Preface: When I began writing this article, the working title was “Training for hypertrophy: is muscle damage actually helpful?” I started out believing that damage did play a role; I just wasn’t sure to what extent. However, as I researched the topic, I became more and more convinced that damage plays a minimal role (and perhaps even no causative role) in muscle hypertrophy. I hope you enjoy my take on the topic, and I welcome your comments.
Training for hypertrophy: the case against muscle damage
If you’ve been bodybuilding for any length of time, you’ve probably heard the following explanation: “Training damages your muscles. Your muscles then repair, getting bigger and stronger in the process.” But is it really true? I dug into the science to find out.
In 2010, Brad Schoenfeld published what would become a classic paper in our field: “The mechanisms of muscle hypertrophy and their application to resistance training.” In that paper, he hypothesized that three primary factors are responsible for initiating the hypertrophic response to resistance exercise: mechanical tension, muscle damage, and metabolic stress.
Regarding muscle damage, Schoenfeld wrote that under certain conditions, damage “is theorized” to generate a hypertrophic response. He cited four reviews, a study on rats, and a study on older men injected with testosterone who did not train. In other words, it seems that at the time, this hypothesis had not yet been tested formally in a training study.
Two years later, in 2012, Schoenfeld published a brief review on that very topic: “Does exercise-induced muscle damage play a role in skeletal muscle hypertrophy?” He concluded that “a cause-effect relationship directly linking [muscle damage to hypertrophy] is yet to be established.”
Four years later, in 2016, he reached the same conclusion in his textbook Science and Development of Muscle Hypertrophy. In that book, he also discussed the “challenges to the exercise-induced muscle damage hypothesis” and noted that downhill running can induce significant damage to muscle tissue without corresponding growth, citing a review by Brentano and Kruel (2011). Based on this observation, he concluded that “muscle damage by itself is not sufficient to induce significant muscle growth.” And that if it does play a role, “it can do so only in the presence of resistance-based mechanical overload.” In epidemiology (my field of study), we would call this a component cause. As we’ll see shortly, this component cause does not seem necessary for hypertrophy. This suggests it’s of lesser importance and leads me to believe that it plays a minimal role in muscle hypertrophy overall.
More evidence against the role of muscle damage in muscle hypertrophy
Flann et al. (2011) assigned 14 young, healthy men and women at random to two groups. Subjects in the first group trained at a low intensity for three weeks to gradually acclimate their muscles. Subjects in the second group did not. Then, both groups engaged in eccentric cycle ergometry at a “somewhat hard” level (based on rating of perceived exertion) for 20 minutes, 3 times a week, during 8 weeks. Although there was more muscle damage in the second group, both groups made similar gains in hypertrophy. Another study on elderly individuals found that damage was not a prerequisite for inducing muscle growth with eccentric contractions (LaStayo et al. 2007). In addition, Damas et al. (2016) found that myofibrillar protein synthesis was correlated with muscle hypertrophy in beginners only after three weeks of training, when muscle damage was attenuated. Based on these results, the results of Flann et al. (2011) (cited above), and others, some of these authors concluded in a recent review that: “muscle damage is not the process that mediates or potentiates resistance training-induced muscle hypertrophy” (Damas et al. 2018).
Data on blood flow restriction (BFR) training also de-emphasize the role of muscle damage. We know that low-load training with BFR leads to similar hypertrophy as heavier training without BFR, as demonstrated in a 2018 meta-analysis by Lixandão et al. However, low-load training with BFR doesn’t seem to cause nearly as much muscle damage as heavy training. Wilson et al. (2013) found that moderate blood flow restriction resulted in greater acute metabolic stress, muscle swelling, and muscle activation – all without increasing muscle damage. In a follow-up study from the same lab, Lowery et al. (2014) found that both “high-intensity” (not defined) and low-load, blood flow-restricted training led to significant and similar gains in biceps brachii muscle thickness after four weeks. In a more recent study, Sieljacks et al. (2016) did find that blood flow-restricted training performed to failure caused muscle damage acutely. However, they used untrained subjects, who are prone to damage. After their second session, all subjects saw: “attenuated response in several of the indicators of muscle damage.” In a review, Loenneke et al. (2014) concluded that: “minimal to no muscle damage is occurring with this type of exercise.” In agreement, Pearson and Hussain (2015) noted in their review that this type of training does not seem to increase direct markers of muscle damage (such as interleukin-6) to any meaningful degree. They pointed out that these levels reach only one-quarter of those reported in response to high-intensity eccentric exercise, and they concluded that damage “may not contribute to blood flow-restricted, resistance training-induced hypertrophy, due to its low-intensity nature.” Taken together, these observations challenge the role of damage as a cause of muscle hypertrophy.
Data on hypertrophy and nonsteroidal anti-inflammatory drugs (NSAID) such as ibuprofen also de-emphasize the role of muscle damage. One would think that by blocking inflammation as a mediator between muscle damage and hypertrophy, these drugs would hinder hypertrophy. However, the evidence is mixed. In one study, hypertrophy was indeed lower in young adults taking maximal over-the-counter doses of ibuprofen (Lilja et al. 2018). In another, hypertrophy was actually greater in older adults taking NSAID (Trappe et al. 2011). Other studies found no differences between groups (Krentz et al. 2008; Petersen et al. 2011). With that said, it should be noted that inflammation is not the only hypothesized mediator between damage and hypertrophy.
Concluding on the role of muscle damage: causation or correlation?
There is no doubt that exercise damages muscles. However, there is little evidence that this damage causes subsequent muscle hypertrophy. Based on the evidence I have reviewed in this article, it seems that damage plays a minimal role in muscle hypertrophy. It may even be correlated to hypertrophy without causing it, playing no causative role at all. I hypothesize that lifting damages muscles, but that this damage does not directly cause muscle hypertrophy (and may not even contribute to hypertrophy). Other mechanisms at work when you lift probably do (via mechanical tension and metabolic stress).
I have not carried out a systematic review, so it is likely that I have missed studies that would have added meaningfully to this discussion (please comment on this blog post or get in touch with me if you would like to discuss any). Also, some of the studies I’ve cited used older and untrained subjects (LaStayo et al. 2007; Trappe et al. 2011). We should be careful when generalizing their results to other populations, especially younger, trained lifters and elite athletes. On a related note, a limitation to this body of literature is that there is a lack of research looking specifically at the role of muscle damage in trained lifters who have already achieved substantial muscle hypertrophy and for whom, perhaps, damage may be important for satellite cell activation and myonuclear accretion.
Practical applications: training for muscular hypertrophy
Since it seems that damage only plays a minimal role in muscle hypertrophy, when training for hypertrophy, I’d recommend you focus on the other mechanisms of muscle growth (such as tension and metabolic stress).
I’d like to thank Brandon Roberts and Greg Nuckols for their comments on the draft of this article.