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.
A common controversy in the fitness field is whether to use high-intensity interval training (HIIT) or moderate-intensity continuous training (MICT) for optimizing fat loss. The debate rages on, with proponents on both sides of argument supporting their positions with logical rationale.
To help bring clarity to the topic, our group recently carried out a meta-analysis of existing literature. This paper came to fruition after a previous meta-analysis showed superior body comp benefits for HIIT, going as far as alluding to HIIT as a “magic bullet” for fat loss. The paper received a huge amount of media attention, with some of the most prominent magazines and news outlets touting the findings in feature articles. However, a subsequent letter to the editor noted that the paper had multiple issues in reporting and analysis. Sadly, the inconsistencies were never addressed by the authors, ultimately leading to the paper’s retraction.
In short, our results refute those of the previous meta, providing compelling evidence that HIIT and MICT produce very similar decreases in fat loss and increases in fat-free mass over time. In technical terms, the point estimates for all measures hovered around zero with very narrow confidence intervals (see the accompanying figures below). In layman’s terms, there were virtually no differences in body composition between methods under the conditions studied. None. Intriguingly, there were similar rates of adherence (high) and adverse events (low) between methods as well.
Take-home: We can confidently state that HIIT cannot be considered a “magic bullet” for fat loss; MICT is equally as effective for achieving this outcome.
It’s important to note that the absolute amount of fat loss from cardio in the studies analyzed was quite small, amounting to an average of less than a pound over 12 weeks. Tightly controlled research shows that cardio can produce meaningful reductions in body fat, but it requires a large time commitment to achieve these results (in this case, ~11 hours per week)—a commitment beyond what most people are willing and able to dedicate. This finding reinforces the fact that diet is the most effective way to lose fat. That said, emerging evidence indicates that cardio is a beneficial supplement to fat loss regimens, particularly for sustaining long-term weight maintenance (ideally combined with resistance training, which is arguably of even greater value in this regard).
There are several important caveats to findings: First, the vast majority of studies instructed subjects to follow their usual diet as opposed to providing a structured nutritional regimen. Thus, it’s not clear if and how combining HIIT or MICT with a diet-induced energy deficit may affect results. Second, the studies did not take into account the effects of combining cardio with resistance training (a.k.a. concurrent training). It’s possible there may be a differential interaction (i.e. one condition has a more pronounced interaction than the other) when the two modalities are combined, either from an acute interference effect or perhaps chronically from overtraining. Third, there is a paucity of research on those with low body fat levels (e.g. bodybuilders, athletes, etc.); it remains to be determined if different cardio methods may impact the ability to further reduce body fat (i.e. into single-digit percentages) in these individuals. Finally, the meta-analysis is specific to the effects of cardio on body composition. There is evidence that HIIT training may confer additional health-related benefits over and above that seen with MICT, at least in certain outcomes.
The bottom line is that, from a body comp standpoint, you should choose an aerobic method based on preference. Results with HIIT are accomplished in less than half the time as MICT, but HIIT requires a higher level of exertion that heightens temporary discomfort. For situations specific to the study limitations (i.e. cardio performed in combination with restrictive diets, resistance training, and/or those with low body fat levels), experimentation is warranted to tailor prescription to your individual results. Finally, note that the choice does not necessarily have to be binary; you can opt to perform some HIIT sessions and some MICT sessions. Research can help to guide exercise prescription, but ultimately you must determine the best course of action based on individual needs, abilities, and goals.
It’s well-established that mechanical tension is the primary mechanism responsible for muscle hypertrophy (i.e., increases in muscle size). Simply stated, mechanical tension can be defined as the stress applied to a muscle, generally (although not exclusively) from an external resistance. Resistance can be applied to the muscle in various forms including but not limited to free weights, cable pulleys, pneumatics, hydraulics and body weight.
Here’s how things play out in practice. Let’s say you perform a set of dumbbell arm curls. During each repetition, the imposed load from the dumbbells place a stress on your arm flexors (i.e. biceps brachii, etc). Receptors in the working muscle fibers (i.e. mechanoreceptors) sense the applied forces and consequently convert the associated mechanical signals into chemical signals via a phenomenon called mechanotransduction. A cascade of intracellular (i.e. within the muscle fiber) enzymes then facilitate anabolic processes from these chemical signals, which drives the synthesis of proteins that build muscle. Numerous anabolic and catabolic pathways have been identified, and the extent of their activation/de-activation ultimately determines how much muscle you build.
Based on the aforementioned information, it may seem that using very heavy weights would necessarily be ideal for maximizing muscle mass; the heavier the better. After all, heavier loads impose greater forces on muscles, and thus there theoretically should be higher levels of mechanical tension created during such training, right? Well, if that were in fact the case, then powerlifting routines would be optimal for bodybuilding. Both controlled research and anecdotal experience in the field tell us that’s not the case.
How can this be?
Intrigued? Then stay tuned for Part 2 of this series, which will delve into the nuances of mechanical tension and discuss why the topic is much more complex than simply focusing on the absolute amount of weight lifted.
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]
10.1096/fj.13-229799
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
Nakagawa S, Cuthill IC (2007) Effect size, confidence interval and statistical significance: a practical guide for biologists. Biol Rev Camb Philos Soc 82:591-605. doi:BRV27 [pii]
10.1111/j.1469-185X.2007.00027.x
Rahbek SK, Farup J, Moller AB, Vendelbo MH, Holm L, Jessen N, Vissing K (2014) Effects of divergent resistance exercise contraction mode and dietary supplementation type on anabolic signalling, muscle protein synthesis and muscle hypertrophy. Amino Acids 46:2377-2392. doi:10.1007/s00726-014-1792-1
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
Today marks the first day of the new year and the gyms are going to be packed with people whose resolution is to get into shape. Problem is, the vast majority will have quit working out before the end of February. A few things to remember if you’re new to training or getting back after a lengthy layoff:
1. You’re not going to change your body in a week, so don’t overdo it at the beginning; you’ll just end up overly sore which will diminish your ability and desire to train. Start off slow and don’t push it the first few sessions so that your body acclimates to the stress of exercise. As you progress, gradually increase the intensity of training over time in a manner necessary to continually challenge your body to realize continued positive adaptations.
2. Have a plan. If you’re aimlessly walking around the gym deciding what to do, chances are you won’t get optimal benefits. Exercise is a science and should be approached accordingly. Set your goals, create a program consistent with your goals, and then follow the program you’ve laid out. If it’s not working the way you want over time, then assess and refine as required. One of my favorite quotes: Those who fail to plan, plan to fail.
3. Know how to perform exercises properly. Overall the form I see people use in the gym is anywhere from poor to horrendous. Not performing an exercise with good biomechanics at the very least will diminish your results, and at worst will get you injured; both outcomes are demotivating. If needed, consult with a qualified personal trainer. Alternatively, there are plenty of excellent video tutorials from top fitness pros on exercise performance; watch them and learn before setting out on your own.
4. Most importantly, choose a program that fits your lifestyle. Getting results is a lifetime commitment. If a program is not sustainable over the long-term then it’s meaningless.
Below is an excerpt from my book, Strong & Sculpted that discusses my current approach to warming up prior to resistance training. I neglected to include a chapter on the topic in my book, M.A.X. Muscle Plan so for those following this program, the same info applies.
Warm-Up
To prepare your body for the demands of intense exercise, you should warm up prior to your lifting session. The warm-up contains two basic components: a general warm-up and a specific warm-up. Here’s what you need to know about each component for a safe, effective workout.
General Warm-Up
The general warm-up is a brief bout of low-intensity, large muscle–group, aerobic-type exercise. The objective is to elevate your core temperature and increase blood flow, which in turn enhances the speed of nerve impulses, increases nutrient delivery to working muscles and the removal of waste by-products, and facilitates oxygen release from hemoglobin and myoglobin.
A direct correlation exists between muscle temperature and exercise performance: when a muscle is warm, it can achieve a better contraction. As a rule, the higher a muscle’s temperature is (within a safe physiological range), the better its contractility. And because better contractility translates into greater force production, you’ll ultimately achieve better muscular development.
What’s more, an elevated core temperature diminishes a joint’s resistance to flow (viscosity). This is accomplished via the uptake of synovial fluid, which is secreted from the synovial membrane to lubricate the joint. The net effect is an increase in range of motion and improved joint-related resiliency. Better yet, these factors combine to reduce the risk of a training-related injury.
Suffice it to say that the general warm-up is an important part of a workout.
Virtually any cardiorespiratory activity can be used for the general warm-up. Exercises on equipment such as stationary bikes, stair climbers, and treadmills are fine choices, as are most calisthenic-type exercises (e.g., jumping jacks, burpees). Choose whatever activity you desire as long as the basic objective is met.
The intensity for the general warm-up should be low. To estimate intensity of training, I like to use a rating of perceived exertion (RPE) scale. My preference is the category-ratio RPE scale, which grades perceived effort on a scale from 0 to 10 (0 is lying on your couch, and 10 is an all-out sprint). Aim for an RPE of around 5, which for most people is a moderate walk or slow jog. You can use the talk test as an intensity gauge. With this method, you base intensity on your ability to carry on a conversation; if you have to pause to take a breath while speaking a sentence, you’re working too hard.
Five to ten minutes is all you need for the general warm-up—just enough to break a light sweat. Your resources should not be taxed, nor should you feel tired or out of breath either during or after performance. If so, cut back on the intensity. Remember, the goal here is merely to warm your body tissues and accelerate blood flow—not to achieve cardiorespiratory benefits or reduce body fat.
Specific Warm-Up
The specific warm-up can be considered an extension of the general warm-up. By using exercises that are similar to the activities in the workout, the specific warm-up enhances neuromuscular efficiency for the exercise you are about to perform. In essence, your body gets to rehearse the movements before you perform them at a high level of intensity, translating into better performance during your working sets.
To optimize transfer of training, the exercises in the specific warm-up should mimic the movements in the workout as closely as possible. For example, if you are going to perform a bench press, the specific warm-up would ideally include light sets of bench presses. A viable alternative would be to perform push-ups because the movement pattern is similar to that of a bench press, although the specificity, and thus transfer, would not be as great as with light sets of the given movement. Always stop specific warm-up sets well short of fatigue. The object is not to fatigue your muscles, but rather to get a feel for the exercise so that you’re physically and mentally prepared for intense training.
The specific warm-up is particularly important when training in low-repetition ranges (~ five reps or fewer). I recommend at least a couple of specific warm-up sets per exercise during low-rep training. As a general rule, the first set should be performed at ~40 to 50 percent of 1RM; and the second set, at ~60 to 70 percent of 1RM. Six to eight reps is all you need in these sets—any more is superfluous and potentially counterproductive. Following the specific warm-up, you should be ready and able to plow into your working sets.
The need for specific warm-up sets in medium- to high-rep-range training remains questionable. I recently collaborated on a study that investigated the effects of a warm-up on the ability to carry out repetitions to failure at 80 percent of 1RM (a weight that allows performance of about eight reps) in the squat, bench press, and arm curl (Ribeiro et al., 2014). The verdict: Warming up showed no beneficial effects on the number of repetitions performed in medium- to high-rep-range training nor in a measure called the fatigue index, which is a formula that assesses the decline in the number of repetitions across the first and last sets of each exercise.
At face value these results suggest that warming up is pretty much useless prior to submaximal resistance training. Despite the currently held belief that a specific warm-up enhances exercise performance, no benefits were seen when compared to no warm-up at all. Intuitively, this seems to make sense given that the initial repetitions of a submaximal lifts are in effect their own specific warm-up, and increasing core temperature might be superfluous from a performance standpoint when multiple reps are performed.
It should be noted, however, that we found a slight advantage to performing a specific warm-up prior to the squat (although results did not rise to statistical significance); the specific warm-up prior to the biceps curl seemed to be somewhat detrimental. Thus, more complex movement patterns seem to benefit from the practice effect of a specific warm-up, although this would be of no value prior to simple exercises.
Taking the evidence into account, here’s my recommendation: When performing medium-rep-range work (8 to 12 reps per set), perform a specific warm-up prior to multijoint free weight exercises. One set at about 50 percent of 1RM is all you need to obtain any potential benefits.
Specific warm-up sets are not necessary when training with high reps (15+ reps per set). In this instance, because you’re already using light weights, the initial repetitions of each working set serve as rehearsal reps. What’s more, performance of warm-up sets is counterproductive to the goal of maximizing training density to bring about desired metabolic adaptations.
What About Stretching?
Static stretching is commonly included as part of a prelifting warm-up. This method of flexibility training involves moving a joint through its range of motion to the point where you feel slight discomfort, and then holding the position for a period of time (generally about 30 seconds). Most protocols involve performing several sets of static holds and then moving on to stretches for other muscles. It’s commonly believed that the addition of stretches to a warm-up further reduces injury risk while enhancing physical performance.
In recent years, however, the benefits of preexercise static stretching have come under scrutiny. A large body of research shows that the practice does not decrease injury risk (Thacker et al., 2004). Yes, improving flexibility can conceivably help in injury prevention. Tight muscles have been implicated as a cause of training-related injury, and improving flexibility can reduce this possibility. Because a stretching exercise improves range of motion, including it in an exercise program can enhance overall workout safety. However, the benefits are not specific to stretching prior to training. All that matters is achieving adequate range of motion to properly carry out exercise performance.
The most important consideration here is to make sure your muscles are warm before performing static stretches. This reduces joint viscosity, ensuring that muscles and connective tissue are sufficiently prepped to endure passive or active lengthening.
So you might be thinking, Why not include some basic stretches after the general warm-up? After all, your core temperature is elevated and joint viscosity is reduced. What’s the harm, right?
Interestingly, evidence shows that static stretching performed before a workout can have a detrimental impact on exercise performance. This is most applicable to activities requiring high force output, such as heavy resistance training. The primary theory proposed to account for these performance decrements is a decrease in musculotendinous stiffness. The musculotendinous unit (the muscle and its associated tendons) is responsible for generating force to carry out movement. Like an overstretched rubber band, the musculotendinous unit with increased laxity following stretching impairs force transmission. The upshot is a reduced capacity to lift a given load.
However, caution needs to be used when applying this research to a lifting session. First, most of the studies in question used excessive stretching protocols, in some cases upwards of 30 minutes stretching a single joint! Most preworkout stretching routines involve only a few minutes per joint, and it’s highly questionable whether such brief stretching bouts have any performance-related detriments. Moreover, the vast majority of research on the topic is specific to high- strength and high-power activities. Whether negative effects are associated when training with medium- to high-rep schemes remains speculative.
Given the uncertainty of evidence, you’re best off performing static stretches immediately after your workout. Your body is already warm from engaging in intense exercise, and it generally feels good to cool down by elongating muscles that have been repeatedly contracted. Some research even shows that postworkout stretching may alleviate delayed-onset muscle soreness (see the sidebar What Causes Muscle Soreness After a Workout?), although the extent of the reduction probably isn’t all that meaningful (Henschke & Lin, 2011).
If you want to include some flexibility work prior to lifting, consider dynamic stretches: slow, controlled movements taken through their full range of motion. Examples are arm swings, shoulder circles, high steps, and hip twists. Choose dynamic stretches that are specific to the joint actions being trained in your workout. Perform several sets for each dynamic stretch, attempting to move the body segment farther and farther in a comfortable range with each set.
Contrary to popular belief, you don’t necessarily have to include a stretching component in your regular routine for general health and wellness. Increased flexibility results in decreased joint stability. Being too flexible, therefore, actually increases injury risk. Thus, stretch only those joints that are tight, and avoid any additional flexibility exercise for those that already have adequate range of motion to carry out your required activities of daily living.
Moreover, it’s important to note that resistance training in itself actually improves flexibility. Provided that you train through a complete range of motion, multiset lifting protocols produce similar increases in flexibility to those seen with static stretching routines (Morton et al., 2011). In essence, resistance training is an active form of flexibility training whereby a muscle is contracted and then immediately lengthened. When performed on a regular basis, it can keep you mobile and limber. We can therefore put to rest the myth that lifting slows you down and binds you up!
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