Cold water immersion (a.k.a., “ice baths”) has become a popular method amongst exercise enthusiasts and athletes to enhance recovery after an intense training bout. The strategy involves exposing either the trained limb or the whole body to very cold liquid temperatures. According to p...
Brad Schoenfeld, Ph.D, C.S.C.S., is an internationally renowned fitness expert and widely regarded as one of the leading authorities on body composition training (muscle development and fat loss). He is a lifetime drug-free bodybuilder, and has won numerous natural bodybuilding titles.
The following is the foreword to my book, M.A.X. Muscle Plan 2.0, written by John Meadows. John epitomized what it is to be a fitness pro. Always curious, always learning, always striving to improve himself and those around him. There was no one better at bridging the gap between science and practice from a bodybuilding standpoint. He passed far to soon, but made a huge impact on all those he touched. I consider myself truly fortunate to have known John personally; he will be forever missed. RIP.
2012 was one of my best yet most scary years ever. It was then that I ventured out of the comfortable corporate world at JP Morgan Chase and dove full time into the health and fitness industry. I had grown up a bodybuilder and loved to help others, so this transition was exciting, but scary, as now it was either sink or swim. I was also keenly interested in the science of what makes things happen to our bodies so now I would have more time to devote to learning. I decided to start my own website and figured that interviewing experts would be a great place to start. With a little fear behind me, I decided I had better knock my interviews out of the park so I wouldn’t have to crawl back to Bank and ask for my old job back.
I had been hearing about a guy in New York named Brad Schoenfeld. In fact, I was studying everything he said. I found myself nodding my head as I read his work. It made sense. Much of what I had done had worked in the bodybuilding and nutrition realms, but the truth is, it was more of a gut feeling based on experience then a deep knowledge of the details of why things happen. Brad seemed to be filling in the blanks for me. Oh, this is why this works, this is why this doesn’t work etc. I reached out to him hoping he would have time for a quick interview, and he responded with a quick yes. I was ecstatic. We ended up doing 2 parts because, well honestly, I just wanted to learn more myself, but the side effect was my website followers got some very advanced knowledge dropped on them.
After the interview Brad and I kept in touch and I had begun carrying his “mechanisms of muscular hypertrophy” paper around with me like a bible. I read it over, and over, and over. I wasn’t the only one. Many bodybuilders I knew started referencing his work. If you know the bodybuilding community, you know we can be a bit of a meathead bunch when it comes to accepting “science” or evidence outside of our own personal experience. Somehow Brad was bridging this gap. I kept noticing more and more of my colleagues popping in and asking Brad questions or sharing his work. It helped that Brad has competed as a bodybuilder himself, but what really helped the most, was Brad acknowledging a lot of the good things bodybuilders had done, and when challenging long held beliefs, he did it with class and an obvious good intention in his heart. You can search the bodybuilding community high and low and you won’t find a single successful person that doesn’t respect Brad’s work. This is quite remarkable.
Brad eventually asked me to guest lecture to his class, which was absolutely amazing for me, as having the respect of someone in his league, really meant a great deal. Eventually Brad visited and trained together made videos for my YouTube channel that were wildly popular. I am looking forward to doing more of this in the future with him!
You are in for a treat reading this book. Brad is going to teach you how to think about exercise at a high level, and at a more detailed level. Simply put, you are going to have the information you need, to allow you to build the best program for YOU, and how to reach your ultimate potential!
Few topics in the field of exercise are as controversial as training to failure. Views on the topic tend to be polarizing, with some fitness pros strongly advocating the need to go all-out for optimal muscle adaptations, and others claiming failure training not only isn’t necessary, but in fact may be detrimental to gains.
Who’s right?
Our recent systematic review and meta-analysis provides some answers on the topic, while at the same time raising many more questions. The paper is open access and thus free for all to read, but I think it’s essential to delve beyond the numbers to fully appreciate its practical implications. Here’s the scoop…
What We Did
We searched the current literature to locate all randomized control trial studies that directly compared measures of strength and hypertrophy when carried out to muscle failure versus not to failure. Only human studies with healthy subjects that had a minimum duration of six weeks were considered for inclusion; we excluded studies that used blood flow restriction resistance training or concurrent training interventions (e.g., combined resistance and aerobic training). We then carried out a random effects meta-analysis that pooled results of all included studies to quantify the effects of failure training on muscular adaptations. A subgroup analysis of training status, body-region, exercise selection and training volume was performed to determine their potential influence on results.
What We Found
A total of 15 studies were identified that met inclusion criteria. A basic meta-analysis of pooled results found no statistical differences between training to failure versus stopping short of failure for both strength and hypertrophy outcomes; the trivial to small observed effect size differences between conditions in both outcomes (-0.09 and 0.22, respectively), suggest that any effects were of little practical meaningfulness.
Subgroup analysis showed a moderating effect of training volume on strength gains, whereby studies that did not equate volume favored non-failure training; the effect size differential was of a moderate magnitude (ES: –0.32). Alternatively, subgroup analysis found a moderating effect of training status on muscle growth, whereby trained individuals achieved a small hypertrophic benefit (ES = 0.15) from failure training.
What are the Practical Implications of Findings
On a general level, our meta-analysis indicates that training to failure isn’t necessary for maximizing muscular strength or hypertrophy. That said, numerous gaps in the literature preclude our ability to draw strong conclusions on the topic. The following points need to be considered when attempting to translate the research into individual program design:
• The choice doesn’t have to be binary: All failure-training studies to date have employed designs where one group trains to failure in every set while the other group does not train to failure in every set. This doesn’t necessarily reflect real-world programming. Fact is, you don’t have to take all sets to (or not to) failure. Training to failure on each set ultimately tends to compromise volume load, which in turn may impair hypertrophic adaptations. Moreover, there is some evidence that continually training to failure across multiple sets brings about markers of overtraining, which in turn may negatively impact muscle-building capacity. There are numerous strategies to employ failure training in a program. For example, you can perhaps limit its use to the last set or two of an exercise…perhaps use it selectively on certain exercises (see below)…perhaps reserve its use for higher rep sets (see below)…perhaps periodize its implementation across workouts or training cycles (see below)…the possibilities are almost endless. Thing is, no study has yet endeavored to study these possibilities, so all we have to go on at this point is anecdote and logical rationale.
• If not failure, then what is the appropriate set end point? : Assuming we take the results of the meta-analysis at face value and accept that training to failure isn’t obligatory for optimizing muscular adaptations, the ensuing question would be: “How close to failure do you need to train?” Unfortunately, there isn’t enough evidence to answer the question. Given that a muscle has to be sufficiently challenged to promote adaptation, we can logically make the case that at least some sets would need to be taken relatively close to failure. However, what value would that equate to in the repetitions in reserve (RIR) scale? An RIR of 1? An RIR of 2? An RIR of 3…or more? And consistent with what was mentioned in the above bullet point, how does this play out across multiple sets of an exercise? At this point, there is considerable room for debate on the topic.
• Does training frequency enter into the equation? : Although controlled evidence is lacking, it logically follows that training to failure increases recovery time between sessions. Assuming so, it makes sense that those training with higher session frequencies (>3 or 4 sessions per week) may not be able to tolerate as much (or any?) failure training. A case can be made that failure training not only has recovery implications for the targeted muscle groups, but on the neuromuscular system as a whole. At this point no research has endeavored to investigate the need to manage the level of effort based on how often you train.
• Is the need to train to failure load-dependent? : It has been speculated that you must train (closer) to failure when using higher rep schemes, both to recruit and simulate fast twitch fibers. Despite this speculation, there is a paucity of controlled research on the topic. The evidence we currently do have appears to support that higher rep training requires a higher level of effort, but whether all-out failure is obligatory remains somewhat equivocal. It is also important to note that failure in low repetition training is brought about by neuromuscular factors whereas failure in high-rep training is brought about by peripheral factors; are these factors associated with mechanisms that may elicit different hypertrophic responses and, if so, would failure be a modifying variable in the response? And given that higher rep sets involve a higher perception of discomfort, is true “failure” actually reached by most lifters when training with lighter loads before they simply give up due to the displeasure sensation? These questions require further investigation.
• What about training experience? : Our meta-regression showed that failure training was more beneficial in those with resistance training experience compared to novice trainees. However, there are a couple of caveats to this finding. For one, the overall magnitude of effect of was relatively small (ES = 0.15), calling into question the practical meaningfulness of the finding. Moreover, as noted in the exclusion criteria, we excluded a study by Carroll et al. (that employed trained lifters), due to the fact that it had an aerobic training component as part of the design (research indicates that aerobic training can interfere with muscular adaptations, and the degree of interference may be more pronounced in trained lifters). However, whether the aerobic training component actually influenced results remains unclear. Had this study been included, the result favoring failure training for trained lifters would have been nullified. I’d also note that a recently published study was just published showing no benefit to failure training in trained men; the study came out after publication of our paper and thus was not included for analysis, but certainly would have further reduced the observed effect. With all this said, no study to date has investigated failure training in highly trained lifters. It is conceivable that when lifters get increasingly closer to their genetic ceiling, a greater intensity of effort is required to achieve muscular gains. On the other hand, highly trained lifters also tend to be able to use heavier loads and are able to “dig deeper” to push the limits of failure training. Perhaps this means elite lifters should take fewer sets to failure because of the resultant neuromuscular stress on the body?
• Is age a consideration? : It is fairly well-established that recovery ability tends to decline as people age; all other things being equal, older lifters require more time to recuperate after a resistance training session compared to younger trainees. Given that failure training negatively impacts recovery, perhaps it should be employed more sparingly in this population? Unfortunately, there is scant research to date on the effects of failure training in older individuals, limiting our ability to draw strong conclusions on the topic.
• Does the type of exercise matter? : All exercises are not necessarily created equal when it comes to failure training. For example, taking sets of deadlifts or bent rows to failure can be highly taxing to the neuromuscular system. Alternatively, I’ve never heard anyone say they were crushed from going all-out on cable lateral raises. Single vs multi-joint…free weight vs machine…upper vs lower body…each of these variables concerning exercise selection requires consideration when deciding on the level of effort to expend. Unfortunately, the literature to date has not endeavored to investigate the complexities of this topic.
Take-Home Conclusions:
So where does this leave us from a practical standpoint? As with most applied exercise-related topics, research can only provide general guidelines into application for program design. Hence, here is my evidence-based take on the topic that synthesizes the current research in combination with insights from personal experience.
First, muscular adaptation requires a stimulus that challenges the body beyond its present capacity. In novice lifters, this can be achieved stopping quite a ways away from failure; even cardio is sufficient to cause appreciable muscle growth in this population! As you gain training experience, the need to train closer to failure becomes increasingly more important. Although it’s difficult to provide specifics, I’d say that at least some sets need to be within a rep or so of volitional failure. I’d also speculate that for highly trained lifters (e.g. competitive bodybuilders), there is a need to take some sets to failure to optimize muscle-building. Along these lines, as you get older, failure training should be employed more sparingly to allow for adequate recovery.
Second, when failure training is warranted, it should be applied somewhat conservatively, erring on the side of caution. A good rule-of-thumb is to limit its use to the last set of a given exercise; other sets should employ an RIR of 1 to 3. Moreover, you may need to further limit failure training with higher frequency routines. Periodizing failure training is a viable option, whereby more sets are carried out to failure prior to a peaking phase, potentially followed by a tapering phase. I’d note that numerous research studies show robust strength and hypertrophic gains when multiple sets are carried out to failure over short-term interventions (~8 to 10 weeks); however, continuing to train in this fashion likely will bring about negative consequences (i.e. overtraining). Thus, alternating periods using very high levels of effort with reduced levels of effort potentially may promote supercompensation of gains without devolving into an overtrained state.
Third, failure training should be prioritized in single-joint movements. These exercises induce less stress on the neuromuscular system, and thus don’t tax your recuperative abilities as much as multi-joint movements. Alternatively, limit the use of failure training on compound movements, particularly structural exercises using free weights (e.g. squats, bent rows, etc.). Machine-based exercises, in addition to being somewhat less taxing from a neuromuscular standpoint, provide a degree of safety when training to failure if you don’t have a spotter.
Finally and importantly, how all these considerations play out in practice will be specific to individual needs and abilities. Both genetic and lifestyle factors have a major role in program design. Ultimately, continued experimentation is required to optimize individual response over time.
However, there is a well-established phenomenon called the repeated bout effect, whereby continual performance of the same routine markedly attenuates damage-related symptoms compared to the initial bout. In fact, there is evidence that just one additional bout of the same exercise protocol reduces the swelling response to only one-third of the initial bout. Consistent training with the same routine further diminishes these effects, as eloquently shown in a study by Damas et al who tracked indices of muscle damage across 10 weeks of regimented resistance training carried out to volitional muscular failure. As shown in the graph above, damage was substantial after the initial training session. By the fifth workout, damage was substantially reduced and by the 19th workout, damage was practically inconsequential as measured 48 hours post-exercise. Post-testing for our study was done 48 to 72 hours after the last bout of a routine that was performed 24 times over an 8-week period. Thus, while I can’t completely rule out the possibility that there was swelling in the muscles, it would seem highly unlikely that this would have confounded our findings. This is particularly true given that our subjects were resistance-trained men with 4+ years training experience, who were already acclimated to the stresses of regular lifting.
On a separate note, in the discussion section of our paper we briefly discussed the results of another study on the topic carried out by Ostrowski et al. We noted that, similar to our study, the results of Ostrowski et al supported the hypothesis that volume is a primary driver of hypertrophy. Some have asked why we did not discuss the dose-response implications between their study and ours. This was a matter of economy. Comparing and contrasting findings would have required fairly extensive discussion to properly cover nuances of the topic. Moreover, for thoroughness we then would have had to delve into the other dose-response paper by Radaelli et al, further increasing word count. Our discussion section was already quite lengthy, and we felt it was better to err on the side of brevity. However, it’s certainly a fair point and I will aim to address those studies now.
Ostrowski et al carried a study in resistance-trained men, who were randomized to perform either 1, 2 or 4 sets per exercise. For triceps, our results were somewhat inconsistent with theirs. Whereas we showed that muscle thickness increased by 1.1%, 3% and 5.5% for the low, middle and high volume groups, respectively, they showed increases of 2.3%, 4.7% and 4.8%, respectively. The primary difference between findings is that Ostrowski showed similar growth between middle and high volume groups while ours showed a graded increase from low to middle to high. The overall differences were modest on this outcome. Possible reasons for the discrepancy could be due to differences in methods. Ostrowski et al used a typical bodybuilding-type routine that involved a four day split. Subjects trained legs on Day 1; chest and shoulders on Day 2; back and calves on Day 3; and arms on Day 4. On the other hand, our study employed a total body routine where all muscles were trained in the same session, three times per week. Ostrowski et al also had subjects perform single joint exercises for the triceps in addition to their contribution in pushing movements, whereas subjects in our study just performed pushing movements. As discussed in the limitations of our paper, there is evidence that multijoint movements produce similar hypertrophy to single joint movements, but we cannot rule out that inclusion of targeted training for the triceps influenced differences in results. I’d note that the triceps data from our study was the least compelling of the four muscles measured for showing an effect of volume on hypertrophy. Thus, given the fairly low response across conditions, the discrepancy also could be due to the effects of random chance.
With respect to lower body hypertrophy, our results are somewhat in concert with those of Ostrowski et al. Ostrowski et al found quadriceps thickness increased of 6.8%, 5%, and 13.1% for low, middle and high volume groups, respectively. These findings are fairly consistent with ours, which found an increase in mid-thigh hypertrophy of 3.4%, 5.4, and 12.5%, and lateral thigh hypertrophy of 5.0%, 7.9, and 13.7% in the low, middle and high volume conditions, respectively. The fact that their low and middle volume conditions did not show differences may be related to the low volumes performed in both of these conditions (3 and 6 sets per muscle per week, respectively) whereas the high volume condition performed 12 sets per muscle per week. It’s also interesting that much greater levels of volume were required to achieve similar hypertrophic responses in the quadriceps between our study and that of Ostrowski; the reasons for this are not clear.
Our findings are consistent with those of Radaelli et al, who randomized young men to perform either 1, 3 or 5 sets per exercise per week. The subjects were military personnel who regularly performed calisthenic-type exercise but were not involved with resistance training at the time of the study. They reported increases in biceps thickness of 1.1%, 7.8% and 17% whereas our study found post-study increases in biceps thickness of 1.6%, 4.7% and 6.9% for the low, middle and high volume groups, respectively. For the triceps, Radaelli et al found pre- to post-study increases of 0%, 1.7%, and 20.8% for the low, middle and high volume groups, respectively. As noted above, we found 1.1%, 3% and 5.5% for the same conditions. Thus, both studies showed a dose-response relationship between volume and hypertrophy, albeit Radaelli et al reported much greater increases for the highest volume condition. Radaelli et al did not report results for lower body hypertrophy, so we cannot contrast findings in this regard. The reasons for similarities between findings potentially can be attributed to the fact that our designs were similar. Both studies employed graded doses of 1, 3 and 5 sets per exercise per session and both had subjects perform a total body routine, three days per week. A difference between studies is that subjects in Radaelli performed single joint exercises for the biceps and triceps whereas our study only performed multijoint movements for these muscles. Moreover, their study lasted 6 months whereas ours lasted 2 months.
Since acceptance of our paper, two additional studies have been published on the topic. I’ll discuss the ultrasound results, as they are specific to our findings. Heaselgrave et al randomized resistance-trained men to perform either 9, 18 or 27 sets of biceps training each week. Subjects performed a combination of multi and single joint exercises for the muscle. Although results did not rise to a level of statistical significance, scrutinization of the individual data appears to show a fairly clear hormetic response (i.e. inverted U), with results peaking in the middle volume condition as shown in the graph above. This study had a couple of notable limitations. For one, subjects were allowed to train on their own outside of the study but were advised not to perform any direct biceps exercise. Although subjects did not report significant confounding from outside training, it is known that self-report can lack accuracy and it therefore remains questionable whether additional training was in fact carried out. Moreover, the subjects in the higher volume conditions trained two days per week while the lowest volume condition trained one day per week. Thus, this study in actuality had two treatment variables, confounding the ability to draw causality on volume alone.
Finally, Haun et al recently carried out a study in resistance-trained men. The study employed a somewhat unusual design, whereby volume was ramped up each week over the course of 6 weeks, beginning with 10 sets per muscle per week and progressing to 32 sets per muscle in week 6. Only 4 exercises were employed: back squat, bench press, stiff legged deadlift, and lat pulldown. A strong point of this study was that they employed midpoint testing after the 3rd week, thereby providing insights into how changes occurred over time. Muscle thickness for the biceps brachii increased from baseline to the midpoint, but then attenuated by the end of the study. This suggests results peaked at 20 sets per muscle per week. Alternatively, results for the vastus lateralis showed no significant changes from mid to post testing, but significantly increased from midpoint (20 sets/muscle/week) to the end of the study (32 sets/muscle/week). Interestingly, the authors also carried out biopsy testing and found that CSA of the vastus lateralis significantly decreased from baseline to mid but then significantly increased from mid to post. It should be noted that the overall magnitude of the increases in this study were quite modest. That may be due to the design, whereby subjects performed 10 reps at 60% of 1RM each set. This is a relatively light load for trained subjects, and it can be speculated they weren’t sufficiently challenged. Another factor to consider is that volume was progressively increased each week, so subjects only trained at a given volume for 1 week. It is therefore difficult to extrapolate the effects of training at a prescribed volume over multiple weeks.
In summing up the literature to date, the one thing that appears clear is that volume plays a fairly prominent role in maximizing growth, but nevertheless significant hypertrophy can be obtained at fairly low volumes. It’s difficult to reconcile discrepancies between studies given differences in methodology. And as as is almost always the case in an applied science such as exercise, prescription will be specific to the individual as there are large interindividual variances associated with response to volume. The astute fitness pro will take the current research into account and then use his/her expertise to customize program prescription, taking into account the potential benefit balanced against the time commitment involved.
For as long as I can recall, bodybuilders have been preaching the importance of a mind-muscle connection for maximizing muscle development. In case you’re not aware, a mind-muscle connection (a variation of the concept in the field of motor learning known as an “internal focus of attention”) is the process of actively thinking about the target muscle during training and then feeling it work through the full range of motion. According to theory, this strategy maximizes stimulation of the muscles you’re trying to target in a given exercise while reducing the involvement of “secondary” movers. This combination hypothetically should result in greater growth.
Hypothetically….
Numerous studies have confirmed that a mind-muscle connection does in fact increase activation of the target muscle as measured by a technique called electromyography. However, higher activation of a muscle doesn’t necessarily mean it will hypertrophy to a greater extent over the course of a long-term training program. To my amazement, no one had endeavored to investigate whether adopting a mind-muscle connection during training actually had a beneficial effect on muscle growth in a controlled, long-term study.
So the curious science nerd that I am, I took it upon myself to find out. Here’s the scoop on our recently published paper on the topic.
What We Did
30 college-aged men agreed to participate in the study and were randomly assigned to either train with an internal focus (mind-muscle connection) or an external focus. All participants performed 4 sets of arm curls and leg extensions for 8 to 12 RM on 3 non-consecutive days per week, with sets carried out to muscular failure. Every rep of every set was supervised by one of my research assistants. The mind-muscle group was instructed to “squeeze the muscle” on each rep while the external focus group was instructed to “get the weight up.” The exercise portion of the program lasted 8 weeks with a week taken for testing immediately before and immediately following the training period.
As those of you who follow my work undoubtedly know, the vast majority of my studies are carried out in subjects with resistance training experience. However, in this case I decided to use untrained subjects.
Why?
Well, trained individuals tend to get hardened into a given attentional focus (called a “deep basin” in motor learning). It’s therefore difficult to get these individuals to change their focus during training. This would be especially problematic in a study such as this since there is no way to be sure what the lifter is actually thinking when training. An untrained lifter is a blank slate and thus we could be more confident that he would follow the prescribed attentional focus strategy.
I also chose to use only single joint exercises for the study. The reasoning here is that it’s easier to focus on a given muscle during a single joint lift. Squats, rows and presses involve multiple primary muscle movers that makes it difficult for a lifter – particularly one with no training experience – to focus on a given single muscle. What’s more, multijoint exercises require more of a learning curve to coordinate movement patterns in the early stages of training, which would further impair the ability to develop a mind-muscle connection as well as delaying the onset of hypertrophy in favor of neural adaptations.
What We Found
After 8 weeks of consistent training, subjects who used a mind-muscle condition had almost double the muscle growth in the biceps brachii compared to those using an external focus (12.4% vs 6.9%, respectively). Alternatively, muscle growth for the quadriceps was similar between conditions. From a maximal strength standpoint, isometric strength of the elbow flexors increased substantially more for the internal focus group while knee extensor strength was markedly greater for the external focus group.
What We Learned
The novel finding of the study was that superior gains in biceps hypertrophy were made by employing an internal focus of attention. Based on these findings, it appears the bros were right; employing a mind-muscle connection enhances muscle growth.
But wait a sec; if that’s the case, then how come attentional focus did not seem to matter for thigh hypertrophy…?
Although it’s impossible to say for sure since we didn’t attempt to investigate mechanisms, a possible reason is that subjects simply found it easier to focus on the biceps as opposed to the quads. This is logical given that the upper extremities are used for fine motor skills (i.e. picking things up, writing, etc) while the lower extremities are involved in gross motor skills (i.e. walking, kicking, etc). Thus, people tend to be more conscious of their arm muscles and less so of the leg musculature. The fact that the subjects were untrained would seemingly contribute to this discrepancy. I’d hypothesize that well-trained lifters would be better able to focus on the quads when training and thus achieve better hypertrophy. This needs further study.
Here’s the take home: It appears beneficial to adopt a mind-muscle connection if your goal is to maximize muscle growth. Instead of worrying about a specific tempo, simply focus on the muscle being trained and visualize it working throughout the full range of motion. Now this comes with the caveat that findings are specific to a moderate rep range; using heavy loads (i.e. 3-5 reps) may preclude the ability to take advantage of this strategy as your focus would conceivably have to shift to just getting up the weight as efficiently as possible. Importantly, this is just one study and shouldn’t be taken as the be-all-end-all on the topic. Hopefully more longitudinal studies will be conducted on the topic to draw more definitive conclusions. Future research should look to compare internal versus external focus strategies using multi-joint exercises in trained lifters to better understand how a mind-muscle connection impacts growth.
For further insights, check out the video I did for Omar Isuf’s YouTube channel below. I discuss the nuances of the topic and their relevance to practical application in a lifting program.
In a recent blog post , I, along with my colleague Bret Contreras, published a “letter to the editor” that raised issue with various claims made in a review of exercise-induced muscle damage. In the spirit of scientific discourse, we invited the authors of the paper – Felipe Damas, Cleiton Libardi, and Carlos Ugrinowitsch – to publish a rebuttal to our letter on my site. They have obliged and what follows is their response.
We acknowledge the authors of the letter to the Editor for the opportunity to continue the debate on the interesting topic of mechanisms related to resistance training (RT)-induced skeletal muscle hypertrophy. While we agree that the role of muscle damage on muscle hypertrophy needs further scientific scrutiny, as we pointed out in our article (Damas et al. 2018a), current evidence indicates that muscle damage promoted by initial resistance exercise (RE) does not predict, explain, or potentiate skeletal muscle hypertrophy induced by weeks of RT (Damas et al. 2016; Flann et al. 2011). Moreover, if muscle damage magnitude is severe, the exercise-induced stress results in maladaptation, segmental necrosis or even muscle atrophy (Butterfield 2010; Eriksson et al. 2006; Foley et al. 1999; Lauritzen et al. 2009). That said, it remains to be elucidated if disturbances within muscle fibres, e.g., Z-band streaming, muscle repair and remodelling are required in early RT phases to prepare muscle tissue to endure further stresses; albeit delayed onset muscle soreness, muscle proteins (e.g., creatine kinase) leakage to bloodstream, or large decreases in muscle function can be avoidable if the goal is muscle hypertrophy (see p.493 of Damas et al. (2018a).
In their letter, the authors mentioned that our original article (Damas et al. 2016) was not designed to test if muscle damage have a role on muscle hypertrophy, what we respectfully disagree. While more intelligent study designs could be drawn to test the hypothesis, we agree with the authors that an investigation that would modulate only the ‘muscle damage’ variable is virtually impossible. However, some points regarding the rational of the research design presented by Schoenfeld and Contreras to test the damage vs hypertrophy paradigm requires further considerations. The comparison between two groups with one demonstrating significant damage in the beginning of RT and another experiencing minimal damage throughout RT has already been performed by Flann et al. (2011) (using muscle soreness and plasma creatine kinase as markers), and they showed similar levels of hypertrophy between groups. Alternatively, maintaining significant damage throughout RT is, as far as we understand, somewhat unfeasible. Firstly because muscle damage is potently attenuated within the first training sessions – repeated bout effect (Barroso et al. 2010; Chen et al. 2009; Clarkson and Hubal 2002; Damas et al. 2016; McHugh 2003), and secondly, to the best of our knowledge, there is no empirical evidence that ‘strategies’ (e.g., changing resistance training variables – volume, intensity, exercises) could overcome the repeated bout effect and further increase or even maintain an initial level of muscle damage. Accordingly, Zourdos et al. (2015) demonstrated that changing elbow flexors exercises between training sessions does not minimize the repeated bout effect. Therefore, in our original article (Damas et al. 2016), we opted to use a reverse logic, maintaining training stimulus as constant as possible, and use the repeated bout effect as strategy to produce distinct muscle damage magnitudes to test the relationship between changes in muscle damage magnitude, myofibrillar protein synthesis (MyoPS) and muscle hypertrophy. Accordingly, we used previously untrained subjects to achieve distinct magnitudes of muscle damage (through direct and indirect muscle damage markers, to form a more complete picture of the process), investigating an early RT phase (i.e., after only 4 RT bouts) as a first ‘attenuated damage’ time-point in which muscle hypertrophy is not significant yet (thus hypertrophic potential is maintained compared to baseline), and relate to acute MyoPS response after the same RT bouts and to muscle hypertrophy induced by 10 weeks of RT. Doing so, we isolated the best way we could the ‘damage’ variable. We also provided the same data for a RT session in the last week of RT. Importantly, our longitudinal design testing the same subjects over time, maintaining exercise mode (isoinertial RT, involving concentric and eccentric phases) with every set to muscle failure (same relative load), allowed significant internal validity while providing ecological validity of our results. We demonstrated that the subjects that had a greater magnitude of muscle damage in the early phase of RT were not the same subjects that showed greater muscle hypertrophy after 10 weeks of RT (correlation analysis). In addition, we showed that MyoPS does not correlate to muscle hypertrophy when damage is the largest (in response to the first RT session), but MyoPS presented a trend to moderately correlate (r ~ 0.6, p = 0.09) to the degree of damage in response to the same RT bout. After progressive attenuation of muscle damage throughout RT, MyoPS strongly correlated (r ~ 0.9) with muscle hypertrophy induced by 10 weeks of RT (but MyoPS showed no association with damage anymore) (Damas et al. 2016). Most likely, the increase in MyoPS at the beginning of RT is directed to repair and remodel muscle tissue and with RT progression and thus damage attenuation, MyoPS increase is focused on muscle hypertrophy. Overall, more (or less) damage, throughout the entire RT program did not correlate at any point with muscle hypertrophy induced by RT. Thus, we suggested, based on our previous work (Damas et al. 2016) and mainly on the discussion developed in our review (Damas et al. 2018a) that muscle damage was not predictive, did not potentiate or explained the magnitude of RT-induced muscle hypertrophy. We are in line with the authors when they argue in their letter that is impossible to determine whether damage is required to occur previously to muscle hypertrophy, repairing and remodelling muscles to be prepared for further stress (Damas et al. 2018a). In fact, in the article the authors cite in their letter (Lilja et al. 2018), the high doses of anti-inflammatory drugs could be interfering in muscle repair and remodelling (involving, for example, enhanced protein turnover, addition of sarcomeres in parallel in response to Z-band streaming). Successful muscle repair and remodelling might be possibly required to endure subsequent RE sessions in the RT program, which in turn, would supress muscle hypertrophy. Indeed, more work is required on this topic.
The authors suggested that we misinterpreted a finding from their previous work (Schoenfeld et al. 2017), as eccentric RT produced an effect size point estimation of 0.25 when compared to concentric RT. In addition, the authors provided the 95% confidence interval of the point estimation of all of the studies included in their meta-analysis. Even though Schoenfeld and Contreras supported their claim based on Hopkins’ magnitude-based inference work, one should consider that confidence intervals, when using a frequentist approach (or credible intervals for a Bayesian approach) are critical to determine the region in which the true population effect value should be included or the actual probability of an event to occur. Nakagawa and Cuthill (2007) provided a good example on the topic:
“The approach of combining point estimation of effect size with CIs provides us with not only information on conventional statistical significance but also information that cannot be obtained from p values. For example, when we have a mean difference of 29 with 95% CI = –1 to 59, the result is not statistically significant (at a level of 0.05) because the CIs include zero, while another mean difference 29 with 95% CI = 9 to 49 is statistically significant because the CI does not include zero.”
This idea is particularly important as the effect size point estimation obtained in a meta-analysis depends on the articles retrieved from the search and may not represent “the true population value”. Thus, effect size confidence interval analysis is imperative as the actual effect size could be any value within the interval. As their confidence interval [-0.03, 0.52] included zero (Schoenfeld et al. 2017), it is possible that the alleged advantage of eccentric RT over concentric RT may be rather smaller or even does not occur. Furthermore, that was not the main point of our argument in the review (Damas et al. 2018a), which was that the evidence indicating superior hypertrophy for eccentric RT is, at least, controversial (please see p.492). The mechanical tension (which should not be confounded as a direct indicator of muscle damage) is greater in a maximal eccentric contraction compared with a maximal concentric contraction, possibly resulting in a greater hypertrophic-induced effect per repetition for the eccentric exercise mode. Indeed, training with the same number of maximal repetitions showed superior hypertrophy for eccentric vs concentric RT (Farthing and Chilibeck 2003). However, when both exercise modes are matched for total work, Moore et al. (2012) showed similar magnitudes of muscle hypertrophy between them. Yet, it needs to be highlighted that different contraction modes seems to rely on distinct mechanisms to induce muscle hypertrophy. For example, it was showed that total work per repetition is greater in eccentric vs concentric RE (Moore et al. 2012; Rahbek et al. 2014), but the voluntary activation of motor units is lower for eccentric RE (Beltman et al. 2004) and metabolic stress is greater following concentric RE (Durand et al. 2003). Therefore, concluding about the role muscle damage to RT-induced muscle hypertrophy using distinct isolated contraction modes, which rely on several mechanisms to promote hypertrophy, may be equivocal. That was imperative for the design choice in our original study (Damas et al. 2016). We maintained exercise mode throughout RT with the same relative load (as explained above), which would rapidly attenuate damage providing different magnitudes of damage to be compared in the same subjects longitudinally. In addition, even with protocols that induce high levels of muscle damage, i.e., maximal eccentric RE, muscle damage is quickly attenuated with RE repetition (Chen et al. 2009) (actually, as curiosity, the greater is initial damage, the stronger is the protective effect (Chen et al. 2007)), questioning the real importance of damage in the long run (i.e., several weeks, months or years of RT). Contributing to this line of argumentation, Rahbek et al. (2014) demonstrated that MyoPS increase post-RE was similar between eccentric and concentric RE after only three RT bouts (i.e., small period of adaptation to RT), despite eccentric RE resulting in greater muscle damage and MyoPS response after a first RT session (Moore et al. 2005).
Finally, we do not claim that satellite cells (SC) are solely involved in muscle regeneration or repair, and not in muscle hypertrophy. We clearly state that “Chronic repetition of RE will maintain SC elevation, replenishing SC niche and enhancing myogenic capacity for future stressful events or muscle fibre hypertrophy” (p.495). However, SC increase early on into RT, as in the scenario in which muscle damage is pronounced, did not result in increased myonuclear number after either isoinertial concentric-eccentric RE (Damas et al. 2018b; Kadi et al. 2004) or a high volume eccentric RE (i.e., 300 repetitions) (Hyldahl et al. 2015). If such an increase in SC resulted in increased myonuclear number due to damage early on into RT, one could suggest increased transcription capacity due to damage, but this was not the case (Damas et al. 2018b; Hyldahl et al. 2015; Kadi et al. 2004). Thus, to this point it is highly speculative to relate the early increase in SC niche, due to stress/damage, to a later on into RT support of muscle hypertrophy, which would undeniably be interesting in low-responders to RT and elderly. Although, one might argue that these populations might not reach a theoretical myonuclear domain threshold that would require an increase in myonuclear number donated by SC (Conceicao et al. 2018; Kadi et al. 2004). SC pool increase in response to unaccustomed stress and muscle damage, and repeated exercise stress seem to keep SC pool elevated, probably as an anticipatory mechanism to aid in possible future stressful events or to support large muscle fibre hypertrophy (to a more in depth discussion see p.493-495). However, there is evidence demonstrating that SC pool was increased in a non-hypertrophic (i.e., aerobic) training (Joanisse et al. 2013), favouring a major role for SC activity related to stress response.
Although we acknowledge that the theme of muscle damage vs hypertrophy requires further testing and elucidations as we mentioned above, it is our understanding that based on current evidence the ball is on the other side of the court, i.e. the hypothesis of damage having a minor (or even large) role in explaining or potentiating muscle hypertrophy is speculative at this point. We look forward to novel study designs testing the damage vs hypertrophy paradigm to continue solidifying evidence-based knowledge on the theme.
References
Barroso R, Roschel H, Ugrinowitsch C, Araujo R, Nosaka K, Tricoli V (2010) Effect of eccentric contraction velocity on muscle damage in repeated bouts of elbow flexor exercise. Appl Physiol Nutr Metab 35:534-540
Beltman JG, Sargeant AJ, van Mechelen W, de Haan A (2004) Voluntary activation level and muscle fiber recruitment of human quadriceps during lengthening contractions. J Appl Physiol 97:619-626
Butterfield TA (2010) Eccentric exercise in vivo: strain-induced muscle damage and adaptation in a stable system. Exerc Sport Sci Rev 38:51-60. doi:10.1097/JES.0b013e3181d496eb
Chen TC, Chen HL, Lin MJ, Wu CJ, Nosaka K (2009) Muscle damage responses of the elbow flexors to four maximal eccentric exercise bouts performed every 4 weeks. Eur J Appl Physiol 106:267-275. doi:10.1007/s00421-009-1016-7
Chen TC, Nosaka K, Sacco P (2007) Intensity of eccentric exercise, shift of optimum angle, and the magnitude of repeated-bout effect. J Appl Physiol (1985) 102:992-999
Clarkson PM, Hubal MJ (2002) Exercise-induced muscle damage in humans. Am J Phys Med Rehabil 81:S52-69. doi:10.1097/01.PHM.0000029772.45258.43
Conceicao M et al. (2018) Muscle fibre hypertrophy to myonuclei addition:A systematic review and meta-analysis. Med Sci Sports Exerc in press
Damas F, Libardi CA, Ugrinowitsch C (2018a) The development of skeletal muscle hypertrophy through resistance training: the role of muscle damage and muscle protein synthesis. Eur J Appl Physiol 118:485-500. doi:10.1007/s00421-017-3792-9
Damas F et al. (2018b) Early- and later-phases satellite cell responses and myonuclear content with resistance training in young men. PLoS One 13:e0191039. doi:10.1371/journal.pone.0191039
Damas F et al. (2016) Resistance training-induced changes in integrated myofibrillar protein synthesis are related to hypertrophy only after attenuation of muscle damage. J Physiol 594:5209-5222. doi:10.1113/JP272472
Durand RJ et al. (2003) Hormonal responses from concentric and eccentric muscle contractions. Med Sci Sports Exerc 35:937-943
Eriksson A, Lindstrom M, Carlsson L, Thornell LE (2006) Hypertrophic muscle fibers with fissures in power-lifters; fiber splitting or defect regeneration? Histochem Cell Biol 126:409-417. doi:10.1007/s00418-006-0176-3
Farthing JP, Chilibeck PD (2003) The effects of eccentric and concentric training at different velocities on muscle hypertrophy. Eur J Appl Physiol 89:578-586. doi:10.1007/s00421-003-0842-2
Flann KL, LaStayo PC, McClain DA, Hazel M, Lindstedt SL (2011) Muscle damage and muscle remodeling: no pain, no gain? J Exp Biol 214:674-679. doi:10.1242/jeb.050112
Foley JM, Jayaraman RC, Prior BM, Pivarnik JM, Meyer RA (1999) MR measurements of muscle damage and adaptation after eccentric exercise. J Appl Physiol (1985) 87:2311-2318
Hyldahl RD et al. (2015) Extracellular matrix remodeling and its contribution to protective adaptation following lengthening contractions in human muscle. FASEB J 29:2894-2904. doi:10.1096/fj.14-266668
Joanisse S, Gillen JB, Bellamy LM, McKay BR, Tarnopolsky MA, Gibala MJ, Parise G (2013) Evidence for the contribution of muscle stem cells to nonhypertrophic skeletal muscle remodeling in humans. FASEB J. doi:fj.13-229799 [pii]
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Kadi F, Schjerling P, Andersen LL, Charifi N, Madsen JL, Christensen LR, Andersen JL (2004) The effects of heavy resistance training and detraining on satellite cells in human skeletal muscles. J Physiol 558:1005-1012. doi:10.1113/jphysiol.2004.065904
Lauritzen F, Paulsen G, Raastad T, Bergersen LH, Owe SG (2009) Gross ultrastructural changes and necrotic fiber segments in elbow flexor muscles after maximal voluntary eccentric action in humans. J Appl Physiol (1985) 107:1923-1934. doi:10.1152/japplphysiol.00148.2009
Lilja M et al. (2018) High doses of anti-inflammatory drugs compromise muscle strength and hypertrophic adaptations to resistance training in young adults. Acta Physiol (Oxf) 222. doi:10.1111/apha.12948
McHugh MP (2003) Recent advances in the understanding of the repeated bout effect: the protective effect against muscle damage from a single bout of eccentric exercise. Scand J Med Sci Sports 13:88-97
Moore DR, Phillips SM, Babraj JA, Smith K, Rennie MJ (2005) Myofibrillar and collagen protein synthesis in human skeletal muscle in young men after maximal shortening and lengthening contractions. Am J Physiol Endocrinol Metab 288:E1153-1159. doi:10.1152/ajpendo.00387.2004
Moore DR, Young M, Phillips SM (2012) Similar increases in muscle size and strength in young men after training with maximal shortening or lengthening contractions when matched for total work. Eur J Appl Physiol 112:1587-1592. doi:10.1007/s00421-011-2078-x
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Schoenfeld BJ, Ogborn DI, Vigotsky AD, Franchi MV, Krieger JW (2017) Hypertrophic Effects of Concentric vs. Eccentric Muscle Actions: A Systematic Review and Meta-analysis. J Strength Cond Res 31:2599-2608. doi:10.1519/JSC.0000000000001983
Zourdos MC et al. (2015) Repeated Bout Effect in Muscle-Specific Exercise Variations. J Strength Cond Res 29:2270-2276. doi:10.1519/JSC.0000000000000856
Recently, Damas et al (2018) published an interesting review on the role of exercise-induced muscle damage in muscle hypertrophy. Although the paper was well-done overall, my colleague, Bret Contreras, and I felt there were several issues that needed to be highlighted. We endeavored to send a letter to the editor at the journal in which the paper was published (European Journal of Applied Physiology). Unfortunately, the journal has a strict word count for letters to the editor, and the editor asked us to cut down the length of our letter to accommodate the journal’s guidelines. We attempted to comply with this request and submitted a revision, but the editor stated the letter would have to be cut down still further to meet requirements. At that point, we declined a further revision as we did not want to water down our points simply to have the letter published.
Thus, we have decided to post the letter online so that it can be read in its entirety. We have the utmost respect for the authors of the paper and would welcome to publish their rebuttal here if they so choose. Hopefully this will further discussion and point out the nuances of drawing conclusions on a topic as complex as this.
We read with interest the paper by Damas et al (Damas et al. 2017) titled, “The development of skeletal muscle hypertrophy through resistance training: the role of muscle damage and muscle protein synthesis,” which, in part, endeavored to review the role of exercise-induced muscle damage on muscle hypertrophy. This is a multifaceted topic and the authors are to be commended for attempting to delve into its complexities. That said, we feel there are a number of issues in interpretation of research and extrapolation that preclude drawing the inferences expressed in the paper that muscle damage neither explains nor potentiates increases in muscle hypertrophy. The intent of our letter is not to suggest that a causal role exists between hypertrophy and microinjury. Rather, we hope to provide balance to the evidence presented and offer the opinion that the jury is still very much out as to providing answers on the topic.
Firstly, the authors cite a study by Damas et al (Damas et al. 2016) as evidence that muscle damage is not involved in the hypertrophic response. However, this study was not designed to investigate a cause-effect relationship, or even correlation, between muscle damage and growth. While the study eloquently demonstrated that an initial bout of damage was explanatory as to why muscle protein synthesis is not associated with exercise-induced hypertrophy over time, it in no way can be used to draw inferences as to the long-term effects of damage on muscular adaptations. To properly study the topic would require carrying out a longitudinal resistance training (RT) study whereby one group experienced a predetermined level of damage and then comparing with another group that experienced minimal damage. Unfortunately, such a design is problematic as attempting to isolate damage in this fashion would invariably involve altering other RT variables that would confound the ability to draw causality. With respect to the Damas et al (Damas et al. 2016) study, it is impossible to determine whether some level of muscle damage experienced by subjects contributed to the observed hypertrophic changes in the study. Moreover, it is not clear whether more (or less) damage may have influenced hypertrophy over time. The only thing that can be concluded in this regard is that an initial exercise bout in untrained individuals appears to be directed toward structural repair as opposed to hypertrophy; the effects of repeated exposure to varying levels of damage beyond the initial bout cannot be extrapolated from the study design.
Second, the authors go on to cite the recent meta-analysis from our group (Schoenfeld et al. 2017) as evidence that there are no hypertrophic differences between the performance of concentric and eccentric actions and thus, given the well-established link between eccentric actions and micro-injury, indirectly inferring that muscle damage does not play a role in muscle growth. The authors’ conclusion was based on a priori alpha analysis, whereby the reported p-value (p = 0.07) did not reach “statistical significance.” However, null hypothesis testing at a predetermined alpha level has been widely criticized as a flawed statistical method that should not be used to draw practical inferences (Bernards et al. 2017; Gelman and Stern. 2012; Hopkins et al. 2009). A closer inspection of our data using the reported magnitude-based statistics show that eccentric actions may indeed promote a superior hypertrophic response. As noted in our paper, the effect size difference (0.25) showed a modest but potentially meaningful magnitude of effect favoring eccentric exercise, and the 95% confidence intervals (-0.03, 0.52) clearly favored the eccentric condition. Moreover, based on the guidelines for statistics in exercise science proposed by Hopkins et al (Hopkins et al. 2009), results were likely/probably not due to chance alone. Thus, our data actually lend support to a hypertrophic benefit for eccentric actions. It also should be noted that eccentric actions have been shown to produce differential intracellular anabolic signaling responses compared to other muscle actions (Eliasson et al. 2006; Franchi et al. 2014), and the regional hypertrophic changes demonstrated between concentric and eccentric actions in several longitudinal studies have been hypothesized to be resultant to damage along the length of myofibers (Franchi et al. 2014; Hedayatpour and Falla. 2012). It remains speculative as to whether microinjury contributes to these differential effects between muscle actions, but the possibility that it may play a role cannot be dismissed based on current evidence.
Lastly, the authors make the claim that satellite cells (SC) derived from damaging exercise are not involved in hypertrophic adaptations but rather function solely to mediate tissue regeneration. In support of this view, the authors cite a study by Hyldahl et al (Hyldahl et al. 2015) who found no evidence of myonuclear addition for up to 27 days following an initial bout of lengthening contractions. However, as the authors note in their review, myonuclear addition is not realized until an increase in muscle size exceeds ~26%; the theoretical threshold above which additional myonuclei are necessary to support continued growth. A lack of increase in the incorporation of myonuclei therefore would be expected in the Hyldahl et al (Hyldahl et al. 2015) study as minimal hypertrophy would necessarily occur from an acute bout of RT. Accordingly, under these circumstances there would be no impetus for SC-mediated myonuclear addition. Whether SC accretion from exercise-induced damage potentiates hypertrophic increases over time with repeated exercise damaging exercise bouts would require a longitudinal study comparing the effects of two distinct levels of muscle damage. It also is interesting to speculate that an increase in SC via damage may be particularly important for low responders to RT as well as older individuals, as evidence shows that their ability to expand the SC pool is suppressed, which may in turn explain the observed blunted hypertrophic response (Petrella et al. 2006; Petrella et al. 2008).Whether SC derived from micro-injury could enhance hypertrophy in these populations requires future study.
To summarize, the paper by Damas et al (Damas et al. 2017) addresses an important topic for understanding the mechanisms of muscle growth and raises some pertinent considerations as to what role, if any, muscle damage plays in the process. However, in the quest to provide answers to mechanistic questions we must avoid the temptation to prematurely infer conclusions that cannot be supported by the available literature. The question at hand is not whether muscle damage is the primary driver of hypertrophy; clearly it is not as compelling evidence indicates mechanical stress is predominant in this regard. The relevant question is whether muscle damage may enhance the hypertrophic response to regimented RT over time. And to this question, we contend that the current body of evidence is not sufficient to draw conclusions with any degree of confidence. There would seem to be a sound rationale for a potential beneficial effect as previously detailed in the literature (Schoenfeld. 2012). Moreover, Lilja et al (Lilja et al. 2017) recently demonstrated that high doses of anti-inflammatory drugs suppressed hypertrophic adaptations in young, healthy individuals, conceivably by inhibiting the cyclooxygenase (COX) pathway. It is intriguing that the inflammatory response elicited by muscle damage has been implicated in COX induction, and thus raises the possibility that repeated micro-injury from RT may augment its hypertrophic effects. How all this theory plays out in practice remains to be determined and highlights the need for more rigorous research. Until such research is carried out and in the absence of sufficient quality evidence on the topic, scientific protocol dictates the importance of remaining prudent, inquisitive and cautiously skeptical.
References
Bernards JR, Sato K, Haff GG, Bazyler CD (2017) Current Research and Statistical Practices in Sport Science and a Need for Change. Sports 5:87
Damas F, Libardi CA, Ugrinowitsch C (2017) The development of skeletal muscle hypertrophy through resistance training: the role of muscle damage and muscle protein synthesis. Eur J Appl Physiol . doi:10.1007/s00421-017-3792-9 [doi]
Damas F, Phillips SM, Libardi CA et al (2016) Resistance training-induced changes in integrated myofibrillar protein synthesis are related to hypertrophy only after attenuation of muscle damage. J Physiol 594:5209-5222. doi:10.1113/JP272472 [doi]
Eliasson J, Elfegoun T, Nilsson J, Kohnke R, Ekblom B, Blomstrand E (2006) Maximal lengthening contractions increase p70 S6 kinase phosphorylation in human skeletal muscle in the absence of nutritional supply. Am J Physiol Endocrinol Metab 291:1197-1205
Franchi MV, Atherton PJ, Reeves ND et al (2014) Architectural, functional and molecular responses to concentric and eccentric loading in human skeletal muscle. Acta Physiol (Oxf) 210:642-654. doi:10.1111/apha.12225 [doi]
Gelman A, Stern H (2012) The Difference Between “Significant” and “Not Significant” is not Itself Statistically Significant. The American Statistician 60:328-331
Hedayatpour N, Falla D (2012) Non-uniform muscle adaptations to eccentric exercise and the implications for training and sport. J Electromyogr Kinesiol 22:329-333. doi:10.1016/j.jelekin.2011.11.010 [doi]
Hopkins WG, Marshall SW, Batterham AM, Hanin J (2009) Progressive statistics for studies in sports medicine and exercise science. Med Sci Sports Exerc 41:3-13. doi:10.1249/MSS.0b013e31818cb278 [doi]
Hyldahl RD, Nelson B, Xin L et al (2015) Extracellular matrix remodeling and its contribution to protective adaptation following lengthening contractions in human muscle. FASEB J 29:2894-2904. doi:10.1096/fj.14-266668 [doi]
Lilja M, Mandic M, Apro W et al (2017) High doses of anti-inflammatory drugs compromise muscle strength and hypertrophic adaptations to resistance training in young adults. Acta Physiol (Oxf) . doi:10.1111/apha.12948 [doi]
Petrella JK, Kim JS, Cross JM, Kosek DJ, Bamman MM (2006) Efficacy of myonuclear addition may explain differential myofiber growth among resistance-trained young and older men and women. Am J Physiol Endocrinol Metab 291:E937-46. doi:10.1152/ajpendo.00190.2006
Petrella JK, Kim J, Mayhew DL, Cross JM, Bamman MM (2008) Potent myofiber hypertrophy during resistance training in humans is associated with satellite cell-mediated myonuclear addition: a cluster analysis. J Appl Physiol 104:1736-1742
Schoenfeld BJ, Ogborn DI, Vigotsky AD, Franchi MV, Krieger JW (2017) Hypertrophic Effects of Concentric vs. Eccentric Muscle Actions: A Systematic Review and Meta-analysis. J Strength Cond Res 31:2599-2608. doi:10.1519/JSC.0000000000001983 [doi]
Schoenfeld BJ (2012) Does exercise-induced muscle damage play a role in skeletal muscle hypertrophy? J Strength Cond Res 26:1441-1453. doi:10.1519/JSC.0b013e31824f207e
The beauty of science is that is self-correcting. When a study is published, others get to scrutinize the data and methods. When issues arise, the scientific community gets to discuss and debate the findings, and when appropriate, challenge their veracity.
Recently, I collaborated with some of the world’s top sports scientists on a letter to the editor about a study published in the Journal of Strength and Conditioning Research, that showed an extremely large anabolic effect to consuming a supplement containing HMB+ATP. We wrote an extensive letter that covered our issues with the paper in hopes of seeking truth in science. However, we had to substantially cut down our response to conform to the journal’s policy of allowed only 400 words in such letters. This watered down our points so that the true impact was markedly diminished.
Thus, I wanted to present the unedited version of our letter here so that further discussion can be had on the topic. Only through discourse can we maintain confidence in the research process and facilitate true evidence-based practice.
Extraordinary changes in body composition and performance with supplemental HMB-FA+ATP
Stuart M. Phillips, Ph.D., McMaster University
Alan Aragon, M.S., California State University, Northridge
Shawn M. Arent, Ph.D., Rutgers University
Graeme L. Close, Ph.D., Liverpool John Moores University
D. Lee Hamilton, Ph.D., University of Stirling
Eric R. Helms, M.S., M.Phil, Sports Performance Research Institute New Zealand
Jeremy P. Loenneke, Ph.D., The University of Mississippi
Layne Norton, Ph.D., Owner BioLayne LLC
Michael J. Ormsbee, Ph.D., Florida State University
Craig Sale, Ph.D., Nottingham-Trent University
Brad J. Schoenfeld, Ph.D., Lehman College
Abbie Smith-Ryan Ph.D., University of North Carolina
Kevin D. Tipton, Ph.D., University of Stirling
Matthew D. Vukovich, Ph.D., South Dakota State University
Colin Wilborn, Ph.D., University of Mary Hardin-Baylor
Darryn Willoughby, Ph.D. Baylor University
The authors of this letter read with skepticism the recent report from Lowery et al. (10), employing a supplement that provided 3g of beta-hydroxy-beta-methyl butyrate as a free acid (HMB-FA; three doses of 1g each) plus 400mg of oral adenosine triphosphate (ATP) in young men who resistance-trained for 12wk. Lowery et al. (10) report gains in lean mass and performance that are greater than those reported in a similarly surprising earlier study from Wilson et al. (18). Our skepticism of the results reported by Lowery et al. (10) exists on several levels. However, our collective disbelief of these data rests on the collective experience of the authors of this letter, who have conducted more than 60 resistance training studies, and who have never observed gains in lean body mass that are of a similar incredibly uniform magnitude as those reported by Lowery et al. (10). As opposed to the often-observed heterogeneity in resistance training-induced hypertrophy, Lowery et al. (10) must have observed remarkably consistent between-group changes in muscle mass to find statistical significance between the supplemented and placebo groups. What makes this more remarkable in that this was seen in a total of 17 subjects (n=9 placebo, n=8 HMB-FA+ATP). We are particularly nonplussed on this point since the sharp ‘divergence’ between the HMB-FA+ATP versus placebo groups occurred in the face of what the authors refer to as an optimal training paradigm, with optimal nutritional support, and the advice of an experienced dietitian. And thus the difference is due, ostensibly, to two compounds (HMB-FA and/or ATP), which have been studied previously and resulted in a trivial training-induced adaptive advantage (13). Would the authors be willing to share subjects’ individual data? We ask since the mean gain in lean body mass in the supplemented group was ~8.5kg (10), meaning there had to be some subjects who gained more and uniformly so for the treatments (in only 17 subjects) to be so robustly different! This is also an astounding gain of lean body mass when one considers that the subjects were previously resistance-trained and so would have had less propensity to gain lean body mass (11). We could not ascertain the absolute values for the beginning and final values for body composition and so readers would have to make assumptions (since the reported data were incomplete and given as percentages) as to how much body composition changed. Would the authors be willing to present these data?
We are aware of a previous letter from Hyde et al. (7) asking for clarification from Lowery et al. (10) on their methods. Thus, our concern is clearly shared by others and, given the number and research experience of the authors on this letter, quite widespread. In their reply to this letter (7) Lowery et al. (10) went to great lengths to compare their rates of hypertrophy with those previous reported by other studies. Importantly, however, a number of studies discussed by Lowery et al. (10) as having comparable ‘rates’ of hypertrophy were markedly (5wk) shorter than their 12wk intervention (14). Thus, while ‘rates of hypertrophy’ (assessed with different methods and in different labs (3, 9, 14, 16), in different study populations, being overfed and not exercising (3), with different dietary backgrounds (3, 9, 14, 16), and/or consuming different supplements (i.e., creatine) (9, 14, 16), may have been similar (or greater) to those seen by Lowery et al. (10) the total accrued (over 12wk) lean body mass cannot be assumed to be linear and extrapolated to that seen in their study. Further, what is revealing is the astonishing performance differences reported by Lowery et al. (10), which implies not only greater total lean mass gains but an extraordinary functionality to the accrued lean mass or by some other unexplained mechanism. That is, why did HMB-FA+ATP impart an astonishing ‘functional overreaching’ response with the optimal training paradigm, with great dietary support, and in highly trained and motivated subjects and not in the placebo group?
It is important to understand the limitations of dual-energy x-ray absorptiometry (DXA), which derives by difference fat- and bone-free mass, which is a variable that is not equivalent to muscle (6, 12). The limitations of DXA and ultrasound, the two muscle-based outcome measures have been clearly outlined in a recent review (6). As stated, DXA “Cannot specifically discern skeletal muscle mass [bold added] and quality as can CT [computerized tomography] and MRI [magnetic resonance imaging]” and is subject to changes in hydration status (6). For ultrasound, “Technical skill required. Excess transducer pressure and orientation can influence muscle size measurements. Identification of reproducible measurement sites critical. Care needed to make sure muscle is in relaxed state. Conditions such as proximity to exercise bout, hydration, are important to control” (6). Lowery et al. (10) report nothing with respect to the ultrasound machine used, the hydration or feeding status of their subjects, or proximity to an exercise. It would be useful for readers if Lowery et al. (10) would detail for the readers the training level of the researcher(s) who conducted the ultrasound tests (inter-rater reliability of more than one researcher was used), noted whether more than one researcher carried out testing, whether these testers were blinded to the group assignment while completing/analyzing the thickness measures, and clarify the temporal aspects of testing to determine if there may be any associated confounding issues.
In the response to Hyde et al (7) Lowery et al. (10) purport to have selected “…a responsive population who possess a quantity of lean mass indicative of previous responses to resistance training…” Notwithstanding the scientific inaccuracy of this statement, the authors must have gone through a screening process of sorts to recruit 17 subjects with lean mass “…an order of magnitude [we note that an order of magnitude is defined as 10-times greater so this cannot be the case] higher than average lean mass typically seen in recreationally trained subjects…” Could the authors please state what the exact criteria for inclusion as a subject in this study were? Can the authors please detail the screening process describing how many subjects were recruited and screened, final entered the study, and dropouts, to reach this number of subjects meeting these criteria and who completed the protocol? Please also clarify if the subjects were randomised to treatment and placebo groups or pair matched based on body mass, lean body mass, strength or other variable.
The only form of HMB for which there is plausible data showing a mechanistic underpinning for its potential role aiding in muscle protein turnover is for calcium-HMB (15). We are unaware of any similar proof-of-principle mechanistic data for the free acid form of HMB despite apparently greater bioavailability and uptake (into what tissue is unclear) (4). Do the authors know of any data showing that HMB-FA has a similar credible effect as calcium-HMB on human muscle protein turnover (15)? We note that leucine had the same anabolic effects as calcium-HMB (15). We also note that dietary protein can exert a positive effect on gains in muscle mass with resistance training (1) and yet the placebo group did not appear to respond at all to the overreaching phase. As another ingredient of the supplement used by Lowery et al (10), ATP would appear to be, given an extraordinarily low bioavailability (2), to be unusable. However, we note that Wilson et al. (17), using the same study protocol as that employed by Lowery et al. (10), reported that ATP (400mg/d) resulted in a positive effect on muscle mass, strength, and power gains. This seems to us highly improbable given that oral ATP even up to doses of 5000mg/d [more than an order of magnitude greater than the dose used by Wilson et al. (17) and Lowery et al. (10)] for 4wk leads only to increases in circulating uric acid with no detectable changes in ATP in the blood (2) let alone muscle. Thus, as opposed to an inconsequential increase in post-exercise blood flow induced by the ATP (8) in the HMB-FA+ATP supplemented group, we find it biologically implausible that 400mg/d of oral ATP would exert any effect on processes leading to enhanced performance let alone hypertrophy. What is remarkable is that given the expert dietary advice and total protein intake of the subjects studied, the optimal training program, and ‘responsive’ subjects that the differences in lean mass (and performance) between the HMB-FA+ATP and placebo groups are as impressive as they are (10). Moreover, that these differences are statistically significant in such a small sample of subjects and ascribed to an, as yet, mechanistically untested form of HMB and a biologically unavailable quantity of ATP.
We ask, in accordance with all reasonable guidelines regarding full disclosure of potential conflicts of interest now in place at many journals (including the Journal of Strength and Conditioning Research – http://journals.lww.com/nsca-jscr/Pages/InstructionsforAuthors.aspx – accessed Oct 1, 2016) that Dr. Wilson and Mr. Lowery disclose here whether they have ever received travel expenses, stipends, or honoraria, or shares associated with their work and the companies involved with ATP and/or HMB and/or whether they or their spouses have any public or private interests with Metabolic Technologies, Inc. and/or companies selling or dealing in oral ATP supplements or their affiliates? This is not an accusation and we fully accept that neither Dr. Wilson nor Mr. Lowery may have ever received such support, but believe this is an honest and reasonable question to ask on both scientific and ethical grounds (5) and it is standard practice to make such disclosures.
Reference List
1. Cermak NM, Res PT, de Groot LC, Saris WH and van Loon LJ. Protein supplementation augments the adaptive response of skeletal muscle to resistance-type exercise training: a meta-analysis. Am J Clin Nutr 96: 1454-1464, 2012.
2. Coolen EJ, Arts IC, Bekers O, Vervaet C, Bast A and Dagnelie PC. Oral bioavailability of ATP after prolonged administration. Br J Nutr 105: 357-366, 2011.
3. Forbes GB, Brown MR, Welle SL and Lipinski BA. Deliberate overfeeding in women and men: energy cost and composition of the weight gain. Br J Nutr 56: 1-9, 1986.
4. Fuller JC, Jr., Sharp RL, Angus HF, Baier SM and Rathmacher JA. Free acid gel form of beta-hydroxy-beta-methylbutyrate (HMB) improves HMB clearance from plasma in human subjects compared with the calcium HMB salt. Br J Nutr 105: 367-372, 2011.
5. Gorman DM. Can We Trust Positive Findings of Intervention Research? The Role of Conflict of Interest. Prev Sci 2016.
6. Heymsfield SB, Gonzalez MC, Lu J, Jia G and Zheng J. Skeletal muscle mass and quality: evolution of modern measurement concepts in the context of sarcopenia. Proc Nutr Soc 74: 355-366, 2015.
7. Hyde PN, Kendall KL and LaFountain RA. Interaction of beta-hydroxy-betmethylbutyrate free acid and adenosine triphosphate on muscle mass, strength, and power, in resistance trianed invidividuals. J Strength Cond Res 30: e10-e14, 2016.
8. Jager R, Roberts MD, Lowery RP, Joy JM, Cruthirds CL, Lockwood CM, Rathmacher JA, Purpura M and Wilson JM. Oral adenosine-5′-triphosphate (ATP) administration increases blood flow following exercise in animals and humans. J Int Soc Sports Nutr 11: 28, 2014.
9. Jowko E, Ostaszewski P, Jank M, Sacharuk J, Zieniewicz A, Wilczak J and Nissen S. Creatine and beta-hydroxy-beta-methylbutyrate (HMB) additively increase lean body mass and muscle strength during a weight-training program. Nutrition 17: 558-566, 2001.
10. Lowery RP, Joy JM, Rathmacher JA, Baier SM, Fuller JC, Jr., Shelley MC, Jager R, Purpura M, Wilson SM and Wilson JM. Interaction of Beta-Hydroxy-Beta-Methylbutyrate Free Acid and Adenosine Triphosphate on Muscle Mass, Strength, and Power in Resistance Trained Individuals. J Strength Cond Res 30: 1843-1854, 2016.
11. Morton RW, Oikawa SY, Wavell CG, Mazara N, McGlory C, Quadrilatero J, Baechler BL, Baker SK and Phillips SM. Neither load nor systemic hormones determine resistance training-mediated hypertrophy or strength gains in resistance-trained young men. J Appl Physiol (1985) 121: 129-138, 2016.
12. Prado CM and Heymsfield SB. Lean tissue imaging: a new era for nutritional assessment and intervention. JPEN J Parenter Enteral Nutr 38: 940-953, 2014.
13. Rowlands DS and Thomson JS. Effects of beta-hydroxy-beta-methylbutyrate supplementation during resistance training on strength, body composition, and muscle damage in trained and untrained young men: a meta-analysis. J Strength Cond Res 23: 836-846, 2009.
14. Stone MH, Sanborn K, Smith LL, O’Bryant HS, Hoke T, Utter AC, Johnson RL, Boros R, Hruby J, Pierce KC, Stone ME and Garner B. Effects of in-season (5 weeks) creatine and pyruvate supplementation on anaerobic performance and body composition in American football players. Int J Sport Nutr 9: 146-165, 1999.
15. Wilkinson DJ, Hossain T, Hill DS, Phillips BE, Crossland H, Williams J, Loughna P, Churchward-Venne TA, Breen L, Phillips SM, Etheridge T, Rathmacher JA, Smith K, Szewczyk NJ and Atherton PJ. Effects of leucine and its metabolite beta-hydroxy-beta-methylbutyrate on human skeletal muscle protein metabolism. J Physiol 591: 2911-2923, 2013.
16. Willoughby DS, Stout JR and Wilborn CD. Effects of resistance training and protein plus amino acid supplementation on muscle anabolism, mass, and strength. Amino Acids 32: 467-477, 2007.
17. Wilson JM, Joy JM, Lowery RP, Roberts MD, Lockwood CM, Manninen AH, Fuller JC, De Souza EO, Baier SM, Wilson SM and Rathmacher JA. Effects of oral adenosine-5′-triphosphate supplementation on athletic performance, skeletal muscle hypertrophy and recovery in resistance-trained men. Nutr Metab (Lond) 10: 57, 2013.
18. Wilson JM, Lowery RP, Joy JM, Andersen JC, Wilson SM, Stout JR, Duncan N, Fuller JC, Baier SM, Naimo MA and Rathmacher J. The effects of 12 weeks of beta-hydroxy-beta-methylbutyrate free acid supplementation on muscle mass, strength, and power in resistance-trained individuals: a randomized, double-blind, placebo-controlled study. Eur J Appl Physiol 114: 1217-1227, 2014.
Dating back to my early years as a personal trainer in the mid-90’s, I began to become intrigued by the concept of “loading zones” whereby different rep ranges purportedly could bring about differential effects on muscular adaptations. Prevailing wisdom at the time was that heavy loads (1-5 RM) promote maximal strength gains, moderate loads (6-12 RM) elicit maximal increases in muscle mass, and light loads (15+ RM) produce the greatest improvements in local muscular endurance. This concept, discussed extensively in exercise science texts, was termed the “strength-endurance continuum” (see the image below) although direct research on the topic was limited.
The topic of rep ranges was so intriguing to me that I ultimately made it a focus of my doctoral work. Several years ago I published the data collected in accordance with my dissertation study. In brief, the study looked at muscular adaptations in a “bodybuilding-type” routine versus a “powerlifting-type” routine in resistance-trained men when the routines were equated for volume load. Consistent with the “strength-endurance continuum” concept, the study found that the powerlifting-type routine produced the greatest strength increases. Contrary to prevailing wisdom, however, both routines produced similar increases in hypertrophy of the biceps brachii. You can read my write-up of the routine in this blog post.
Importantly, the findings of that study are specific to the respective routines being equated for volume load. While this provides interesting insights on the topic, it is impractical to carry out long-term training with very heavy loads at the volumes used in that study (in fact, the majority of subjects in the powerlifting-type group displayed clear signs of overtraining by study’s end). So the question arises as to whether results would differ if an equal number of sets were performed between heavy and moderate loads?
What We Did
Nineteen college-aged men were recruited to participate in the study. All subjects had at least one year of resistance training experience lifting at least three times per week. Subjects were randomized to either a group that trained in a heavy loading range of 2-4 repetitions per set (HEAVY) or a group that trained in a moderate loading range of 8-12 repetitions per set (MODERATE). All other aspects of the subjects’ program were kept constant between groups. The training protocol consisted of seven exercises that worked all the major muscles of the body each session, with three sets performed per exercise. Training was carried out on three non-consecutive days per week for eight weeks. Subjects were instructed to maintain their normal daily nutritional intake and no differences in either calories or macronutrient consumption was found between groups over the course of the study.
What We Measured
We tested hypertrophy of the elbow flexors, elbow extensors, and quads using b-mode ultrasound. Maximal strength was assessed in the squat and bench press via 1 repetition maximum (RM) testing. Upper body local muscular endurance was determined by assessing the subject’s initial 1RM in the bench press for as many repetitions as possible to muscular failure.
What We Found
The infographic to the left (courtesy of Thomas Coughlin) illustrates the results of the study. In general, overall muscle growth was greater for MODERATE compared to HEAVY. Increases in thickness of the elbow flexors (i.e. biceps brachii and brachialis) modestly favored the use of moderate reps (~5% vs ~3% for MODERATE vs HEAVY, respectively) while gains in the quads substantially favored the moderate rep group (10% vs 4% for MODERATE vs HEAVY, respectively). Interestingly, growth of the triceps was similar between groups.
On the other hand, strength gains were decidedly greater when training with heavy loads. This was seen for improvements in both the 1RM squat (29% versus 16%) and bench press (14% vs 10%), which favored HEAVY compared to MODERATE. Muscle endurance increases were similar between rep ranges.
What are the Practical Implications
The study provides evidence that training with heavy loads helps to maximize muscle strength and training with moderate loads promotes greater increases in muscle mass. Importantly, these findings are specific to routines where the number of sets are equated. At face value, this is consistent with the “strength-endurance continuum” and supports what gym bro’s have been preaching for years in regards to rep ranges.
However, when the results are taken into account with my previous study on the topic that equated volume load, an interesting hypothesis emerges. Since strength gains were greater with heavy loads in both studies, it can be concluded that low-rep training is best for maximizing strength regardless of volume load. On the other hand, since the previous study showed no differences in hypertrophy between conditions when volume load was equated, it can be inferred that volume load is a greater driver of muscle growth irrespective of the rep range. In other words, strength is maximized even with lower training volumes provided heavy loads are used, but higher volumes are needed to maximize gains in size whether you train with moderate or heavy weights.
The study had several limitations including a relatively small sample size, the use of a single-site measurement for muscle growth on each of the respective muscles, and possible confounding from the “novelty factor” (i.e. virtually all the subjects trained with moderate loads, so it is possible that the novel stimulus for those in the heavy load group might have impacted results). These issues must be taken into account when attempting to draw evidence-based conclusions. Most importantly, one study is never the be-all-end-all when it comes to answering questions on an applied science topic. Rather, each study should be considered a piece in a puzzle that lends support to a given theory. The practical implications of programming loading zones will become increasingly clear as we continue to build on this line of research. For now, though, the evidence suggests to train heavy if your goal is maximal strength, and to focus on accumulating volume for maximal gains in muscle mass.
Wanted to update everyone on all that’s been happening; so much to share!
First, I’ve agreed to write a textbook on muscle hypertrophy, to be published by Human Kinetics — one of the leading publishers on the science of exercise and nutrition. The book will be geared towards fitness professionals and university programs. I’m totally stoked to provide an evidence-based resource on a subject that has long relied on gym lore and bro-science. Estimated pub date is April of 2016.
I’ve also agreed to write a monthly column for Flex Magazine. The column will discuss science-based application of hypertrophy and fat loss practices. It’s a real kick for me to be a regular columnist for a mag that I grew up reading. My first column is slated for the November issue.
Research-wise, I’m currently finishing up a study on body comp changes associated with fasted cardio and another on muscle activation during different loading intensities in the bench press. During the fall I have multiple studies set to get underway including a training frequency study investigating muscular adaptations in split vs. total body routines, another comparing functional transfer between the squat and leg press, and yet another that will evaluate the effects of protein timing pre- versus post-workout on muscle hypertrophy in well-trained subjects. I look forward to sharing the results of these and other studies currently in review when they become available.
Okay, that out of the way, here are some links that I thought you’d find informative. As always, I appreciate your continued support.
• I recently lectured at the CanFitPro Conference in Toronto. While there, I got a chance to record a few interview segments for Omar Isuf’s YouTube channel. In this segment we discuss repetition ranges for maximizing muscle hypertrophy. Give this a watch and you’ll see why Omar lives up to his nickname, King of YouTube Fitness.
• I was interviewed along with my partner-in-science, Alan Aragon, on the We Do Science Podcast. Here Alan and I discuss the complexities of nutrient timing, delving into both the science and practical applications on the topic. Bonus discussion on a related topic: whether there is any fat loss benefit to doing fasted cardio. Click on Episode #8.
• I’ve appeared numerous times on Superhuman Radio; this segment might be my favorite yet. Here I discuss whether it’s possible to gain muscle simultaneously while simultaneously losing fat. Host Carl Lanore is consistently one of the best interviewers in the biz and he again shows why by asking all the right questions. l
• My friend and colleague Tom Venuto wrote an excellent post on delayed-onset muscle soreness and its relevance to muscular gains. The article covers the science in an understandable fashion, and provides solid take-home advice.
• Speaking of Tom Venuto, he wrote what I think is the most detailed review of my book, The M.A.X. Muscle Plan. Always an honor to receive praise from a true fitness pro such as Tom.
• In case you missed it, I recently published this study showing muscle activation during the leg press at 30% 1RM to failure produced significantly lower muscle activation compared to 75% 1RM. I also wrote an accompanying blog post where I break things down into consumer-friendly language and discuss the study’s implications.
• Finally, my good friend Bret Contreras wrote this terrific article that delved into the free-weights vs. machines debate. As mentioned earlier, I will be collaborating on a study examining this topic; Bret’s post provides excellent commentary on its complexities. While you’re at it, make sure to read through the references at the end of the article; it’s patently clear research doesn’t support the claims made by certain fitness pros.
Been a little while since my last blog post. Here’s an update on what’s been going on:
• I just received acceptance from the Journal of Strength and Conditioning Research on study showing that you can target different areas of the hamstrings by varying exercise selection. The study evaluated muscle activation during performance of the stiff legged deadlift and the leg curl. We looked both at activation of the medial hamstrings (semiteninosus and semimembranosus) versus lateral hamstrings (biceps femoris), as well as the upper and lower aspects of the muscle. While previous studies have shown that the medial versus lateral hamstrings can be targeted, this is the first study to document differences in the upper and lower portions. Very interesting findings with novel practical implications. I’ll have lots more to say when the study is officially published, which should be soon.
• The internet has given rise to a legion of arm-chair scientists who have little appreciation for what it actually takes to carry out a research study. The upshot is rampant misinterpretation of data and absurd criticisms about study design, often based solely from reading the abstract. That’s why it’s refreshing to see when someone writes an insightful commentary on a study. Such is the case here, where Lyle McDonald provides an excellent critical analysis of my recent study comparing muscular adaptations in bodybuilding- vs. powerlifting-type training. The write-up shows keen insight into understanding the nuances of research methodology and the ability to draw applicable conclusions from the results. Really well done and worth the read.
• I have a number of speaking engagements coming up in the next few weeks. First, I’ll be at the ISSN Annual Conference in Clearwater Beach, Florida discussion how to periodize a muscle-building routine. Next, I’ll be at the NSCA International Conference in Murcia, Spain speaking on a new paradigm for hypertrophy training based on my recent research. Final stop is the NSCA National Conference in Las Vegas, Nevada where I’ll co-present with the incomparable Alan Aragon on practical applications for nutrient timing. If you’re attending any of these events, make sure to stop by and say hello.
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