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.
It has been well documented that mechanical tension associated with resistance exercise promotes hypertrophic gains. The forces associated with lifting weights alone are therefore capable of producing muscular growth. What is becoming increasingly clear, however, is that metabolic stress associated with moderate to higher repetition exercise also can promote increases in muscle mass. The mechanisms by which this occur are still not entirely clear, but recent research is beginning to give us insight into the possibilities. As discussed in my recent review, several potential factors have emerged as likely candidates. For those who want the cliff notes, here is an overview of each:
Fiber Recruitment: Perhaps the most established way that metabolic stress appears enhance growth is by increasing recruitment of fast-twitch (i.e. type II) muscle fibers. Recruitment follows the so-called “size principle” whereby the smaller slow-twitch (i.e. type I) fibers are recruited first during muscular activity and then larger fast-twitch fibers are progressively called into play as needed to carry out the action. It is believed that the effects of metabolic stress promote fatigue of slow-twitch fibers, thereby forcing activation the fast-twitch fibers. Understand that fibers must be recruited in order to grow; without such stimulation, there is no impetus for the fiber to adapt. Thus, increased recruitment enhances the growth potential of the muscle as a whole.
Myokines: Another possible means by which metabolic stress may enhance muscle mass is by increasing production of local growth factors. Muscle tissue directly produces a number of growth-promoting substances, which have been termed myokines. Local production of a variant of insulin-like growth factor, called mechano-growth factor (MGF), is thought to be particularly important to muscle development and metabolic stress has been shown to increase its production. Numerous additional myokines have also been implicated in the growth process including various interleukins, fibrobrast growth factor, hepatocyte growth factor and others–and many of them appear to be regulated, at least in part, by metabolic stress. Moreover, there is evidence that metabolic stress may reduce various catabolic factors, ultimately increasing the extent of muscle protein accretion.
Reactive Oxygen Species: The term reactive oxygen species (ROS) generally conjures up negative images. The popular media has demonized ROS as injurious substances that wreak havoc on bodily tissues, causing disease and even death. While this view has some credence with respect to chronically elevated levels of ROS, their acute production following exercise has actually been shown to confer positive effects on muscle development. Specifically, ROS are thought to function as key cellular signaling molecules that promote muscle anabolism. There is evidence that metabolic stress heightens ROS production, potentially helping to increase hypertrophy.
Cell Swelling: One of the most novel mechanisms by which metabolic stress may promote muscle growth is via an increase in the hydration of the muscle fiber. This phenomenon, known as cell swelling, has been found to increase protein synthesis and reduce protein breakdown. Well, it just so happens that metabolic stress is a causitive factor in cell swelling, largely from the corresponding accumulation of lactate. Lactate acts as an osmolyte, attracting fluid into the muscle cell. This, in turn, causes sensors in the cell to perceive a threat to its integrity, thereby initiating a signaling cascade that ultimately enhances anabolism.
Acute Hormonal Elevations: This is one of the more controversial areas of research. Studies clearly show that bodybuilding style training (i.e. multiple sets of moderate reps with fairly short rest intervals) substantially increases post-exercise anabolic hormonal levels. What is less clear is whether these transient hormonal spikes actually play a role in the growth process. Evicence is conflicting and there are large gaps in the literature making it difficult to draw firm conclusions on the topic. I have a review paper just published-ahead-of-print that specifically addresses this topic; I’ll have more to say about it soon. Stay tuned…
Summing up, there is compelling evidence that metabolic stress can serve to augment muscle growth. Although we have yet to fully understand precisely how this occurs, it would appear that a combination of factors detailed above are involved in the process. Note that these mechanisms remain largely theoretical at this time, and there may well be others that have not yet been determined.
So how can you use this information? From a practical standpoint, metabolic stress is heightened during resistance training protocols that involve moderate to higher repetitions and fairly short rest intervals. This is typical of the common “bodybuilding-style” method of training and if your goal is to maximize hypertrophy, it appears prudent to include such training as a primary component of your routine. What is not clear as yet, however, is whether metabolic stress provides an additive benefit over-and-above what can be achieved by simply training with very heavy loads. My lab will be exploring this topic over the coming months and I hope to be able to provide some answers in the near future. Stay tuned!
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
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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
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A popular theory among fitness professionals is that taking short rest periods between sets maximizes muscular growth. The theory is primarily based on the hormone hypothesis, whereby limiting inter-set rest promotes greater elevations in post-exercise growth hormone, IFG-1 and testosterone, and thus enhances the anabolic response to resistance training. One little problem: Emerging evidence indicates that acute increases in anabolic hormones have little if any effect on muscular adaptations, as detailed in my comprehensive review of the topic
In an effort to directly test the theory, our group published a study last year titled, Longer inter-set rest periods enhance muscle strength and hypertrophy in resistance-trained men. In brief, the study not only refuted the claim of a hypertrophic benefit to short rest periods, but in fact showed that resting 3 minutes between sets actually produced superior growth compared to resting 1 minute. Importantly, the study was carried out using a moderate rep range (8-12 reps/set) with all sets performed to muscular failure. The question therefore arises whether results would be applicable when training with lighter weights. No study had ever investigated the topic.
What We Did
Subjects were 21 young collegiate athletes who had not performed resistance training for at least 2 years prior to the study. The subjects were randomly divided into two groups: A short rest group (SHORT) that rested 30 seconds between sets and a long rest group (LONG) that rested 2.5 minutes between groups. The load was set at 40% of the subjects’ 1RM in the back squat and bench press using a tempo of 1-0-2 (1 second on the concentric, 2 seconds on the eccentric). Four sets were performed for each exercise, with all sets taken to muscular failure. Training was carried out twice a week for 8 weeks.
What We Tested
Measures of muscle hypertrophy and strength were assessed pre- and post-study. Muscle cross sectional area (CSA) of the triceps and thigh was measured by MRI. A 1RM bench press and squat was employed to measure changes in maximal strength.
What We Found
With respect to hypertrophy, the SHORT group increased muscle CSA by 9.8% while LONG showed an increase of 10.6%. Thigh CSA increased by 5.7% in SHORT versus 8.3% in LONG. No statistically significant differences were noted between any measure of muscle growth.
From a strength standpoint, 1RM in the bench press increased by 9.9% in SHORT and 6.5% in LONG while increases in the squat were virtually identical between groups (5.2% versus 5.4) As with the hypertrophy results, no statistically significant between-group differences were observed in the strength measures.
How Can You Apply These Findings
There are a number of interesting takeaways from the study. First and foremost, this is yet another study showing that training with light weights can promote marked gains in muscle mass in a relatively short time period. There is now a large body of supporting research on the topic using varied methodologies across a variety of populations. The evidence is too compelling for even the most ardent critic to dismiss.
Intriguingly, we found that rest interval length had no statistically significant effects on muscular adaptations. On the surface, these results conflict with our previous research showing that 3 minutes rest produced superior increases in strength and hypertrophy compared to resting 1 minute when training in a moderate rep range (~10RM). Our findings here seem to indicate that rest interval length isn’t an important consideration when training with lighter loads.
A closer look at the data, however, suggests a more nuanced take-home message.
It’s important to realize that the term “statistical significance” refers to the probability of an event happening by chance. Our study had a fairly small sample size, which reduces the ability to detect significance. Hence, we have to look beyond whether results were “significant” and consider other statistical measures. To that end, while hypertrophy of the arms was fairly equal between conditions, gains in thigh muscle CSA clearly favored resting longer between sets. A statistic called the effect size, which is a gauge of the meaningfulness of the results, bears out these differences were indeed consequential. The effect size for the LONG group was 0.93 (considered a large effect) while that of the SHORT group was just 0.58 (considered a moderate effect). The chart above illustrates the absolute differences between thigh growth and rest intervals.
When attempting to reconcile the differences between upper and lower body hypertrophy, it may well come down to total training volume. Short rest blunted increases in training volume in both upper and lower training, but the disparity was much more pronounced in the squat than in the bench. This is logical as the leg/glute muscles have much greater muscle mass than those of the upper trunk/arms, and thus the associated fatigue during high-rep training is greater in multi-joint lower body training, particularly a demanding exercise like the squat. Given the known dose-response relationship between hypertrophy and volume (as clearly displayed in our recent meta-analysis on the topic), the substantial decrease in number of reps performed with short rest periods could conceivably explain the lesser muscle growth seen in the thighs.
In addition to the long-term effects, we also measured hormonal elevations from each condition post-exercise. Both SHORT and LONG showed significant acute spikes in growth hormone and IGF-1, but the increases were similar between groups. Since hormonal increases are related to levels of metabolic stress, it can be inferred that metabolic stress was similar between conditions as well. Although short rest periods have generally been shown to enhance metabolic stress, these findings are specific to moderate rep training. Training with very high reps elicits large increases in lactic acid regardless of how long you rest between sets. Thus, rest interval length seemingly has less relevance in promoting metabolite buildup. Whether metabolic stress influenced results in this study is undetermined as we didn’t seek to assess mechanisms of adaptations. That’s an intriguing topic for future research.
The Bottom Line
* Training with light weights can pack on some serious muscle.
* Short rest between sets has a detrimental effect on lower body hypertrophy when squatting while there does not seem to be much if any negative impact on growth from the bench press when training with light weights. Thus, shorter rest periods for light-load upper body work are a viable option to cut down on training time without sacrificing gains.
* Since single joint exercise does not elicit comparable fatigue to multi-joint movements, it is conceivable that short rest would be similarly viable for single-joint lower body exercises such as the leg extension. This remains speculative, however, as the topic wasn’t directly investigated in our study.
Current resistance training guidelines recommend long rest intervals (i.e. 3 minutes) to maximize muscle strength. Alternatively, short rest intervals of around 1 minute are generally recommended for maximizing muscle growth. This is based on the premise that higher metabolic stress associated with limiting rest between sets will promote a greater muscle-building stimulus. Some have specifically pointed to acute post-exercise increases in anabolic hormones as a primary driving factor in the process.
Back in 2014, I co-authored a review paper on the topic with my colleague Menno Henselmans that was published in the journal Sports Medicine. After a thorough scrutiny of the literature, we determined that there was little basis for the claim that shorter rest intervals was beneficial to hypertrophy. As I discussed in this blog post, It would appear from current evidence that you can self-select a rest period that allows you to exert the needed effort into your next set without compromising muscular gains. That said, our recommendations were limited by a dearth of controlled studies on the topic. Moreover, no study had investigated the generally accepted guidelines of taking 3 minutes rest for strength gains and 1 minute for hypertrophy in resistance-trained individuals.
Until now…
I recently collaborated on a just-published study that investigated the effect of rest intervals on strength and hypertrophy. Here’s the scoop:
What We Did
A cohort of 21 young men were randomly assigned to either a group that performed a lifting routine with 1- or 3-minute rest intervals. All other resistance training variables were held constant. Subjects performed a typical bodybuilding-style routine that comprised 7 different exercises working the major muscle groups of both upper and lower body. Three sets of 8-12RM were performed per exercise. Training was carried out 3 days a week for 8 weeks.
We tested subjects immediately before and after the study period. Tests for muscle strength included 1RM for the bench press and back squat. Muscle-specific growth was assessed by b-mode ultrasound for the elbow flexors, triceps brachii, and quadriceps femoris.
What We Found
Maximal strength was significantly greater for both 1RM squat and bench press for the group taking longer rest. No big surprise here. Somewhat unexpectedly, however, muscle thickness tended to be greater when taking longer rest intervals as well. Although we can’t be sure of the underlying mechanisms, we speculated that results may be attributed a reduction in total volume load (i.e. reps /x/ load) over the course of the study. There is a well-established dose-response relationship between volume and hypertrophy, whereby higher volumes correlate with greater muscle growth. Thus, very short rest periods may compromise growth by reducing the amount of weight you can use on subsequent sets. This would indicate that if there are synergistic benefits to heightened metabolic stress, they are overshadowed by the associated decreased volume.
What are the Practical Implications
The obvious take-home here would seem to be that resting 1 minute between sets compromises gains in muscle size. But if 1 minute is in fact too short a rest period, how long should you then rest when maximal hypertrophy is the goal? Well, based on previous work in well-trained individuals, it would seem that 2 minutes provides sufficient recovery so as not to undermine growth.
That said, it’s important to take these results in proper context. Realize that we looked only at effects of the two respective conditions (i.e. 1- versus 3-minutes rest) on muscular adaptations. But rest interval length does not have to be a binary either-or choice. There is no reason you can’t combine different rest periods to potentially maximize hypertrophy.
A viable strategy is to take longer rest intervals on your large-muscle compound exercises such as squats, presses and rows. These movements generate very high levels of metabolic disturbance, particularly when performed with moderate rep ranges (i.e. 8-15 reps). Thus, longer recovery periods are needed to fully regenerate energy levels for your next set so that volume load is maintained across sessions.
On the other hand, single joint movements are not as metabolically taxing and thus you’re able to recover more quickly from set to set. Exercises like biceps curls, triceps pressdowns, and leg extensions therefore could conceivably benefit from shorter rest periods. In this way, you can heighten metabolic stress and its potential hypertrophic benefits without negatively impacting volume load. In this scenario, it’s best to keep the short-rest sets at the end of your workout to ensure they don’t interfere with recovery of compound exercise performance.
A final word: Research is still emerging on this topic. Each study is simply a piece in a puzzle. As more studies are carried out we’ll hopefully develop a better understanding of how programming can be tweaked to maximize the growth-related response. Stay tuned.
Recently, I collaborated with my friend and colleague, Menno Henselmans, to review the literature on the effects of rest interval length on muscle growth. I’m pleased to report that this review has just been published in the prestigious journal, Sports Medicine. If you’re into the science of hypertrophy, I encourage you to read the paper as we delve into all the relevant research on the topic. In the meantime, here is an overview of the take-aways with practical implications.
General resistance training guidelines recommend that rest intervals should remain relatively short to maximize hypertrophy. In a previous review, The Mechanisms of Muscle Hypertrophy and Their Application to Resistance Training I echoed these sentiments, suggesting that rest periods of 60-90 seconds would seemingly provide an optimal balance between mechanical tension and metabolic stress (primary mechanisms in the hypertrophic response) to enhance anabolism. It should be noted, however, that these recommendations were based primarily on a logical extrapolation of mechanistic data; there simply have not been a sufficient number of studies that have investigated the topic in a well-controlled fashion.
In what is the most comprehensive study on the topic to date Ahtiainen et al. found no differences in muscle cross sectional area between 2 versus 5 minute rest periods in a sample of well-trained men. The study had several strengths including a randomized crossover design (which substantially increases statistical power), the inclusion of experienced trainees, and the use of the gold-standard imaging modality, MRI, to measure muscle growth. The one issue here is that the 2-minute rest period employed by the researchers is longer than what is generally advised for hypertrophy-type training. The impact on metabolic stress diminishes with longer rest periods, and this conceivably could have had negatively affected anabolic signaling in this study.
The other study of note that attempted to investigate the effects of rest interval length on hypertrophy was carried out by Buresh et al, whereby 12 untrained individuals performed their workout with either 1 or 2.5 minutes rest between sets. This study actually showed superior results for hypertrophy in the arms and a trend for greater growth in the legs in the subjects using longer intra-set rest intervals. While these results may seem compelling, it should be noted that muscle cross sectional area was determined by anthropometric means (i.e. surface measurements) which can be quite unreliable and thus compromise accuracy. Further confounding matters is the small number of subjects (only 6 in each group) and the fact that subjects were inexperienced with resistive exercise. Thus, while the findings here are interesting they must be interpreted with caution.
So what practical applications can we derive from the literature? Based on current research, it seems highly doubtful that rest interval length has a substantial effect on muscle growth. Bottom line: It would appear that you can self-select a rest period that allows you to exert the needed effort into your next set without compromising hypertrophic results.
That said, the paucity of controlled studies on the topic make it difficult to draw concrete conclusions. Certainly we know that shortening the duration of rest between sets increases metabolic stress, which is known to stimulate muscle remodeling. We also know that well-trained individuals such as bodybuilders are able to sustain a high percentage of their repetition maximum with rest periods as short as a minute. Could the combination of these factors may provide an additional hypertrophic stimulus — albeit a small effect — over time in well-trained subjects? Could other factors such as increased hypoxia and cell swelling also contribute to such a response?
These are questions that require further research. I’m currently in the process of carrying out a study that will provide relevant answers. I hope to begin data collection before the year is out. Stay tuned.
Reference
Henselmans M, Schoenfeld BJ. The Effect of Inter-Set Rest Intervals on Resistance Exercise-Induced Muscle Hypertrophy. Sports Med. 2014 Jul 22. [Epub ahead of print]
I’m stoked to announce that my dissertation study, Effects of different volume-equated resistance training loading strategies on muscular adaptations in well-trained men, was just published ahead-of-print in the Journal of Strength and Conditioning Research. I had actually devised the protocol during my master’s degree course in research methods back in 2008. The study I ultimately carried out had some different wrinkles than the one originally proposed, but overall the essence remained the same. Most importantly, it investigated a topic that’s been debated for many years: What are the differences in muscular adaptations (strength and hypertrophy) between bodybuilding- vs powerlifting-type training programs? Here is an overview of the study and a discussion on its practical implications.
The Methodology
20 well-trained subjects (minimum of 1 year resistance training experience working out at least 3 days/week) were recruited to participate in the study. Subjects were randomly assigned to one of two groups: A hypertrophy group (HT) that performed a bodybuilding style routine or a strength group (ST) that performed a powerlifting-style routine. The HT protocol was a split routine where each muscle was worked once per week with 3 exercises per session, performing 3 sets of 10 reps and resting for 90 seconds. The ST protocol was a total body routine where each muscle was worked 3 times per week with 1 exercise per session, performing 7 sets of 3 reps. The volume load (sets x reps x load) was equated so each group essentially lifted about the same amount of total weight per week. Training was carried out over 8 weeks. All sets were performed to the point of momentary concentric muscular failure.
Strength was measured by 1RM in the squat and bench press. Muscle thickness of the biceps was measured with ultrasound. Testing was carried out pre- and post-study, and results were then compared between groups to assess differences in strength and hypertrophy.
The Results
3 of the subjects dropped out of the study before completion leaving 17 subjects for analysis (9 in the HT group, 8 in the ST group). Both groups significantly increased biceps muscle thickness by ~13% with no differences seen between groups. Both groups also significantly increased 1RM strength, but the ST group had greater increases in the bench press and showed a trend for greater increases in the squat.
Practical Recommendations
On the surface, the study showed that muscle hypertrophy is similar between powerlifting and bodybuilding type routines provided that volume is equated between protocols. Moreover, the study showed that maximal strength is slightly greater in a powerlifting protocol. This could lead to the conclusion that if your goal is hypertrophy then it doesn’t matter what rep range you use (at least in the heavy to moderately-heavy range) as long as you perform equal volumes, but that maximizing strength requires lifting very heavy weights. From a mechanistic standpoint with respect to muscle hypertrophy, the study suggests that either 1) the increased mechanical tension in the ST group was offset by the greater metabolic stress in the HT group on a volume-equated basis or, 2) there is a threshold for mechanical tension and once the threshold is reached, it doesn’t matter as long as the stimulus is maintained for similar timeframes. With respect to strength, this would suggest that neural factors related to training are still relevant in well-trained individuals, and that using very heavy weights does indeed have a greater transfer to maximal lifts compared to moderate intensity loads.
But the devil is often in the details and that is the case here.
First, it is important to point out that total training time in the ST group was 70 minutes while that of the HT group was 17 minutes. So from a time-efficiency standpoint, the bodybuilding-type training produced similar hypertrophy (as well as nearly similar strength increases) in about a quarter of the time as the powerlifting routine. Moreover, exit interviews revealed that those in the ST group were fried by the end of the study. Almost all of them complained of sore joints and general fatigue, and the two dropouts from this group were because of joint-related injury (and these routines were highly supervised with respect to form, so we took every precaution for safety). On the other hand, the HT group all felt they could have worked substantially harder and done more volume.
This brings up an important take-away message: While mechanistically it appears that it does not matter whether heavy or moderately-heavy weights are used for hypertrophy, from an application standpoint it simply isn’t practical to train constantly with the volumes used in this study on multiple body parts. The grinding on the joints and the taxation of the neural system that is involved with repeated performance of very heavy loads ultimately has a negative impact on the lifter; I am certain that if we had continued this program for any longer, most of those in the ST group would have been overtrained and seen performance decrements. If nothing else, these finding reinforce the importance of periodizing programs so that cycles of deloading are interspersed with very heavy loading protocols.
Additionally, realize that only three major muscle groups were worked in the study: the pecs (upper body pushing); the back (upper body pulling) and the thighs. Thus, the HT group could have easily done a couple of extra sets for each muscle group without overtaxing their resources. Although impossible to say for sure, it certainly is plausible that additional work would have enhanced the hypertrophic response in the bodybuilding-style training group. Moreover, the HT group could have performed exercises for other muscle groups, including some targeted work with single joint movements. Working specific muscles (and aspects of muscles) such as the middle and posterior delts, the hamstrings and the calves alone would definitely have benefited overall muscle hypertrophy.
So bottom line: The study indicates that the best approach to building muscle is to perform a combination of heavy and moderately heavy loads. The “hypertrophy range” is applicable from the standpoint that it allows the performance of a greater amount of volume without overtaxing the body’s resources. Adding in loads in the 1-5 RM range can enhance strength (which ultimately allows the use of heavier loads during moderate rep lifting) as well as providing a potent hypertrophic stimulus.
It should be noted that.I made a conscious decision to investigate the two types of routines as lifters usually perform them. Thus, the HT routine was a split routine since the vast majority of bodybuilders train in this fashion, while the ST routine was a total body routine since this is the way most powerlifters train. While staying true to the usual performance gives insight into how muscular adaptations generally play out in everyday practice, they also obscure the ability to attribute results entirely to the set/rep scheme. I will be carrying out a follow up study that seeks to address this issue in the near future. Stay tuned!
Happy to report that I’ll be doing regular fitcasts with my brother-from-another-mother, Bret Contreras, which we somewhat unoriginally call the B & B Connection (what’s in a name, right?). We’ll be discussing the practical application of research on a variety of fitness topics, objectively delving into some of the more controversial issues that currently exist. Each fitcast will be limited to 30 minutes (translation: we’ll cut right to the meat of the topic without any fluff).
Our inaugural fitcast covered the mechanisms of muscle hypertrophy. We explored my review paper, The mechanisms of muscle hypertrophy and their application to resistance training, with specific emphasis on the roles of mechanical tension, metabolic stress, and myodamage on muscle development. For anyone interested in maximizing their muscle mass, this fitcast will serve as a primer to help with optimizing exercise program design.
In our second fitcast we tackled the hotly debated topic of high-intensity resistance training (HIT). For those who don’t know, HIT is a catch-all for single-set training. The discussion was spurred by a recent research study showing that single set training was equally as effective as multi-set training in improving measures of upper body strength. As is often the case, however, the devil is in the details. What does not get mentioned in the abstract (or anywhere in the discussion, for that matter), is that the “single set” group actually performed one set of three exercises for each muscle group. Given that the subjects trained three times per week, this amounted to nine sets per muscle per week. Not exactly what I would consider a “single set” routine, and certainly not consistent with what HIT pioneers such as Ellington Darden have prescribed as optimal for muscular adaptations. Understand that this by no means invalidates HIT as a potentially viable approach. As Bret and I discuss, the issue on training volume ultimately comes down to your personal goals. I highly encourage you to give this one a listen and let us know your thoughts on the topic.
Suffice to say, I’m very much looking forward to our future B & B fitcasts. Stay tuned.
In addition to my collaboration with Bret, I’ve been interviewed on a number of other sites recently. Here’s a rundown of each:
Most recently, I had the pleasure to chat about bodybuilding with Ben Pakulski and John Meadows. In case you don’t know, these two guys are at the pinnacle of the profession. Ben is an elite bodybuilder who placed second in the Arnold Classic this past year; I feel confident in saying he is destined to be an Olympia champion one day. John is a highly ranked NPC competitor who also trains many of the top pros. Listen to the interview and you can tell the level of commitment and understanding these guys have about the practical application of scientific principles; they certainly dispel the frequent notion that bodybuilders simply rely on genetics and gear. Whether you’re a bodybuilding fan or not, this is a must listen for those interested in maximizing muscle development.
Next, I spoke with Carl Lenore on Super Human Radio about whether muscle soreness is a good way to gauge the success of your workout. Carl always does a great job allowing for scientific discussion of fitness topics, and this was no exception. If you’re caught up in how sore you after a workout you should definitely check this one out.
My interview onJay Scott’s Full Disclosure Fitness Podcast provided wide-ranging questions spanning a variety of fitness topics. Rep ranges, diet, and supplements were just a few of the issues covered. Jay did a great job of keeping the interview focused and interesting.
I spoke with Scott Tousignant on the premier episode of his Fitness Frontier podcast. Scott is a natural bodybuilder who shows a true passion for the sport. In addition to discussing training for physique enhancement, I got to recollect on my past experiences as a competitive bodybuilder.
Last but certainly not least, I was interviewed by two top English fitness pros, Luke Johnson and Joseph Agu. Luke and Joseph are organizing my upcoming seminar series in the United Kingdom this January. Lots of interesting topics discussed. As a bonus, they have really cool English accents! This one is a videocast; I’ve embedded the video below.
embedded by Embedded Video
Okay, gotta get back to work on my dissertation now. In the meantime, hope this provides you with enough listening enjoyment for the time being!
Writing a book is a lengthy, arduous process. To do it right involves a great deal of planning. You need to map out everything that needs to be covered and decide on the best way to organize this information into a cohesive, readable format. A diligent author spends countless hours contemplating these complexities before a single word makes it to the page. But no matter how attentive you are to detail, there are always some things you somehow miss that ultimately become apparent once the book is released. The best you can do at this point is to address any omissions ex post facto.
Based on reader feedback and questions, it has come to light that I made such an omission in my book, The M.A.X. Muscle Plan, with respect to warming up prior to training. In retrospect, this is not something that I should have taken for granted. A warm-up heightens blood flow to muscles, enhances speed of nerve impulses, increases energy substrate delivery to working muscles as well oxygen release from hemoglobin and myoglobin, and reduces the activation of energy for cellular reactions and muscle viscosity (Thacker et al. 2004). Suffice to say, it’s an important component of a workout. This post therefore will seek to rectify the oversight and address my recommendedations for the M.A.X. Muscle warm-up.
A warm-up can be divided into two distinct components: general and specific. The general warm-up – which involves performing a brief bout of low-intensity, large muscle group aerobic-type exercise – should be included in all three M.A.X. Muscle mesocycles (i.e. strength, metabolic conditioning, and hypertrophy). The purpose of the general warm-up is to elevate core temperature and increase blood flow. This has implications not only for injury prevention, but for performance as well. In fact, there is evidence that combining a general warm-up with a specific warm-up increases maximal strength to a greater degree than peforming a specific warm-up alone (Abad et al. 2011).
Virtually any cardiovascular activity can be used for the general warm-up. Modalities such as the stationary bike, stair climber, or treadmill are fine, as are most calisthenic-type exercises (such as jumping jacks, high steps). Choose whatever activity you desire as long as the basic objective is met.
As previously noted, the intensity for the general warm-up should be low. To gauge intensity, 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 range of 0-10 (where 0 is lying on your couch and 10 is an all-out sprint). Aim for an RPE of around 5, which for most would be a moderate walk or slow jog. Five to ten minutes is all you need – 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 cardiovascular benefits or reduce body fat.
The specific warm-up augments the general warm-up. It serves to enhance neuromuscular efficiency in performing a given exercise. To optimize benefits, the exercises used in the specific warm-up should be as similar as possible to the actual activities in the workout. For example, if you are going to perform a bench press, then the specific warm-up would ideally involve performance of light sets of bench presses. In this way, the neuromuscular system gets to “rehearse” the movement before it is performed higher levels of intensity. Specific warm-up sets should always be stopped well short of fatigue – the focus here is to facilitate performance of the heavier sets.
For the M.A.X Strength Phase, I recommend at least a couple of specific warm-up sets per exercise. Since this phase employs a total body routine with very heavy loads (>85% 1RM), it is important that each exercise include specific warm-up sets. As a general rule the first set should be performed at ~40-50% of 1RM and the second set at ~60-70% 1RM. Eight to ten reps is all that is needed in these sets –any more than this is superfluous. Thereafter, you’re then ready to plow into your working sets.
For the M.A.X Hypertrophy Phase, I recommend performing a specific warm-up prior to the first exercise for each muscle group only. Since this is a split-routine where multiple exercises are performed per body part, the benefits achieved from the specific warm-up on the intial movement will carry over to the other exercises for the subsequent exercises for that muscle group. Additional warm-up sets can actually be detrimental since they can hinder generation of metabolic stress, which is a desired outcome in this phase.
Specific warm-up sets are not necessary in the M.A.X Metabolic Phase. In this phase you’re already using light weights and the initial repetitions of each working set therefore 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.
Hopefully this addresses the feedback and questions I’ve received on the topic. I’ll look to cover some additional questions I’ve received in future posts. In the meantime, keep the comments coming!
Brad
References
Abad CC, Prado ML, Ugrinowitsch C, Tricoli V, Barroso R. Combination of general and specific warm-ups improves leg-press one repetition maximum compared with specific warm-up in trained individuals. J Strength Cond Res. 2011 Aug;25(8):2242-5.
Thacker SB, Gilchrist J, Stroup DF, Kimsey CD Jr. The impact of stretching on sports injury risk: a systematic review of the literature. Med Sci Sports Exerc. 2004 Mar;36(3):371-8
So much going on that I want to share. First, I just returned from my last semester of PhD coursework at Rocky Mountain University in beautiful Provo, Utah. The attainment of my doctoral degree is finally in sight! I am on schedule to begin data collection on my dissertation research later this summer and, if all goes according to plan, defend my dissertation in January. This has been an amazing–albeit grueling–educational journey. I’ve learned so much about critical thinking, met so many incredible people, and honed my skills as a researcher along the way these past two-and-a=half years. I’ll be blogging about my experience in the near future. Stay tuned…
My review article, Postexercise hypertrophic adaptations: a reexamination of the hormone hypothesis and its applicability to resistance training program design has been published in the current issue of the Journal of Strength and Conditioning Research. The article exhaustively reviews the literature on whether acute hormonal elevations following resistance training play a role in muscle growth. For years, it was believed that spiking hormones after exercise was the key to maximizing hypertrophy. Entire workouts were planned around maximizing the anabolic hormonal response. Turns out, this belief was misguided. Studies are equivocal as to whether post-workout hormonal elevations are involved in the muscle-building process; some show a positive correlation, others do not. Bottom line is that if there is a hypertrophic effect from such elevations, it would be relatively modest. That said, even a modest effect on hypertrophy could be practically meaningful to someone seeking maximal muscle development, such as a bodybuilder or strength athlete. There are still many gaps in the literature that need to be sorted out before a definitive conclusion can me made on the topic–particularly with respect to the effects in experienced lifters. I will be carrying out research in the coming months that hopefully will help to fill in some of these gaps. Will keep you updated here when I have data to share.
I recently did two interviews of interest with Super Human Radio. The first, The Role of Metabolic Stress in Muscle Growth is an extensive discussion of various aspects of muscle hypertrophy. The second, Look Great Naked delves into women’s fitness as well as touching on post-workout nutrition. What I really like about these interviews is that the host, Carl Lanore, is a true science geek. As such, he let’s me expound on the science of these topics in depth. I go into a level of detail generally not afforded in other media outlets. Each interview lasts about an hour so there’s a lot of listening for your enjoyment 🙂
About a year or so ago I wrote an article on glute training that appeared in Fitness Rx for Women magazine. Well, lo and behold, they published the article online for free! The article is called, The Tight and Toned Butt Workout (yeah, I know the title is a bit cheesy, but hey, that’s apparently what sells magazines…). Although the article is geared toward women, it’s a routine that can be used effectively by men too. Check it out.
Book update: Rodale has acquired the mail order rights to my book, The M.A.X. Muscle Plan. In case you don’t know, Rodale is an industry leader in fitness media. They publish Men’s Health Magazine, as well as many other fitness publications. As I’ve mentioned previously, this book was the culmination of many years of of research and practice, and represents the most cutting-edge muscle building program ever developed (and I’m not blowing smoke when I say this!). It’s available at a discount on Amazon.com as well. I hope you’ll give it a read; I’d love to hear your feedback.
Finally and importantly, I have agreed to a consultant role with Reebok International. In my role, I will be providing educational content for fitness professionals as well as making select appearances at Reebok-sponsored events. There are other as-yet undefined areas that may be explored as well. I am honored to be affiliated with such a terrific brand and look forward to partnering with them to share my fitness expertise.
Antioxidant supplements continue to be touted by many fitness professionals as a nutritional panacea. In case you’re not aware, antioxidants are the body’s scavengers. They help to defend against damage caused by reactive oxygen species (ROS) — unstable molecules that can injure healthy cells and tissues — which are produced in abundance each day during the normal course of respiration. The main culprit: oxygen. Every time you breathe, oxygen uptake causes ROS production. Environmental factors such as pollutants, smoke and certain chemicals also contribute to their formation. Their production have been linked to a multitude of ailments including arthritis, cardiovascular disease, dementia and cancer. Not surprisingly, exercise is associated with substantially greater ROS production given that it substantially inreases oxygen consumption. This has led to the supposition that antioxidant supplements are especially beneficial for hardcore exercisers.
Here’s a short-course in how the process works: Your body is made up of billions of cells held together by a series of electronic bonds. These bonds are arranged in pairs so that one electron balances the other. However, in response to various occurrences (such as oxygen consumption), a molecule can lose one of its electron pairs making it an unstable free radical. The free radical then tries to replace its lost electron by stealing one from another molecule. This sets up a chain reaction where the second molecule becomes a free radical and destabilizes a third molecule, which becomes a free radical and destabilizes a fourth molecule and so on.
To prevent rampant ROS production, your body has a sophisticated internal antioxidant system. Various antioxidant enzymes combine with antioxidants from the foods you eat to help keep ROS at bay. There are dozens of known antioxidants including Vitamin C, Vitamin E, coenzyme Q10, alpha-lipoic acid, and carotenoids, amongst others. Although these nutrients are readily obtainable from food sources, it is often postulated that it’s virtually impossible to consume adequate quantities from your daily diet, thus making supplementation mandatory. In theory, supplementing with antioxidants would seemingly make sense since a greater availability should allow for greater protection against ROS. Question is, does theory translate into practice?
I first became interested about the topic a dozen or so years ago. A friend gave me a book to read called The Antioxidant Miracle, which as the title implies touted the wonders of antioxidant supplementation. The book piqued my curiousity. I delved into the research. Lo and behold, the claims seemed legit. A large number of studies showed positive effects of supplementation on a wide array of health-related benefits. What really caught my attention was a review by Dekkers et al. in the journal Sports Medicine, which discussed favorable results of antioxidant supplements during intense physical activity. The article went on to conclude that “human studies reviewed indicate that antioxidant vitamin supplementation can be recommended to individuals performing regular heavy exercise.” At the time, I wasn’t very savvy as to the complexities of research. I jumped on the antioxidant supplement bandwagon.
My bad.
Fast forward several years. Larger randomized controlled trials were conducted. The findings of these studies were at best decidedly mixed, with a majority showing no health-related benefits from supplementing with antioxidants. Alarmingly, several meta-analyses reported that there may even be an increased supplement-associated risk for cancer, stroke, and all-cause mortality. An objective evaluation of the current literature would make it difficult for even the most ardent antioxidant proponent to make a case for improving well-being by supplementation.
What’s particularly interesting to me as an exercise scientist is emerging research suggesting that antioxidant supplements may actually have a *detrimental* effect on training-related adaptations, particularly those associated with muscle hypertrophy. At issue here is the distinction between chronic versus acute ROS production. Evidence does show that chronically elevated levels of ROS can impair muscle function and even bring about muscle wasting conditions. Understand, however, that exercise upregulates the body’s antioxidant defenses. This ultimately helps to reduce chronic elevations in ROS without the need for supplementation.
On the other hand, acute production of ROS during a workout has been implicated in a variety of exercise-related adaptations including enhanced muscle remodeling. ROS production has been found to promote growth in both smooth muscle and cardiac muscle, lending credence to the supposition that these substances may have similar hypertrophic effects on skeletal muscle as well. The mechanisms have yet to be determined, but studies show that ROS can function as key cellular anabolic signaling molecules in the response to exercise. What’s more, there is evidence that they help to mediate the activity of satellite cells, which are responsible for aiding in repair and regeneration of muscle fibers. I have covered these topics extensively in my recent reviews of the roles of metabolic stress and muscle damage in exercise-induced muscle hypertrophy. By suppressing ROS production, antioxidant supplements may inhibit these hypertrophic effects and thus impair the growth and repair process. Indeed, preliminary studies indicate a negative impact of supplementation on exercise-induced adaptations.
There are a couple of take-home messages here, the most obvious of which is that the risk/reward ratio for antioxidant supplementation appears to be poor. Focus on eating a diet replete in vegetables and fruits and you’ll get all the antioxidants you need to support basic health. Overloading on antioxidants via supplements will not confer any additional benefits; it’s possible they may actually cause harm. And although the jury is still out, it is at least conceivable that supplementation can impede muscular development and other exercise-related adaptations. Any way you slice it, antioxidant supplementation doesn’t seem to make sense, at least for otherwise healthy individuals who exercise on a regular basis.
On a broader scale, the overriding message to be gleaned is the importance of using caution when interpreting research. This is particularly true of exercise-related studies, which are usually limited by small sample sizes, the inability to control for various confounders, and the almost unlimited number of variations that encompass exercise program design. All-too-often fitness professionals are quick to form opinions based on limited evidence. Such an approach is decidedly misguided and unscientific. As illustrated here, I was guilty of falling into this trap. Fortunately I learned from the mistake and as a result became a more astute fitness professional.
Extrapolating research findings in an evidence-based fashion can be equated to solving a jigsaw puzzle. Each published study is a piece to the puzzle. In almost every situation there will be conflicting results between studies. Sometimes two studies will report diametrically opposite findings on the same topic. How can you make sense of all this?
The best fitness professionals, guys like Bret Contreras, Alan Aragon, Joe Dowdell, and James Krieger, will weigh the body of evidence by considering factors such as the type of study (experimental vs. observational), the subjects (animal vs. human), and the setting (in vitro, ex vivo, in vivo, etc). They’ll also take into account numerous other factors including study design, statistical power, generalizability, and the quality of the journal in which the study was published. Only after a thorough analysis of the prevailing body of literature can an educated opinion be formed that guides decision-making and provides the basis for practical recommendations. It’s a skill that can be honed. The more research you read, the better you become at critical thinking, allowing you to piece together the puzzle in question.
One last thing: I frequently hear trainers and even researchers cite a study as “proof” of a given opinion. Not! A single study never “proves” anything. Rather, it simply lends support to a given theory. As noted, some studies carry more weight than others. The greater the strength of evidence, the more support there is for the theory. But theories are not set in stone. Case in point: Until recently, it was taken as gospel that saturated fat and cholesterol caused cardiovascular disease. Every nutrition text, bar none, stated such as fact. Recent research has now challenged these assumptions, however, suggesting that any relationship is far more complex than previously thought. Bottom line is that the more knowledge we acquire, the more we realize just how much more there is to learn.
Always be skeptical. Always be willing to change your opinion based on new information. This is what separates the ordinary practitioners from the elite.
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