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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


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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".


Have you been lazy & lost all your gains? 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. One of my good friends and colleague @drandygalpin tweeted today about a novel study in muscle epigenetics on a phenomenon referred to as muscle "epi-memory" & I had to read it & of course do an infographic on it. 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 like resistance training causes changes in the muscles' function & physical appearance/size/mass. 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 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!


This post stems from an experience after a talk I gave at a research symposium. During the Q&A, a gentleman asked me a question, "I heard plant based diets boost metabolism. Do you know by how much?". I replied with two questions, "1. What part of the human metabolism are you referring to, and 2. In what manner would you like me to quantify "boost"?". Then an awkward period of silence. The most widespread misnomers used in the fitness and nutrition community are associated with the term "metabolism". Most times "metabolism" is used interchangeably with caloric expenditure which are not one in the same. Other times it is used as a scapegoat explanation to one's propensity to gain or lose weight, e.g. "I gain weight easily because of slow metabolism". Here are common examples and my responses: 🤚Broscience: "I gain weight easily because I have naturally slow metabolism" 👉 1. How do you know? Did you measure some facet of your metabolism that would explain your weight gain? Metabolism can't be "slow" or "fast" considering what it actually is. If you don't have a diagnosed metabolic dysfunction, then your weight gain is likely attributable to comsuming beyond your needs. 🤚Broscience: "Detox diets will shed the weight and boost your metabolism" 👉Yes, detox diets will likely result in weight-loss. This usually happens when you're not consuming nutrients and calories. However, it will, on the contrary, promote a suppression of basal metabolic rate commensurate to the degree of weight-loss. 🤚Broscience: "Thermogenic fat burn supplements boost metabolism" 👉Thermogenic supplements, if they are in fact thermogenic, may increase energy expenditure, not metabolism, for a brief time but likely failing to manifest in any significant changes to body fat. 🤚Broscience: "To lose weight, eat frequent meals throughout the day to keep your metabolism high." 👉Eating will temporarily increase energy expenditure but this will not at all explain any observed weight loss. You can Broscience your way through until someone asks you to elaborate. Stay tuned for "Weight loss is a matter of mass, not just caloric expenditure" post.


I am reposting this every time someone tells me lactic acid causes DOMS and myofascial pain. ---------------- Although this is a very simplistic breakdown of the mechanisms underlying DOMS, its intention is to contend against unsupported widespread notions that the formation and localized accumulation of lactate is the culprit when it comes to muscle pain or soreness following an unaccustomed bout of exercise or activity. Among the multiple explanations, we must understand that lactate is not a stress inducing molecule. It is actually a very useable energy substrate or "fuel" especially for oxidative cells like type I skeletal muscle fibers and myocardial cells. In fact 75% of the lactate produced during exercise is used in this manner while the remaining may be used to reform glucose (information largely based on the works of Dr. George Brooks of UC Berkeley). Take home message: 1. There is no sense in designing or applying therapeutic modalities with the intent of removing lactate, 2. Acute inflammation and the associated soreness is a part of the tissue healing process. It does not need to be remedied (unless of course you are an in-season athlete and can't afford to be limited by 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, and 3. The absence of soreness does not mean that muscle tissue has been repaired, so modalities that mitigate acute inflammation and soreness are not really recovery aids.


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. IPC involves arterial occlusion while BFR venous occlusion. Big difference!


The various forms of whey protein supplements have been under scientific scrutiny for some time now resulting in a considerable body of research that have examined and compared variables from digestion and absorption rates to muscle protein synthesis. Recently, a product called Native Whey was introduced to the dietary supplement market and has garnered increasing attention by fitness enthusiasts and athletes mainly due it's relatively higher leucine content compared to other supplemental forms or food sources of whey protein. Because of the widely known anabolic effects of leucine on muscle protein metabolism (although largely misunderstood), Native Whey has comparatively been considered a higher quality and more optimum protein supplement as it relates to supporting training-induced muscle growth. However, despite these purported effects, the scientific literature concerning Native Whey is at the moment very limited. Of the few studies, a recent paper by Hamarsland et al. published in JISSN provides some initial insight as to the effects of Native Whey intake post-resistance exercise on muscle protein synthesis (MPS). Following baseline testing and a resistance exercise bout, subjects consumed Native Whey, Whey Concentrate, or Milk (crossover design) and MPS was measured up to 5 hours post exercise. Native Whey raised plasma leucine content 40% greater than whey concentrate. However, despite these discrepancies in plasma leucine, the rise in post-exercise MPS was similar between the two whey protein treatments suggesting that both whey products produce comparable anabolic effects in muscle. Key limitations of this study included a lack of measurement for protein breakdown to deduce total protein balance and of course the limited translation of acute effects to long term outcomes in lean tissue. Regardless, further investigating the effects of Native Whey and other forms of whey supplementation may be worthwhile since whey protein in general is here to stay.


More often than not body fat has been viewed as harmful to human health when in fact it is rather HIGH AMOUNTS of body fat that is the culprit. This common mindset has enabled a negative perception of body fat in that it is a useless organ people just want to get "rid of". On the contrary, however, body fat or adipose has an important role in whole-body metabolism; in fact, it can be beneficial to overall energy expenditure, lipid and glucose homeostasis, and weight-control... it just depends on what kind of adipose we're dealing with. Adipose tissue comprises of three types of fat cells, white, beige, and brown, each with distinct physical and metabolic characteristics. Beige and brown fat cells are more thermogenic, smaller, and conducive to whole-body energy expenditure compared to the white fat cells which are prevalent in obese individuals. Many of the benefits of chronic exercise in general metabolism are commonly attributed to positive metabolic adaptations in muscle while adipose is largely ignored due its negative reputation. Research, however, has shown that chronic exercise also promotes positive metabolic adaptations in fat cells which in part is stimulated by chemicals derived from active muscles during exercise. This effect is referred to as "browning" (or beiging) of white fat cells which results in smaller and more thermogenic beige fat cells. These adaptations in adipose promote improved whole-body energy expenditure, lipid and glucose homeostasis, and control of body fat mass. Overall, chronic exercise has a positive impact on multiple organs beyond muscle, including those with a bad reputation and should be incorporated especially during weight-loss endeavors to promote long-term success.