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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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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 😁. 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.


The efficacy by which restrictive breathing masks (aka Training Masks) simulate altitude training stress and facilitate aerobic conditioning remains yet to be supported by the scientific literature. Most studies have examined the effects of the training mask under endurance training paradigms which again have yielded no evidence of benefits. In a very recent study published in the Journal of Strength and Conditioning Research, the training mask was put to the test on resistance training performance. Subjects were tested for total reps during a bout of lower body resistance exercise with and without the training mask in a cross over design study. Results showed a significant decline in total reps achieved during the squat and leg press, increase in percieved exertion, and no substantial hypoxic environment with the use of the training mask. When considering the long term implications, using the training mask may limit overall training volume which in turn could impede resistance training adaptations. Bottom line: if deciding to use the training mask, it should be strictly used as a conditioning tool despite the lack of supporting evidence. Some do however argue that the training mask improves respiratory muscle endurance which may afford some benefits to performance but I would bet on these effects to be trivial.


High intensity aerobic training (HIT) using high intensity steady state to interval exercise has long been considered advantageous to weight loss efforts compared to lower intensity training mainly due to a purported "after burn" or EPOC effect. However, in short, the body of scientific literature simply does not support this notion. In fact, data shows this after burn effect to be trivial at best and should not be considered the underlying tenet of utilizing HIT to facilitate weight loss efforts. With deeper scientific scrutiny, it appears the benefits of HIT in the context of weight loss may not be so much explained by it's effects on caloric expenditure but rather on caloric intake. For instance, recent studies have shown long term HIT (high intensity steady state or interval training) to reduce ad libitum (volitional) caloric intake. In Prado et al. (2015), subjects consumed approximately 30% lesser calories per day following 12 weeks of high intensity aerobic training (at ventilatory threshold intensity) while low intensity training of matched caloric expenditure had no effect on avg. daily caloric intake. Researchers looked to hormonal appetite regulators to explain these findings and found a significant boost in circulating Peptide YY (PYY) following 12 weeks of HIT. PYY is a gut hormone that suppresses appetite (anorexigenic hormone) through the inhibition of Neuropeptide Y, an appetite stimulating neurotransmitter. The gut is a major player in the regulation of metabolism and energy homeostasis and more evidence has emerged supporting the role of exercise in the modulation of gut hormones/signals. At this point, we must indeed consider the role and benefits of exercise in weight loss beyond just burning calories.


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.


In honor of wrapping up our recent exogenous ketone study in my lab this week, today's post is on a new investigation from a lab highly productive in exogenous ketone research. Ketone ester and salt supplements have been a hot topic in both the performance and health nutrition industries as of late due to recent evidence demonstrating it's effects as a reliable fuel and energy provision for muscle and the brain. It has also shown some degree of efficacy in promoting endurance performance and preserving muscle glycogen (key muscle fuel source) during exercise and even facilitating muscle glycogen replenishment when combined with simple carbohydrates during recovery. In this 2018 study published in Obesity, researchers administered either a ketone ester drink (🔺G) or a dextrose (glucose) drink to subjects after an 8 hour fast. Both drinks were matched for calories and even taste (included additives to the dextrose to match the ketone's bitterness). Hunger and various hormonal appetite regulators were measured each subsequent hour up to 4 hours. Overall, the results showed that subjects following consumption of the ketone drink demonstrated significantly less hunger from 2-4 hrs post-drink comapred to the dextrose drink. They also reported signficantly lower desire to eat and greater feeling of fullness following the ketone drink. These effects of exogenous ketones may have been mediated by lowered ghrelin secretion post-feeding compared to dextrose. Ghrelin is a key orexigenic gut hormone that stimulates hunger through a subsequent release of the neurotransmitter NPY. Now this is not to say that exogenous ketones are the next best weight loss supplement (there is no such thing) but this provides some interesting initial insight as to the role of this "alternative" nutrient in the regulation of whole body metabolism and energy homeostasis. #ketones #ketogenic #nutrition #muscle #abs #gymlife #shredded #instafit #fitnessmodel #gains #physique #aesthetics #strong #cardio #fitnessaddict #fitnessmotivation #bodybuilder #body #exercise #ripped #strength #fitspiration #muscles #flex #beastmode #squat #instafitness #trainhard #lift #ifbb


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.


A classic debate in training programming is whether a higher training frequency (days/week) is more or less beneficial than lower frequencies with regards to muscular adaptations like strength development or muscle growth. However, this debate is naturally complicated by the multitude of interactions with other training program variables such as training volume (total reps x load). For instance, a common assertion is that a higher training frequency yields greater strength gains. And yes, evidence does support this contention as suggested by Grgic et al. in a recent meta analysis. However, with some critical thinking, one may argue that it is not so much the frequency that explains this effect on strength development, but rather the fact that there is simply a greater training volume with increased frequency. The same meta-analysis put this into consideration and found that when weekly training volume was equated/controlled for, frequency demonstrated no effect on the degree of strength development. These findings suggest that the impact of training frequency on strength gains are actually driven by training volume and not just simply frequency itself. From a practical standpoint, this means one may experience a greater degree of strength development with higher frequencies as long as volume is not compromised. In the same context, lower frequencies may yield similar results as long as strategies are implemented to ensure adequate volume is performed. Indeed, the argument regarding frequency is further complicated by other variables like intensity, recovery time, recovery rate, training mode, strength-specific goals, etc, but for now this meta-analysis provides a great perspective on the volume-frequency interaction. @bradschoenfeldphd


Endogenous Nitric Oxide (NO) synthesis has been a focus of attention in the world of sports nutrition and dietary performance supplements for quite some time now. Initially, the notion was that NO synthesis may be increased by way of supplementing its known precursor L-arginine (and L-citrulline) and in so doing muscle blood flow distribution would be enhanced during exercise via NO-induced vasodilation. However, both the efficacy of supplemental arginine and the purported boost in muscle blood flow have been decently refuted, especially by human model studies. This is not to say NO has no relevance to performance but rather an arginine-to-NO-to-enhanced performance connection is unsubstantiated. Recently, another pathway of NO synthesis has been implicated in human performance with a growing body of supporting evidence. Inorganic dietary nitrate via nitrate salt or beetroot juice supplementation or through food (leafy greens) has shown to boost NO levels and performance even with relatively short term supplementation. Nitrate is reduced to nitrite in the body (particularly by salivary bacteria) which is then converted to NO, especially during hypoxic/low tissue oxygen conditions (like during intense exercise). Adding to the evidence published by my lab, Nyakariyu et al. (2017) showed that a 6-day beetroot juice supplementation increased plasma and salivary nitrate and nitrite levels and improved performance in 32 male soccer players when compared to a nitrate-depleted beetroot juice supplement. Nitrate supplementation has shown to reduce the oxygen and thereby ATP and energy costs of exercise, shifting muscle energy metabolism towards improved aerobic efficiency. Others have suggested that nitrate supplementation (likely via NO boosting) promotes oxygen delivery to muscle, especially to type II (low oxidative) fibers that are more susceptible to hypoxic conditions and fatigue. However, this nitrate-induced blood flow enhancement has yet to be substantiated by in vivo human studies. So far, nitrate supplementation especially via beetroot juice has shown promise as a part of a performance nutrition regimen.


It is commonplace for one to attribute obesity or unhealthy weight gain to a "slow metabolism", i.e. low resting metabolic rate (RMR) or even the other way around in that obesity causes a dramatic slowing of one's metabolism. We hear it all the time. These false notions have largely enabled, at least in my opinion, the massive and, unfortunately, growing presence of obscure proprietary weight-loss programs that are claimed to "boost" one's metabolism or RMR where in fact the way one boosts their RMR is by simply gaining weight. I've always said that a "metabolism boosting weight loss program" is one of the biggest oxymorons in the industry. A change in RMR (minimum energy demand and therefore expenditure) does not happen overnight. It is a long term adaptation to a continuous stress that challenges overall energy homeostasis/balance. Specifically, a caloric surplus such as during overnutrition, stimulates a positive energy balance in which the energy/caloric input from excessive nutrient/fuel intake exceeds energy that the body needs and therefore expends. Like most biological organisms, when there are extra energy-containing fuel resources, the body likes to hold onto it. For humans, we like to hold onto it in the form of energy-dense fat molecules which are largely stored in adipose tissue. Over time, the response will be increased body fat and bodymass; this is not the adaptation however. The adaptation to prolonged positive energy balance is an increase in resting metabolic rate or simply, a "boost in metabolism". This adaptive response is simply to re-establish energy balance. If we did not have this adaptability, we would just simply continue to gain weight. Upon adaptation, body mass stabilizes because there is no longer an energy imbalance. Bottom line, obese individuals have a comparatively high metabolic rate and therefore have a large propensity for weight-loss so never buy into any type of weight loss program that is said to boost metabolism.


"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.


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. I, however, do believe that strategies like fasted cardio to slightly boost fat utilization during exercise is more relevant and practically effective in those individuals of already healthy body weight/composition who perhaps want to shed a couple lbs. But 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.


Cold water immersion (CWI) (11-15°C) therapy has been extensively utilized post-workout in efforts to facilitate muscle recovery between sessions or competition. Although a small number of prior evidence supports its efficacy in acutely mitigating soreness (possibly through an anti-inflammatory effect) & restoring performance capacities following strenuous exercise, there is still large debate surrounding its merit in long term training regimens. Roberts et al (2014) provides fresh insight into the effects of CWI on functional, morphological, & molecular adaptations in muscle after long term resistance training. Their key findings were that post-workout CWI in comparison to active rest 1) suppressed satellite cell activity & anabolic signaling in response to a single training bout & 2) attenuated long term improvements in muscle mass & strength. Researchers partly attributed the latter long term effect to the former short term effects although there is likely more to the story. These findings contribute to an emerging theme that CWI & other strategies (e.g. NSAIDs and anti-oxidant supplements) that are intended to mitigate soreness & accelerate "recovery" may actually be counterproductive to muscle adaptation to training. My assertion (along with others) is that modalities w/ anti-inflammatory properties may effectively minimize soreness (DOMS) by inhibiting mechanisms that are also involved in the process of tissue healing (actual recovery) & adaptation. In other words, many of these modalities promote the perception of recovery as opposed to facilitating actual recovery (tissue healing). This in turn would likely blunt the adaptive process. I'm not at all saying CWI is worthless but it (along w/ other modalities) has its time & place. For instance, during the competition phase of an athlete's season when adaptation is not the focus but rather maintainence of performance capacities is of priority, CWI may be of value especially w/ the limited timeframe between practices & competition for tissue healing. But for off-season prepatory phase athletes & especially recreational lifters, post-workout CWI may lack justification and merit.


The ergogenic properties of caffeine have been well documented in the scientific literature and thus has been a staple of pre-workout supplementation for as long as we can remember. Even with recent evidence of genetic predeterminants and habituation factors that differentiate responders to non-responders, caffeine is arguably the most widely trusted and utilized acute performance enhancer in its class. When considering the existing literature, most research have focussed on pre-exercise caffeine applications, however, the earlier work of Battram et al. (2004) and the more recent works of Pedersen et al. (2008) and Taylor et al. (2011) offer a fresh and unique perspective on caffeine use during post-exercise recovery situations. An important element of post-exercise nutrition is to optimize replenishment of muscle glycogen, an essential fuel molecule for muscle. The most pragmatic approach would be to simply comsume carbohydrates post-exercise. Recent studies, however, suggest that co-ingesting carbohydrates post-exercise (i.e. exhaustive exercise) with caffeine facilitates muscle glycogen replenishment compared to carbs alone. Although the underlying mechanisms are vaguely understood, researchers attributed these effects to some caffeine-mediated enhancement of muscle glucose uptake (glucose being the substrate for glycogen synthesis). Despite a relatively small body of evidence demonstrating these effects, there are no known disadvantages. So in my opinion, why not... It wouldn't hurt to have a little caffeine with your post-workout carbs. Perhaps a new caffeinated Gatorade product line in the future with further evidence. Keep in mind these results may only be relevant for athletes with high training and competition frequency and those who actually experience signficant glycogen depletion. In other words, probably not much of an effect for your everyday gym goer.


An oldie but a goodie. One of my favorite topics to teach.... It is with confidence I can say that we have come a long way in our understanding of the physiological mechanisms underlying muscle growth in response to resistance training. Even just around a decade ago, the optimization of training programs towards muscle growth was largely predicated on the best way to maximize "anabolic" hormone levels. With the advancement of muscle biology and exercise physiology research, we have indeed arrived at the conclusion that hormones (that are purported to be anabolic) were given way too much credit for the hypertrophic adaptation in muscle during resistance training. In fact, at least in my opinion, hormone-mediated pathways are only minor contributors to the growth response to training (that is of course in the context of normal physiological ranges). Muscle growth involves a complex multidimensional process as illustrated above and with better understanding of how each of these pathways may be manipulated by various exercise and nutrition strategies can we further advance the optimization of training programs towards muscle growth (in various populations). With that said, we must understand that building muscle whether in a rehab patient or an elite athlete involves critical understanding of these mechanisms to better guide application. While we are on the topic. I would like to also add that although muscle damage may not be a stimulus (or at least a potent stimulus) for muscle growth, it is certainly part of the biological basis for muscular adaptation to resistance training. I've been noticing more individuals dismissing the role of muscle damage in growth and strength adaptations entirely.


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).


Presenting some of the results from our study recently published in Clinical Nutrition. Overall, we add 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 bariatric 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 deficits, 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. If these effects are observed in such extreme conditions, imagine the efficacy of resistance training in those undergoing more moderated caloric deficits. Caloric deficit will drive weight loss quantity, resistance training will add the quality


With the growing use of Blood Flow Restriction (BFR) training for both fitness and clinical applications, there is a concomitant increase in consumer BFR products/devices. Generally, BFR devices can be categorized as pressure-gauged pneumatic systems or non-pneumatic elastic or rigid straps with a ratchet mechanism. Typically in the clinical setting, therapist would use a pneumatic system in order to apply safe and effective pressures which range between 100-150mmHg when using loads about 20 or 30% of max. More often in the fitness setting, the straps are widely used for BFR training. Here is the problem with this. BFR involves mostly venous occlusion and partial arterial occlusion which can be achieved with the aforementioned pressures. When pressures exceed ~200mmHg, there is an increased risk for near-full arterial occlusion and therefore ischemia, subsequently leading to an increased risk for tissue damage. There is also an increased risk for venous thrombosis and unsafe blood pressures for hypertensive individuals. Because the pressures applied by the BFR strap are completely subjective, the aforesaid risks are exponentially increased. Some may argue that they have a good gauge of the pressures when using the strap however in my preliminary pilot study, 25 subjects were asked to apply a BFR strap to a pressure they felt was appropriate according to manufacturer instructions. 22 of the 25 subjects applied pressures exceeding 200mmHg. Pneumatic, pressure-gauged systems, although costly, are the way to go. Occlusion Cuff, Delphi BFR, Kaatsu, and B Strong, and Smart Cuffs are a few of the devices currently on the market. Calibration is another issue which makes the electronic devices ideal (yet way more expensive).


[repost due to typo] Conditioning programs have traditionally been implemented on the basis of a false dichotomous view of exercise bioenergetics. This in turn has enabled a false anaerobic vs. aerobic perspective on conditioning or "metabolic training" with the equally false notion that specific types of conditioning stress specific energy systems which ultimately promote specific adaptations in a particular energy system in isolation. In my opinion, the term "anaerobic exercise or training" is a misnomer because high to max effort exercise (classically known as anaerobic) is in fact highly aerobic. Aerobic ATP production is at its capacity and the cardiovascular system is working at a commensurate rate to supply the oxygen. However, the ATP demand of working muscles during max effort exercise exceeds the rate at which the aerobic systems can provide it, mainly due to limited oxygen availability and mitochondrial factors. This initiates the use of backup systems that do not require oxygen like the phosphagen (ATP-PCr) system and carb metab is cut short prior to the pathway that requires oxygen rendering only few ATP per carb molecule. Therefore during high to max effort exercise the ATP demand is satisfied both aerobically and anaerobically, not just anaerobically. Therefore, you cannot train anaerobic ATP production in isolation. Specificity of conditioning programs should not be based on the sense that one can isolate and "train" any particular bioenergetics system. Conditioning programs should be based on optimally improving the athletes capacity to 1. produce ATP aerobically at higher work loads, 2. reduce reliance on anaerobic ATP contributions at higher work loads, and 3.contend with the fatigue inducing environment of anaerobic conditions (increased carnosine & bicarbonate buffering capacity). These are the factors, at least from a bioenergetics perspective, that promote fatigue resistance, not from some unique improvement in "anaerobic fitness". With that said research demonstrates a wide variety of conditioning modes that promote the aforementioned adaptations, even those commonly referred to as "anaerobic".