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Eddie Jo, PhD, CSCS*D, CISSN

Professor of Sport & Exercise Physiology Director of the Human Performance Research Lab @ Cal Poly Pomona Industry and Personal Consultant

http://www.dreddiejo.com/

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Exercise is Medicine Series ๐Ÿ‘‰Insulin resistance, especially in adipose and skeletal muscle, is a core defect in type II diabetes and metabolic syndrome. In healthy individuals, when blood glucose rises like after consuming carbohydrates, insulin is secreted to signal cells like those in muscle to uptake glucose out of the blood to be used as a fuel molecule by those cells. Insulin resistance in these cells describes a defect in this process, ultimately leading to uncontrolled blood glucose levels, metabolic dysfunction, and increased risk for metabolic disease. ๐Ÿ‘‰Thus, type II diabetics have two goals, 1) improve immediate blood glucose control and 2) long term improvement in insulin sensitivity. The former requires an insulin-independent pathway to stimulate glucose uptake by cells (since these cells are resistant to insulin). Exercise (or more technically, muscle contraction) is a known stimulus for glucose uptake in muscle (both skeletal and cardiac) through an insulin-independent pathway involving the enzyme AMPK. AMPK has been largely implicated in the treatment of type II diabetes because of its role as a potent stimulus for glucose uptake. This is why AMPK-agonist drugs are prescribed to diabetics to improve blood glucose control. However, as indicated above, exercise does the same thing. Exercise is a KNOWN AMPK-agonist. ๐Ÿ‘‰As for the goal to improve insulin sensitivity, longterm exercise and chronic AMPK activation can eventually lead to improved insulin sensitivity, restoring the insulin-dependent pathway of glucose uptake. This effect of exercise is underpinned by multiple AMPK-related mechanisms such as mitochondrial biogenesis and decreased tissue inflammation. These longterm effects do not appear to occur with chronic use of drugs that are AMPK-agonist. EXERCISE IS LITERALLY MEDICINE. ๐Ÿ‘๐Ÿผ

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With recent headlines concerning contaminated sport and health supplements, I thought it would be appropriate to present work from Dr. Cohen who has published several studies examining the contents of various dietary supplement especially oxilofrine-containing "fat burners". Oxilofrine is an amphetamine-related drug and a potent cardiac and nervous system stimulant. It is not an approved drug in the US and is also banned by the World Anti Doping Agency. Recently, US-sold dietary supplements, namely those identified as fat burners, have been under scrutiny for containing pharmaceutical or harmful levels of oxilofrine regardless of the fact that it is illegal in the US for supplements to contain pharmaceutical drugs. The use of a synonym, "methylsynephrine" on labels may mislead regulators and consumers to believe the supplement is free of oxilofrine. As a result, athletes who have consumed these supplements have been banned for oxilofrine and general consumers have experienced serious health issues. A recent study showed that over half of the tested fat burners contained oxilofrine with a large portion containing pharmaceutical to harmful dosages. Based on supplement instructions, consumers could inadvertently take up to 250mg of oxilofrine per day while the prescribed medical dose in Europe is 16-40mg. The supplement industry especially in the context of fat burners, thermogenics, or weight loss pills, is indeed a buyer beware environment. Be mindful of any supplements containing methylsynephrine especially when it is labeled as being derived from plant extracts since oxilofrine has never been identified in any plants. Look for third party accreditations for good manufacturing practices like NSF, BSCG, and informed-choice.org for all dietary supplements and always keep in mind that supplements are never a necessity.

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A couple months 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 adipocyte/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 would require A LOT of work at the molecular and cellular levels. On top of that, underlying these changes from molecular to whole-body levels are epigenetic modifications via environmental or lifestyle factors (e.g. exercise, nutrition, etc). Persistence and patience is key. Just because you don't see observable changes doesn't mean nothing is happening.

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"Exercise is Medicine" is a mantra that is widely and irrefutably accepted by the medical community as well as the general public. It is, although, largely percieved in a more figurative manner with the simple understanding that a lifestyle incorporating exercise is good for health and is thereby, "medicine". However, with growing knowledge of the biological mechanisms underlying the health promoting benefits of exercise, the popularized saying has developed a more literal and technical meaning. There is no question that in the world of metabolic syndrome and related diseases drug prescriptions supercede exercise prescriptions. Medical students are often taught the intricate mechanisms and biological targets for a variety of pharmacological treatments for conditions related to metabolic syndrome, but what is less emphasized is that many of these drugs are in fact exercise mimetics. In other words, they mimic a particular biological effect of exercise. As exemplified by this infographic, common drugs for type II diabetes and dyslipidemia are PPAR (peroxisome proliferator-activated receptor) or AMPK (adenosine monophosphate kinase) agonist/activators. These molecules are the biological targets for these drugs because they regulate and stimulate processes like lipid breakdown, glucose uptake, and mitochondrial biogenesis all of which are conducive to improved metabolic health status. What may be less known and less communicated is that exercise is also an agonist for these very same molecular targets, targets that are implicated in many of the physiological mechanisms through which exercise improves metabolic health. So yes, even from a technical perspective, exercise is indeed medicine. Now only if exercise prescriptions were given more attention.

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Of the studies examining the immediate effects of foam rolling or similar self-myofascial release techniques on performance, a majority (almost all) demonstrate no effects (positive or negative). Thus, on the basis of the available evidence, pre-exercise or -competition use of foam rolling, such as during a warm up routine, holds no merit if applied with the specific intent of performance enhancement. It should be noted that immediate yet transient improvements in ROM are more consistently observed but again without concomitant changes in performance. A new study out of my lab recently published in the Journal of Athletic Enhancement offers a fresh perspective on the application of foam rolling as it relates to immediate performance effects. One of the many settings in which athletes incorporate foam rolling is during situations of exercise-induced muscular fatigue such as during competition (e.g. half-time break) or a training bout (e.g. intra-workout rest periods). In these circumstances, foam rolling is used with the general intent of acutely mitigating fatigue-induced impairments of performance and to preserve functional capacities of the neuromuscular system throughout the remaining period of competition or exercise. However, the efficacy of this strategy remains vaguely understood and is predominately reinforced by anecdotal claims of reduced tightness, improved mobility, and preserved strength. We found that a 7-minute application of foam rolling after a fatigue protocol attenuated the fatigue-induced decline in muscular power and velocity compared to passive rest. It must be noted however that the preservation of power and velocity was not robust enough to minimize the reduction in direct performance measures such as vertical jump height and dynamic reaction time. Still, we believe these findings at least warrant further investigation on the ergogenic value of foam rolling during fatigued situations with intra-competition or -workout implications. It appears that the immediate performance benefit of foam rolling is not relevant to performance enhancement per se but rather performance preservation under muscular fatigue states. Link to paper coming soon!

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It is no question that obesity is associated with a multitude of comorbidities or diseases. Accordingly, it is evident that the state of obesity is conducive to a systemic/whole-body environment that is unfavorable for the general "health" of various cells and thereby organ tissues. In a 2016 paper, I discussed the mechanisms underpinning the development of obesity-related comorbidities with large emphasis on chronic low-grade systemic inflammation being the key interlinking mediator. It is evident that this state of chronic low-grade inflammation (or meta-inflammation) with obesity originates from the dysfunction of two tissues, adipose and the gut. First, obesity provokes changes in accumulated adipose tissue that result in altered fat cell metabolism and dysfunction as well as increased infiltration of immune cells. Altogether, this promotes inflammation of adipose tissue resulting in increased release of a variety of small proteins called adipokines, much of which are pro-inflammatory mediators. Secondly, gut tissue also undergoes changes with obesity, such as gut inflammation, altered gut microbiota, and increased intestinal wall permeability causing continuous endotoxin (LPS) leakage into circulation. Thus, obesity is linked to chronic low-grade endotoxemia. Collectively, these effects of obesity on adipose and gut tissues create a continuous state of low-grade inflammation within the whole body. In turn, other tissues are susceptible to aberrant inflammation and dysfunction. Tissues of the heart, liver, and blood vessels are well known to be affected by this inflammatory environment, and there is recent evidence that converge to show that the brain also undergoes substantial changes that are conducive to the development of neuropsychiatric symptoms and diseases. Bottom line is that obesity is an unsuspecting inflammatory disease and if left unresolved will drastically increase the risk for disease. #cpphprl

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(Reposting due to typo) It's no doubt that the advancement of sport-specific training variables has allowed for more sophisticated and efficient strength and conditioning programs. The scientific community continues to introduce new theories and evidence regarding variables that may influence the transfer of a training program to the playing field. Recently, it has been suggested in theory and by new evidence that development of strength for a given sport movement is specific to the force vector, such that exercises involving vertical force applications (e.g. squats) transfer optimally to vertical sport movements (e.g. vertical jump) with the same relationship for exercises and movements with horizontally directed forces. So what are force vectors? In the context of sport and exercise, force vectors generally describe the direction in which force is applied for a given movement in relation to the whole body position (not to each muscle involved). To put the force vector theory to the test, Contreras et al. (2017) investigated the effects of 6wk front squat (vertical/axial force vector) vs. hip thrust (horizontal/anteroposterior force vector) training on vertical and horizontal jump and sprint performance. The data demonstrated the optimal transfer of training to athletic movements to be force vector specific as axial/vertical training (front squat) improved performance of the vertical jump greater than anteroposterior/horizontal (back to front) training (hip thrust). On the other hand, hip thrust training improved performance of more horizontally-directed movements, i.e. short sprint and horizontal jump performance, greater than front squats (*although sprinting and horizontal jumping does involve also a vertical force vector component). The principle take-away here is not a matter of whether hip thrusts or front squats are better than the other, but rather that force vectors may be an important variable to consider when designing sport specific training programs. Awesome sport science by the man @bretcontreras1 ๐Ÿ‘๐Ÿ‘! #cpphprl

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Free radicals like reactive oxygen species (ROS) produced during exercise has long been a common target of nutritional "therapy" via anti-oxidant consumption to mainly aid in muscle recovery. This is likely due to the notion that free radicals/ROS instigate further cell damage, soreness, inflammation, and is generally a detriment to health. However it is not necessarily free radicals or ROS themselves that invoke damage to cells and tissues but rather a combination of elevated free radicals and lowered levels of anti-oxidants to neutralize them, i.e. oxidative stress. In any case, this negative perception of free radicals, especially as it relates to muscle health, has enabled the common practice of high dose anti-oxidant supplementation by athletes and fitness enthusiasts alike. What is largely misunderstood is that ROS and free radicals have an important role in the adaptive processes muscles undergo during training such as myofiber hypertrophy and mitochondrial biogenesis. Thus, studies have shown blunted muscular training adaptations with excessive anti-oxidant intake due to ROS levels falling below normal physiological ranges. Bottom line: an even-keel, balanced approach to anti-oxidant intake through food and perhaps supplements may best keep your ROS levels optimal. So chill out a bit on that heavy supplement stack of vitamins C (ascorbic acid) and E, ฮฑ-lipoic acid, selenium, coenzyme Q10, etc. #kinesiology #exercisescience #sportsscience

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A common question regarding strength training programming is whether a higher training frequency (days/week) is more or less beneficial than lower frequencies in terms of maximal strength development. This debate is naturally complicated by the multitude of interactions with other training program variables such as training volume (total repetitions performed). A recent meta analysis by Grgic et al. (2018) indicated that training frequency does not impact strength development when total training volume is equated for. Thus on the basis of this analysis, one would hypothetically experience similar strength gains when training 3x per week vs. 6x per week as long as the training volume was equal between the two programs. Colquhoun et al. (2018) specifically tested this hypothesis in a study recently published in the Journal of Strength and Conditioning Research. As hypothesized, results showed similar strength gains between a 3x/week vs. a 6x/week program of equal total volume leading to the conclusion that training volume is indicative of strength development and not frequency by itself (DLs performed at 1x for 3x group and 2x for 6x group). Thus, from a practical perspective, strength athletes or practitioners have some flexibility as to how a prescribed training volume can be spread out across a training week or period without the fear of compromising the rate of strength development. It must be noted however that previous evidence indicates that when comparing lower frequency ranges (i.e. 1x vs. 3x per week), a higher frequency is more advantageous even when volume is equated (but not many train 1x per week anyway). Another important factor to emphasize is that the implications of these findings should be limited specifically to the development of maximal strength and not other strength attributes such as explosive strength/power or endurance simply because we just don't know yet. In other words, interpret within context. As for future research, the question of diminishing returns remains as it relates to training volume.

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#tbt "Fat burner" supplements are generally intended to stimulate fat oxidation through some chemically-induced manipulation of mechanisms that regulate this metabolic process. And yes, there is a decent level of empirical evidence that support this effect for a variety of supplemental substances, but what is most convoluting to this matter are the ways this evidence is being interpreted and communicated. For instance, an increase in energy expenditure or fat oxidation rate after subjects consume a fat burner supplement does not imply long term enhancement in body composition. Also, just because there is a statistically significant increase in fat oxidation following supplementation of a fat burner doesn't mean it is practically or clinically meaningful. In fact, when carefully examining data supporting an increase in fat oxidation after consuming a fat burner, the size of the effect is often times trivial to have any meaningful inferences. From a physiological perspective, the overall purpose of fuel oxidation is to take energy from fuel molecules like fat and release it in the form of heat and/or transfer it to an energy carrier molecule called ATP. Ultimately, the oxidation of fuels like fat is for the purpose of thermoregulation and/or meeting cellular energy needs. Therefore, fuel/fat oxidation is on a per needed basis. These fundamental factors of metabolic control cannot simply be overridden by a supplement (drugs are a whole nother story). Meaning, it is biologically inefficient to burn through fuel when the body doesn't need to. Physiology is not easily tricked.

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Myofascial release (MFR) therapies are often viewed as methods to physically & directly "loosen" myofascia or muscle through manually applied forces (thixotropy). However, this explanation remains insufficient especially in the context of short-term (single-session) release. Moreover, some manual therapies claim or are falsely understood to improve mobility & reduce myofasical pain through the break down of fascial scar tissue. However, prior evidence from sophisticated research methodologies indicates that the compressive or shear forces necessary to deform dense fascial tissue to the point of "breaking up" scar tissue are practically unobtainable through traditional manual therapies. This is not to say that these manual therapies are ineffective. People do indeed feel better and have restored function and mobility through both short- and long-term applications of therapies ranging from foam rolling to more aggressive forms like IASTM. It is rather the mechanisms of their efficacy that require better understanding and elucidation. Recent evidence suggest that short-term myofascial release as well as long-term changes resulting from manual therapies are largely attributable to the mechanical manipulation of sensory nerves and active contributions from the central nervous system. The myofascia is more than connective tissue. It is an integral component of muscular force production and it may be arguably the largest sensory organ in the human body as it is host to a variety of sensory nerves. A large portion of these sensory nerves innervate mechanoreceptors, and when stimulated through mechanical perturbation (as in MFR therapies), the central nervous system may respond in a manner that reduces muscle tone, relaxes contractile components of myofascia, and maybe increases blood flow. In others words, MFR therapies work through neural feedback loops. Various myofacial mechanoreceptors (Golgi organ, ruffini and pacini receptors, and interstitial receptors) are connected to specific sensory nerve types (Type I-IV) and each may be stimulated through specific applications of manual forces through a variety of MFR therapies. Stay tuned for more on other MFR mechanisms.

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We've all heard of blood flow restriction during exercise but what about before exercise? Ischemic Preconditioning or IPC has been used as a method to preemptively limit muscle damage during surgical procedures that is caused by repurfusion injury. Repurfusion injury occurs when blood supply returns to tissues (reperfusion) following a period of ischemia or lack of oxygen. IPC prior to tissue surgery has shown to minimize muscle damage by briefly exposing the muscle to brief cycles of ischemia and reperfusion. Since the underlying mechanisms and effects of repurfusion injury in muscle share similarities to exercise-induced muscle damage, it may be reasonable to suggest that IPC prior to high tension, strenuous exercise would minimize muscle damage and related symptoms (e.g. soreness, loss of contractility and performance, etc). In a recent 2017 study published in Medicine and Science of Sport and Exercise, researchers examined the effects of IPC on exercise induced muscle damage. In this study, one group underwent IPC via 3 cycles of arterial occlusion for 5 minutes of ischemia followed by 5 minutes without occlusion to allow reperfusion. The control group did not undergo IPC. After baseline testing for indirect markers of muscle damage, both groups performed eccentric overload exercise followed by repeat testing immediately, 2hrs, 24hrs, 48hrs, and 72hrs post-exercise. Results showed that IPC significantly reduced soreness, loss of muscle contractility, and biomarkers of muscle damage (plasma CK) when compared to the non-IPC control. These are some intriguing results that warrant further study of IPC's application in athletes. Thus, I have decided to do a follow up study in my lab! I must advise however, that IPC is not recommended until proper training on the procedures has been completed. Please note that IPC procedures are NOT the same as BFR training procedures in particular the pressures used.

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I know I know... Kre-Alkalyn is so 2014 but this study gives me an excuse to 1) provide some evidence for those contemplating the efficacy of buffered creatine vs. creatine monohydrate (CrM) and 2) introduce a giveaway of Dymatize Micronized Creatine Monohydrate (swipe left). Kre-Alkalyn made it's way into the sport supplement market around 2012 with the claim that their "pH corrected" creatine product is less susceptible to breakdown (to creatinine) during digestion and thus less dosage is required for the same bioavailability following a higher dose of standard CrM. Unfortunately this claim has not been well documented or supported in the scientific literature. In fact, it has been shown that there is greater creatinine levels following Kre-Alkalyn compared to similar and higher doses of CrM which opposes aforesaid claims. In this particular study, researchers examined and compared muscle creatine content following supplementation of low dose Kre-Alkalyn vs. higher dose Kre-Alkalyn vs. equated dose CrM. The findings show that CrM supplementation resulted in the greatest increase in intramuscular creatine content (almost 100% greater than Kre-Alkalyn of equal dose). These results a long with others suggest that Kre-Alkalyn does not confer any advantages over standard CrM in terms of raising muscle creatine content (which is the fundamental purpose of consuming creatine as a performance aid). Despite the paucity of supporting data, Kre-Alkalyn still exists in various supplement products. Of course there is always room for further scientific scrutiny such as examining responder vs. non-responder characteristics but at this point if creatine is what you're looking for, good ol' fashion CrM seems to suffice. In light of this topic, I am giving away two 1kilo bottles of micronized creatine fro. @dymatize! 3 winners will be selected. Swipe left for more details!

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In a fresh perspective on the exercise maxim, "use it or lose it", new research findings show a deeper interconnection between neurological health and muscle. New animal model research shows that loaded movement of muscle, particularly in the lower body, sends signals to the central nervous system that are vital for the regeneration of healthy neural cells and overall neurological vitality. In this study, hindlimb suspension, an experimental model of muscle disuse, was implemented to examine neurological effects of deprived movement/exercise and unloading of large lower body (i.e. hindlimb) muscles. After a period of 28 days of muscle unloading, researchers examined an area of the brain called the sub-ventricular zone, which in mammals has the critical role of maintaining neural cell health. Via cellular and molecular level analysis, results show that prolonged muscle disuse reduces the presence of proliferative brain cells and neural stem cell proliferation by 70%. Also, the regenerative capacity of nerve cells was severely limited when movement was restricted and large muscles were unloaded. This study provides fundamental clues as to why individuals who are unable to perform load bearing exercise, such as bed ridden individuals, patients of spinal cord injury and motor diseases, or severely obese individuals with limited mobility, often experience rapid decline of neurological health. This research may also partly explain the underpinnings of the relationship between sedentary lifestyles and neurological decline. One could say that exercise is also brain training.

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Dietary protein has shown to promote weight-loss efforts partly due its effects of enhanced post-meal satiety in comparison to carbohydrate or fat. To elucidate the mechanisms underlying this effect, several researchers have looked to the gut-endocrine system for answers since it is the source of potent hormone regulators of ingestive behaviors. For instance, peptide YY (PYY) is a gut hormone generally secreted in response to a meal to subsequently suppress appetite through the inhibition of Neuropeptide Y (NPY), a potent orexigenic (appetite stimulating) neurotransmitter. In this study, normal weight and obese human subjects demonstrated a greater release of PYY and more pronounced satiety following a high protein meal versus high carbohydrate or high fat meals. Interestingly, post-meal release of other apptetite regulators like leptin and GLP1 were not affected by macronutrient distribution (although other studies have shown greater GLP1 following protein intake). Thus, it appears that protein-mediated satiation is indeed mediated (at least in part for now) by gut hormone regulation of appetite, particularly via PYY. These findings, along with others, suggest that manipulating the release of endogenous satiety factors, such as PYY, through alteration of specific diet constituents could provide a rational strategy for weight loss or therapy for obesity. Also, I previously discussed evidence indicating greater basal PYY levels with higher intensity exercise training. Thus, when considering the practical applications of these findings collectively, higher intensity exercise and a high protein caloric restrictive diet may certianly be the optimum approach to weight loss. As I've emphasized before, the traditional focus of exercise and protein intake with respect to weight loss has been overly and fallaciously directed towards energy expenditure where in fact, much of the evidence demonstrates their benefits to be more so related to the control of energy intake.

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Although very similar in nature, the Hex Bar and Straight Bar deadlift variations should be considered, not as mutual alternatives, but as separate exercises. Due to altered joint angles from one DL variation to the other, muscle activation patterns are also changed. As in the study presented above, the hex bar DL produced approximately 21% greater quad (vastus lateralis) activation than the straight bar DL however 14% and 21% less hamstring (biceps femoris) and erector spinae activation, respectively. In terms of movement characteristics, subjects generated slightly greater force (+2%) and moderately greater power (+13%) and velocity (+10%) during the hex bar DL. Therefore, the hex bar variation may be of interest to those athletes focussed on training these strength attributes. That is not to say however that the straight bar DL should be neglected.

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Have you been lazy & lost all your gains or decided to take a break from the weights? Well a new study provides some initial data from molecular to whole muscle levels suggesting that you may be able to recover those gains & THEN SOME when you get back into training. We've all heard of a loosely defined concept of "muscle memory" & this new study published in Nature: Scientific Reports brings a fresh perspective on this topic. Epigenetics, as it relates to muscle hypertrophy, is the study of how modifications to gene expression (not the genetic code itself) in response to a continuous stimuli or stressor like training causes changes in the muscles' function, metabolism, regulation, etc. Over the years muscle physiologists have continuously built a muscle epigenetic profile that is associated with training-induced hypertrophy. In this study, researchers aimed to assess these muscle epigenetic responses and growth during an initial 7wks of hypertrophy training (loading), then during a subsequent 7wks of detraining (unloading), and finally during a subsequent 7wks of retraining (reloading). Results showed a 6.5% increase in lean mass with the initial training (loading) then a return to baseline levels after 7 wks of detraining (unloading). What is interesting was that during the subsequent 7wks of retraining (reloading), the muscular growth response was almost 100% greater than the initial training/loading period. Also, researchers showed increased expression and hypomethylation of key relevent genes following intitial loading which can explain in part the initial growth. These epigenetic responses were significantly enhanced (just like muscle growth) during reloading, indicating a genetic "memory" of earlier encounters of muscle hypertrophy (as in this case, during the initial 7-week loading). It is exciting to see these type of data and analyses adding to the growing body of exercise and muscle physiology research. Muscle remembers hypertrophy!

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Have you ever heard anyone say that you HAVE to get some protein or BCAAs in every 3 or so hours to stay "anabolic"? Or perhaps you yourself have given this advice to someone ๐Ÿ˜. First we need to get one thing straight. Anabolism simply describes a part of metabolism that is dedicated to building bigger molecules from smaller ones. So synthesizing triglycerides and glycogen are also anabolic processes; anabolism is not just about building muscle proteins. Now, this notion of muscle protein metabolism "staying anabolic" simply by way of frequent amino acid or protein consumption is enabled by past studies that show an acute increase in muscle/myofibrillar protein synthesis (MPS) upon intake or adminstration of amino acids, especially leucine. So many gym enthusiasts/bros immediately thought amino acids=ANABOLIC so as an overexaggerated interpretation of research findings, said people started to believe that MPS can stay elevated all day as long as amino acids or proteins are consumed frequently. Unfortunately, this goes against many basic principles of biochemistry and metabolism and has been debunked by a decent body of evidence such as my favorite from Bohr et al in 2001. Bottom line: you cannot sustain an anabolic state in muscle protein metabolism just by consuming amino acids all day. I think many have lost focus on the fundamental basis for dietary protein intake as it relates to muscle growth, which is to provide a sufficient pool of substrate (in this case amino acid building blocks) for proteins to be constructed and not just on the best strategy to stimulate MPS. Therefore consider your total daily protein needs as priority and then work on other factors like timing and type.

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