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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


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As Part 2 of my post on 1/8, here we have more results from our recent paper published in Clinical Nutrition. As I detailed in the earlier post, periodized resistance training during 12 weeks of severe caloric restirction in obese bariatric patients dramatically improved weight loss quality through the preservation of lean mass while blunting the suppression of resting metabolic rate. In the same study we also examined muscle function and strength through isokinetic and isometric testing and 1 rep max tests of the upper and lower body. Our subjects were all sedentary at baseline. The control group, who were only given general exercise guidelines archetype of current clinical recommendations in the bariatric setting and represented by the blue bars, exhibited a significant decline in muscular force (torque) production capacity as well as max strength relative to total body and lean mass. This means that general, non-specific, non-systematic, exercise recommendations such as "30 minutes of exercise per day" have little added benefits for obese individuals undergoing these dietary treatments in the context of body composition and muscle function. Unfortunately these types of recommendations are the extent of the exercise prescription in most medical obesity treatment programs today. Our study hopes to change that as data shows the significance of a structured periodized resistance training program in dietary weight loss treatments as it relates to enhancing the quality of weight loss, preserving muscle, slowing down drop in resting metabolic rate, and totally reversing the decline of muscle function and strength. Bottom line, resistance training is a must in any structured dietary weight loss program @ormsbeem


A frequent question I receive from students is regarding the efficacy by which exercising under an overnight fasted state facilitates weight/fat loss. In other words does "fasted cardio" = greater weight loss? This is not so much an obscure inquiry considering the general logic behind this theory. That is, if one is exercising under a fasted state, carbohydrate fuel sources may be limited thereby, increasing dependence on fat/lipid fuel sources. Makes sense to some degree but I wish metabolism was just that simple. However there is in fact a decent body of research that suggests an acute augmentation in fat oxidation rate when exercising following an overnight fast. But the question remains whether these acute effects actually translate to overall weight-loss. In a recent meta-analysis of a relatively small body of research investigating this "fasted cardio" theory, subjects who performed 4-6 weeks of steady state exercise 4-6x per week under a fasted state failed to demonstrate any alterations to body mass when compared to training with exercise in a fed state. The key aspect of these culminating findings is that total daily caloric intake was controlled across the two treatment groups. This suggests that regardless of whether one exercises fasted or fed, the ultimate determinant to weight loss over time is indeed caloric intake, more specifically caloric deficit. But there is certainly more to uncover with "fasted cardio" as it relates to long term adaptations in whole body and muscle metabolism. But at least for now this meta analysis provides some initial insight into the effectiveness of fasted exercise training WITHIN THE CONTEXT of weight loss. @bradschoenfeldphd


It has become more apparent that exercise practitioners and enthusiasts experiment with and incorporate various methods of regulating training prescriptions and progression/periodization, primarily for the sake of practicality. With respect to resistance training programming, the traditional method of load assignment is by using a percentage of a pre-determined 1 rep max (1RM). However, although the use of %1RM may be of benefit for the purpose of objectivity, this method indeed accompanies a few issues, such as (but not limited to), 1) 1RM testing specifically for load determination may be generally impractical and inappropriate for certain exercises and 2) it enables one to inadvertently neglect the qualitative aspects of the load (the rep range and perceived "effort" for a certain %1RM varies among individuals, muscle groups, exercises, etc). The work of my good friend Mike Zourdos and Eric Helms @helms3dmj introduces an alternate method of load assignment for resistance training based on a 'reps-in-reserve' rating of perceived exertion (RPE) scale as presented in the second slide (swipe left). In a recent study by Helms et al. (2018), data indicated that a load prescription based on desired RPE in an 8-week periodized bench press and squat training program was just as effective or possibly slightly more effective than %1RM-based loading in strength and muscle size development. What I felt was most interesting was that the average weekly reported RPE was generally greater with RPE-based loading compared to %1RM-based loading lending to the possibility that loads based on %1RM elicit lower perceived efforts for a given sub-failure rep range. Moreover, the loads implemented with the RPE-based loading method were in fact a greater percentage of the subjects' 1RM than the loads applied via the %1RM-based loading method. Therefore, by using the RPE method, a greater relative load for a given rep range can be achieved, thus maximizing training variables such as volume-load. This study demonstrates the efficacy of RPE-based loading as a practical alternative to the traditional %1RM-based loading method. Looking forward to more data on this!


The physiological adaptation to conditioning is multifactorial and is not solely due to an increase in aerobic capacity and/or anaerobic threshold (as often measured by VO2max and lactate or ventilatory threshold, respectively). Specifically, performance enhancements resulting from a conditioning program is also attributable to improved resistance to the muscle-inhibiting effects of acute/temporary metabolic acidosis, a major underlying contributor to fatigue during post-anaerobic threshold, high to max effort exercise. One of the mechanisms by which one may become more fatigue resistant is through an increase in muscle buffering capacity via muscle carnosine, a known intracellular buffer. As demonstrated by Salles Painelli et al. 2018, 12 weeks of high intensity interval training resulted in an average 36% boost in muscle carnosine levels and a significant improvement in muscle buffering capacity when compared to control (no training). The more novel aspect of this study however is that these outcomes were not confounded by dietary beta-alanine consumption, which has been a common limitation in prior studies. Beta-alanine is a pre-cursor to carnosine, and its supplementation has shown to raise muscle carnosine levels. The next steps would be to study various modes of conditioning to see whether these effects are only limited to HIIT (i.e. high intensity steady state, sprint interval training?) #cpphprl


Over the recent years BFR has gained widespread use in both fitness & clinical applications due to the growing body of evidence supporting it's efficacy in facilitating stress-induced adaptations in muscle. Conceptually, proximal limb (upper arm or upper thigh) BFR generally allows one to undergo similar metabolic stress to limb skeletal muscles w/ lower mechanical loading/intensities compared to higher mechanical loading/intensities w/ out BFR. Prior research, accordingly, have shown similar growth of limb muscles w/ lower intensities + BFR compared to higher intensities of = volume w/ out BFR. This may be due to the compensation of the reduced mechanical stress from lower loads w/ higher metabolic stress due to BFR. The two overarching factors that stimulate the processes of muscle growth is metabolic & mechanical (tension) stress. In healthy muscles, this generally means higher loading (mechanical stress) w/ higher volume (metabolic stress). But, for vulnerable muscles, like during soft tissue rehab post-injury/op situations, the mechanical stress & thereby loading must be moderated due to the risk of reinjury. This in turn may limit metabolic stress which altogether limits the rate of adaptation & rehab. Thus, BFR may be advantageous in these scenarios since it allows vulnerable muscles to undergo higher metabolic stresses while using loads that lessen mechanical stress. This has been shown to be beneficial for limb muscles specifically, but less is known on the effects of limb BFR on adaptations in related trunk muscles (pec major) during compound training (bench press). Obviously there are no practical ways to apply BFR directly to trunk muscles nor is it recommended. This study by Yasuda et al. examined how upper arm BFR during lower intensity BP training affects trunk muscle adaptations (i.e pec major). The main take away from this study was that BFR of the upper limb with lower intensity compound training promotes a less proportionate growth response between triceps & pec muscles than higher intensity w/ out BFR. Thus, the application of BFR for trunk muscle adaptation w/ lower load compound training is still questionable. Typo! 2011 not 2018 paper.


Caffeine, primarily in anhydrous form, is one of the most prevalent substances used in exercise and sport due to its acute performance enhancing effects as supported by meta-analysis data. Research suggests that a median dose of 6mg/kg of body mass improves endurance and high intensity exercise performance by an average of 2% up to 4%. There has also been a long-standing paradigm that habitual caffeine intake influences the performance enhancing efficacy of caffeine supplementation. Specifically, it is a common assertion that those with high consumption of caffeine would be "desensitized" to its effects, at least in the context of exercise performance. In this 2017 study, results showed a significant improvement in cycling time trial performance in trained cyclists following a caffeine dose of 6mg/kg of body mass corroborating a history of prior studies. Interestingly, low, moderate, and high caffeine consumers showed similar absolute and relative improvements in cycling time-trial performance following acute supplementation of caffeine. Performance effects of acute caffeine were not influenced by the level of habitual caffeine consumption, suggesting that high habitual caffeine intake does not negate the benefits of acute caffeine supplementation. Please keep in mind that this information is NOT a recommendation of what your daily caffeine consumption should be. It is simply data indicating that habitual caffeine intake does not appear to affect its ergongenicity. Please consider within context because I know there will be readers who will interpret this as a recommendation that they consume 6mg per BW every day. #cpphprl


Over some years now, research findings have continuously implicated chronic low-grade systemic inflammation or meta inflammation as a major link between obesity and the multitude of associated comorbidities, such as type II diabetes and cardiovascular diseases to name a few. Much of the earlier work in obesity research showed that inflammation and dysfunction of adipose was the primaty contributor to systemic meta inflammation during obesity. However, it appears that gut dysfunction brought upon by obesigenic lifestyles or the state of obesity itself is also a major contributor to this damaging inflammatory state. Increased gut permeability and changes to the gut microbiota allow for increased infiltration of unwanted gut "materials" such as endotoxins called LPS. Increased LPS infiltration in turn increases the risk for endotoxemia which is a state conducive to meta inflammation. We clearly see in the scientific literature the damaging effects chronic obesity, especially to something that is so largely impactful to our overall metabolic health, the gut.


Part 2 of 4/9 post. Anaerobic training modes are commonly and falsely viewed to improve one's conditioning based on a fallacious concept of "anaerobic" adaptation as depicted in the bottom figure. This is the principle of specificity misunderstood and misapplied likely due to a false dichotomous view of exercise bioenergetics and metabolic training, i.e. anaerobic training=anaerobic fitness and aerobic training=aerobic fitness. Anaerobic ATP production only exists because there are situations like during max physical effort in which the ATP demand of working muscles exceeds the rate at which aerobic metabolism can generate it. Anaerobic metabolism is synonymous with fatigue and it is a state of metabolic stress. Increasing anaerobic contributions to ATP demand (expanding the red area under the curve) would in fact promote fatigue as opposed to fatigue resistance. This happens with detraining NOT training. Despite the terminology, "anaerobic" training modes like high to max intensity interval training promote conditioning through AEROBIC adaptations which involve integrative changes in both the cardiovascular and skeletal muscle systems. The key principles to conditioning at least from a bioenergetic standpoint is to 1. improve the capacity to produce ATP aerobically at higher work loads (increase white area under curve), 2. reduce the reliance on anaerobic ATP production (minimize red area under curve), and 3. better contend with the fatigue-inducing environment of post-anaerobic threshold conditions (e.g. increased pH buffering and fatigue resistance). Even till this day, we see many exercise science instructors and practitioners preach the false dichotomy of exercise bioenergetics. It is important not to forget the fundamentals of human metabolism and biochemistry. Bottom line... conditioning programs should not be based on the false notion that one can train any particular energy system in isolation. It is all aerobic conditioning. #cpphprl


A fairly novel application of blood flow restriction (BFR) that has been recently explored in exercise science is during post-exercise recovery periods or, in the case of interval training, during recovery intervals. Two studies have explored the potential physiological and performance benefits of a sprint interval training (SIT) program with BFR either applied post exercise or during the recovery intervals between each sprint. In the earlier study, Taylor et al (2016) demonstrated a 4.5% improvement in VO2max following 4 weeks of SIT with post-exercise BFR while SIT alone showed no significant change. Authors also demonstrated evidence of improved angiogenic signaling which could have explained the observed enhancement of aerobic capacity in BFR-treated subjects. However, the question remained on how these effects translate to cycling performance which is highly predicated on critical power (among other power output variables). Thus in a follow up study as presented here, researchers found similar improvements in VO2max as their prior study, but these effects were not accompanied by improvements in any power output variable, including critical power. However, the enhancement of VO2max in both studies and improved markers of angiogenesis and possibly mitochondrial biogenesis in their earlier study are outcomes of interest as these effects may translate to improved performance capacities with the "right" conditions. For instance, a 4 week training period may have induced positive physiological adaptations conducive to endurance performance; however, perhaps due to the short training period, these adaptations were not robust enough to manifest in any observable performance enhancement. Also, the SIT protocol used in these studies may require modifications as it failed to induce any positive physiological or performance adaptations without the BFR intervention. Further research would be required of course but in the meantime it is interesting to see alternate applications of BFR in sport and exercise. #cpphprl


👉The traditional strength training intensity prescription spectrum, as shown above, encourages a false perspective in that muscle hypertrophy is unobtainable with higher (>85%) or lower (<67%) relative loads and is only achieved within a narrow range of intensities. Muscle hypertrophy is a result of a continuous balance of mechanical and metabolic stress which can be achieved through a wide range of intensities even as low as 30% max and as high as 90% max. Intensity ranges are more relevant to the development of specific strength attributes (muscle hypertrophy is not a strength attribute). 👉There are multiple variables outside of intensity that can be manipulated to facilitate hypertrophic adaptations. Volume has shown to be a key factor in optimizing progress towards muscle growth via manipulation of sets, muscle specific exercise selection, weekly frequency, and/or time under tension. For example, a 2 week periodization of intensities outside traditional zones ranging between 85 to 90% 1RM (~6RM to 3RM) with higher sets and muscle specific exercises would be appropriate within a hypertrophy program. At the same time a periodization of intensities ranging from 40 to 60% 1RM with less sets (since higher reps), higher frequency, and a few eccentric overloaded lifts would also be appropriate. 👉As an important note, we have to remember that not everybody responds similarly to any single program (just like we see in research). I've had many clients who responded favorably to lower intensity ranges while others found optimum progress with higher intensity ranges in the context of growth. It really just depends on the individual. Therefore, in the context of muscle growth, we should not be limited by an intensity range and it is ok to periodize intensities across a wide, non-traditional range. #cpphprl


Here is some evidence from our lab that counters the notion that preserving or perhaps even improving lean mass during caloric restriction is not possible. We put this to the test under one of the most severe caloric restriction conditions. Our paper was recently accepted for publication in Clinical Nutrition adding onto the growing body of research focussed on practical exercise and nutritional strategies to optimize weight loss quality during caloric deficit (a concept of maximizing fat loss while preserving or improving lean mass). In our study, obese patients at our clinical site underwent 12 weeks of a formulated Very Low Calorie Diet (VLCD) with supplemental protein support providing about 1000kcals per day. Although a fixed caloric intake treatment presents a potential study limitation, subjects were pair matched by caloric deficit and placed in separate groups. One group concurrently performed a structured, supervised periodized resistance training program while the control group was assigned the typical exercise recommendations associated with these VLCD treatment programs which is a pedometer based walking program (basically there is currently no real exercise Rx for these VLCD treated patients). Despite undergoing severe caloric restriction, resistance trained subjects experienced drastically superior weight loss quality through the preservation of lean mass with no differences in fat loss between groups. Only 4% of the total weight loss was due to a reduction in lean mass while 96% was due to fat loss. This can be viewed as "high quality" weight loss when compared to the control who lost about a quarter of their weight loss from reduced lean mass. Resting metabolic rate was also better maintained in those undergoing resistance training which may have some important long term implications. High protein and resistance training is a MUST when restricting calories no matter how severe. It works! Full text available on my Researchgate profile. Resistance Training During A 12-Week Protein Supplemented VLCD Treatment Enhances Weight-Loss Outcomes in Obese Patients


There is no question that sleep research has gained increasing attention over the recent years due to the emerging evidence linking inadequate sleep to poor health and fitness outcomes. On the other hand, adequate sleep has shown to improve metabolic and cognitive health while reducing oxidative stress and inflammation (of course in combination with active and healthy lifestyles). A fairly recent body of sleep research has focused on the effects of sleep restriction on weight loss during caloric restriction. In this 2018 study, researchers investigated the effects of sleep restriction on body composition changes over 8 weeks of caloric restriction. In the sleep restricted group, subjects had an avg. decrease in sleep by 169 min per week. When compared to the unrestricted sleep group, total absolute weight loss was similar. However, the composition and therefore quality of the weight loss significantly differed between groups. The sleep restricted subjects on avg. lost approximately 39% of their total weight loss as lean mass and 58% as fat mass. When sleep was not restricted, weight loss was only 17% attributable to lean mass loss while fat loss accounted for 83%. Interestingly, the sleep restricted group demonstrated a decrease in fasting leptin which is a hormone (adipokine) that suppresses hunger (anorexigenic effect). These findings along with others over the years strongly suggest that sleep is an integral component of weight loss endeavors along with dietary and exercise modifications. I know it's hard at times but get your 8 hours in. It's a game changer. #cpphprl


The optimum daily protein intake to support muscle growth with resistance training (RT) has been a topic of debate for quite some time now. However, it is safe to say that the scientific literature has converged on a consensus that the U.S. RDA of 0.8g/kg bodyweight/day is not inadequate per se, but rather suboptimal for muscle growth during RT. A recent meta analysis on this very research inquiry examined 42 study groups from multiple published investigations who underwent a resistance training program with some prescribed experimental dosage of dietary protein relative to bodyweight. Results indicated that a variable degree of growth in lean mass was observed with protein dosages between 1.0 to 2.2g/kg/day with a breaking point around 1.6g/kg/day. When consuming less than 1.6g/kg/day at baseline, protein supplementation appeared to augment RT-induced lean mass growth up to a daily intake of 1.6g/kg. Among the studies examined, the average intake at baseline was about 1.4g/kg/day which is 75% higher than the RDA, and an average supplementation of about 35g of protein per day still boosted gains in lean mass with RT. This analysis demonstrates that protein supplementstion, at least when daily intake is less than 1.6g/kg, is advantageous to optimize lean mass growth during RT. Sufficient protein intake is especially critical during energy deficit and in older adults. Indeed the arguably most critical factor in lean mass growth is training program efficacy which makes the determination of optimal protein intake difficult to ascertain. However, from a practical standpoint, consuming near 1.6g/kg/day would likely compliment and support your training program for muscle growth.


A widely used method for muscular power development (i.e. "explosive" strength) is centered around maximizing rep by rep velocity during resistance training. This velocity-based training method is predicated on the notion as well as some empirical evidence that power (as a function of force x velocity) may be optimally improved when each training rep is performed w/ or close to peak velocity. During a traditional set, velocity may decrease w/ continuous reps due to acute fatigue effects & thus the later reps may likely be performed w/ slow velocities. Technologies that assess barbell velocity like linear position transducers or accelerometer devices can be used to provide real-time feedback on velocity during a set allowing an athlete to stop the set whenever velocity falls under a predetermined velocity threshold (usually ~80% of peak velocity). Another practical way of performing velocity-based training is by implementing cluster sets. For example, instead of performing 6 sets of 6 continuous reps, one may split each set into 3 sub-sets of 2 reps w/ about 30 sec rest in between each sub-set. This way each rep may be performed with greater velocity. In a 2018 study published in JSCR training w/ cluster sets allowed for greater rep by rep velocity than traditional sets, especially the last 3 reps of each set (top right figure). With traditional sets, barbell velocity dropped w/ each continuous rep during a set as expected due to acute fatigue effects. However, w/ cluster sets, each rep was performed close to peak velocity since each set was divided into 3 sub-sets of 2 reps. As for the overall performance adaptations, and when total work was matched between treatment groups, power-centric training incorporating a cluster set configuration yielded superior development of muscular power than traditional sets mainly due to a superior development of velocity (force development similar between groups) and increased neural drive. Power development was positively and strongly correlated to rep by rep velocity production during training (greater rep by rep velocity, greater power development).


Exercise is Medicine Series 👉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. 👉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. 👉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. 👍🏼


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.


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.


"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.