 12:1:1 leucine to isoleucine to valine ratios even. 🔬My lab recently conducted a study on 4:1:1 leucine enriched BCAA supplementation to examine whether it would offer any advantages over a conventional 2:1:1 BCAA formulation for performance recovery from exercise induced muscle damage. We found through performance, perception-based, and biochemical measurements that a leucine enriched BCAA supplement failed to offer any further benefits over the conventional formulation. Also, a 10g leucine-only supplement demonstrated less efficacy in facilitating recovery of muscular power and range of motion and mitigating soreness than both BCAA treatments. This study does not however demonstrate the efficacy of BCAA in attenuating damage or improving recovery nor do these findings have clear implications for training adaptations. Always important to consider context. Awesome job by my lab team!

Adding onto the growing body of research supporting the benefits of high protein intake in efforts to optimize body composition, a recent 2018 study published in the International J. of Sports Nutrition & Exercise Metabolism compared body composition outcomes between high vs. low protein diets across 8 weeks of training in aspring female physique competitors. The high protein diet (2.5g/kg/day) resulted in a significant loss of fat mass while the lower protein diet failed to elicit any significant change. The high protein diet also produced a significant increase in fat free mass which was a change signficantly greater than the low protein diet. Although this study presented with some methodological limitations (like every study to some degree), the body of scientific literature corroborates these findings, further adding to the importance of protein intake in the optimization of body composition across multiple scenarios including, caloric deficit, muscle hypertrophy training and body recomposition efforts (improving muscle mass while reducing fat mass).

Impatient with your muscles? Let's go back to the basics of physiology. As we train to improve muscle size and mass, we can only assess (at least practically) the efficacy of a program by changes that are observable. And often times we grow impatient when there is a lack of observable change and are quick to label the program ineffective or we simply quit. But when you understand that growth of muscle tissue is a process that begins all the way down to the most micro level of the body, the molecular level, you would understand that there is a huge element of time and scale. The size and mass of any given muscle is really (at least for the most part) composed of the size and mass of all of the associated cells/fibers (hundreds of thousands of them). The size and mass of a single fiber is determined by the total mass of "stuff" inside said fiber. This stuff taking up intracellular space are the various molecules that have specific roles in the cell's functioning. Although the majority of the molecules found in muscle cells are water molecules, a large portion are proteins. Resistance training is the most potent stimulus for building these muscle proteins as an adaptive response to the repeated overloading mechanical and metabolic stress to the muscle. So the fundamental point of achieving observable growth of muscle tissue is to train in a way that consistently and effectively drives protein synthesis at a rate that exceeds degradation so that individual cells can expand (hypertrophy). Even with that, a sufficient amount of cellular hypertrophy needs to occur to see visual and observable changes in the muscle tissue size and mass. As you can see, even a kg improvement in muscle mass requires A LOT of work at the molecular and cellular levels. Think of muscle growth as building a concrete wall one grain at a time. Although grains are being added you won't see any changes in the mass and size of that wall until some time has passed and tons of repeated work has been put into it. Patience and consistency are the basis of any effective training program.

Often times we hear debates on effective training programs and almost equally as often one would use the outcomes of a single study to defend a training method. We see it all the time in social media. A single research study is not intended to directly affect real life application. Rather, a single study is intended to contribute to a body of research which in time would establish principles that would ultimately affect real life application.
This graph indicates the individual subject responses for lean mass to a 6 week resistance training protocol from one of my past studies. Although the results show that the 4% average gain was statistically signficant, it does not imply a uniform, exact response for all individuals. As you can see every single one of the 38 subjects responded differently to the same training protocol. This is what happens in real life applications. Thus programs should not be designed by a copy and paste of research protocols. Training programs should rather be based on training principles derived from a BODY of research such as overload stress, periodization, and specificity. These evidence based principles help build a foundation for a training program while systematic variations should be applied on the basis of both quantitative and qualitative feedback as well as empirical and anecdotal evidence.

From online fitness blogs to gym talk, it is clear that modern day concepts of protein nutrition overemphasize the purported significance of "anabolic" amino acids, i.e. BCAA or leucine, and strategies to maximize muscle protein synthesis. This was largely facilitated by earlier research demonstrating an acute and transient anabolic response upon administration of BCAAs or leucine. On one end, these findings provided novel scientific insight to the unique anabolic properties of nutrients and shaped the definition of "quality" dietary protein sources. However, on the other end, these findings also enabled a fallacious view on optimum protein nutrition in that a net anabolic state in muscle protein metabolism can be achieved by way of abundantly consuming these key nutrients (hence the boom in the BCAA market). Muscle proteins, like every protein found in the body, are constructed by a unique combination of essential and non-essential amino acids which your body can't and can produce, respectively. Thus, without a sufficient dietary EAA provision, a net anabolic state to facilitate muscle growth would be difficult to achieve regardless of whether BCAAs are consumed abundantly. Bottom line: optimum protein nutrition should be predicated on meeting total daily protein needs and inclusion of EAA rich protein sources. It should not be centered on the amount and frequency of BCAA or leucine intake. Not saying BCAA supplementation is useless. Just depends on the context in which we are asking ourselves if it "works".

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