Can stretching directly cause muscle growth?

A recent study by Warneke et al is the first great proof-of-concept study investigating the direct impact of stretching on muscle growth.

Stretching is one of a handful of topics where I consistently find myself at odds with other “evidence-based” fitness folks. The popular narrative is that stretching is useless at best (“It doesn’t actually increase range of motion long-term!” and “It doesn’t reduce injury risk!”) and counterproductive at worst (“It hinders performance!” and “It reduces muscle growth!”). However, when you actually dig into the research on stretching, an interesting, nuanced picture emerges. For example, intense stretching immediately before exercise might reduce muscle growth (study), but light stretching between sets may actually increase muscle growth (study). Similarly, intense, long-duration stretching right before an exercise test may reduce force and power output, but longitudinal stretching interventions may actually increase strength over time (study). In short, stretching isn’t all good or all bad – whether it helps or hinders you largely depends on the timing, intensity, and duration of your stretching sessions.

Lately, there’s been more interest in stretch-mediated hypertrophy. We pretty consistently observe that training through a full range of motion results in more muscle growth than training through the top part of a range of motion (i.e., deep squats cause more quad growth than half squats). There are two key differences between training through a full range of motion and training through the top half of a range of motion: 1) the total range of motion is different, and 2) training through the top part of a range of motion generally involves not training your prime movers at long muscle lengths. So, which of these differences explains why training through a full range of motion results in more muscle growth?

Recent research suggests that the second factor – training at long muscle lengths – is far more important than the total range of motion you train through. If that weren’t the case, only training the top half of a lift would result in just as much muscle growth as only training the bottom half of a lift, and both would result in less muscle growth than training through a full range of motion. However, that’s not what the research shows. Partial range of motion training at long muscle lengths (for example, just doing the bottom half of a squat) causes at least as much muscle growth as training through a full range of motion, and considerably more muscle growth than partial range of motion training at short muscle lengths.

This research suggests that there’s something special about training at long muscle lengths. At the moment, the leading hypothesis to explain these findings is the existence of “stretch-mediated hypertrophy.” In other words, there’s something about tension on a muscle in a stretched position that more effectively promotes hypertrophy than tension on a muscle in a shortened position. And, while I personally think that the existence of stretch-mediated hypertrophy provides us with a plausible, elegant idea that ties this entire line of research together, there’s one problem with it: there’s not a ton of evidence that stretching can directly cause hypertrophy. We do know that stretching can put a lot of tension on a muscle – sufficiently intense stretching can lead to muscle damage and DOMS, much like resistance training – so sufficiently intense stretching should directly result in muscle hypertrophy if the notion of stretch-mediated hypertrophy is correct. If it doesn’t, then we need to find some other explanation for why training at long muscle lengths results in more muscle growth than training at short muscle lengths.

At this point, there have been dozens of studies on stretching, but hypertrophy following stretching interventions has only been observed a handful of times, so a skeptic could easily argue that these findings were false positives, swimming in a sea of “true” null results. Furthermore, the positive findings aren’t complete slam dunks. For example, Panidi and colleagues found that a stretching intervention increased gains in gastrocnemius cross-sectional area in adolescent volleyball players, but a skeptic might note that while gains in cross-sectional area differed between conditions, increases in muscle thickness didn’t differ between the stretching and non-stretching conditions. Furthermore, Simpson and colleagues found that a six-week stretching intervention increased gastrocnemius thickness in a sample of 11 males, but this finding also has a slight asterisk: when comparing stretched versus nonstretched legs, the increase in muscle thickness was slightly greater in the stretched legs (p = 0.04 for the time-by-condition interaction effect), but you can see the results for yourself in Figure 1. It’s certainly not a night-and-day difference.

Graphic by Kat Whitfield

So, the stretch-mediated hypertrophy hypothesis finds itself in a weird spot. It would explain the results of studies examining the effect of range of motion on hypertrophy. It would explain why isometrics at long muscle lengths may result in more muscle growth than isometrics at short muscle lengths. It also has a lot of support from animal studies (on birds, rodents, and cats), finding that intense stretching interventions result in a ton of muscle growth (both hypertrophy and fiber hyperplasia). However, there’s not much human evidence supporting the idea that a stretch stimulus effectively and independently promotes muscle growth.

In situations like this, it’s nice to have a proof-of-concept study to fall back on. In proof-of-concept studies, you stack the deck in favor of the effect you’d like to observe. We’ve discussed this concept previously in the context of concurrent training. The first concurrent training study by Hickson was a great proof-of-concept study. It found that when you put subjects on a really intense resistance training program and a really intense endurance training program, subjects gain less strength than they would when following a program without any endurance training. After Hickson established the existence of this “interference effect,” subsequent research was able to flesh out the details: how much endurance training is required to result in significant interference? What populations are most likely to experience the interference effect? How does the timing of endurance and resistance training affect the interference effect?

Until recently, however, there wasn’t a great proof-of-concept study investigating the direct impact of stretching on muscle growth. The ideal proof-of-concept study would use an intervention that would likely exceed anything that would ever be used in the “real world,” to simply establish that stretching can independently cause hypertrophy. If such a study failed to find that stretching directly causes hypertrophy, that would put the concept of stretch-mediated hypertrophy on shakier footing. However, if such a study did find that stretching can cause hypertrophy in humans, it would put the idea of stretch-mediated hypertrophy on firmer evidentiary grounds, and open the door for subsequent studies to flesh out the details.

As you might suspect, the study I’m reviewing in this research spotlight is the exact sort of proof-of-concept study I’ve been waiting on.

52 subjects were randomized into two groups: a stretching group and a non-stretching control group. Furthermore, the legs of the subjects in the stretching groups were randomly divided within-subject: one leg underwent the stretching intervention, and the other leg served as a non-stretching control leg. All subjects were “athletically active,” having “performed two or more training sessions per week in a gym or a team sport continuously for the previous six months.” 

The stretching intervention was quite intense. Each subject used an orthotic device that locked the foot in place while pulling the ankle into dorsiflexion. The orthotic is illustrated in Figure 2. The amount of stretch provided by this device could be manually adjusted, and subjects were instructed to cinch the stretching mechanism to the point that the stretch resulted in pretty significant discomfort (an 8 on a subjective 1-10 pain scale). From there, they sat upright in a chair, propped their leg up on another chair of the same height, and stretched their calf for a full hour. This setup can be seen in Figure 2. The stretching intervention lasted for six weeks, and subjects stretched their calf for a full hour every day. As their range of motion improved, they were instructed to pull their ankle into more and more dorsiflexion using the orthotic device, to maintain the same discomfort rating throughout the intervention. Subjects were also instructed to keep a stretching diary, noting their daily stretching duration and intensity (the dorsiflexion angle of the orthotic device).

Graphic by Kat Whitfield

For our purposes, the most important outcome was the change in gastrocnemius thickness. However, changes in dorsiflexion range of motion were also assessed, as were changes in dynamic and isometric plantarflexion strength. Hypertrophy was assessed via ultrasound. Flexibility was assessed via the knee-to-wall test, and by measuring the maximal dorsiflexion angle that could be achieved on the orthotic device used in the stretching intervention. Strength was assessed unilaterally on a leg press (subjects performed maximal isometric contractions and calf raise 1RM tests).

Isometric strength increased significantly more in the stretching leg of the stretching group (+16.8%) than in the non-stretching leg of the strength group (+1.4%), whereas the control group experienced small reductions in strength (reductions of 1.4-1.6%). Dynamic strength followed a similar pattern, though the non-stretching legs in the stretching group also experienced a notable increase in strength, suggesting that some amount of cross-education occurred: calf raise 1RMs increased by 25.1% in the stretching leg of the stretching group and 11.4% in the non-stretching leg of the stretching group, whereas the control group experienced small reductions in strength (reductions of 1.2-3.6%). These results can be seen in Table 1.

Graphic by Kat Whitfield

Changes in flexibility followed a similar pattern. Knee-to-wall test performance increased substantially in the stretching leg of the stretching group (+13.2%), while all other groups and conditions experienced small reductions in performance (reductions of 0.8-2.4%). Maximum dorsiflexion angle on the orthotic device increased by 27.3% in the stretching leg of the stretching group and 7.5% in the non-stretching leg of the stretching group (suggesting that some cross-education occurred), whereas the control group experienced minimal changes (increases of 0-0.7%). These results can be seen in Table 2.

Graphic by Kat Whitfield

Finally, and most importantly, gastrocnemius thickness increased substantially in the stretching legs of the stretching group (+15.3%), while the non-stretching legs experienced a much smaller increase (+2.1%). This was a large (η2 = 0.406; an eta squared of 0.406 is comparable to a Cohen’s d effect size of about 1.65), statistically significant (p = 0.015) difference. These results can be seen in Table 3.

Graphic by Kat Whitfield

This study demonstrates that static stretching with sufficient intensity and volume can directly cause hypertrophy in humans. While this isn’t a completely novel finding (Simpson and Panidi previously observed similar effects), the results of this study are stronger and more conclusive than those observed in prior research. This is a pretty important finding, because it places the idea of stretch-mediated hypertrophy on firmer evidentiary grounds. Furthermore, this study confirms that longitudinal stretching interventions can directly increase dynamic strength and isometric force output.

At first, I was tempted to write that, like most proof-of-concept studies, the results of the present study likely can’t be directly translated into “real world” practice. However, upon further reflection, I actually think that someone could directly apply the intervention used in the present study. If you don’t mind shelling out some money for an ankle stretching orthosis, and you spend at least an hour per day sitting around (watching TV, playing video games, working on your computer, etc.), you could conceivably try this intervention out for yourself, with minimal disruption to your day-to-day life. It’s just a question of how much discomfort you’re willing to endure to grow your calves.

Realistically, though, this study is just a first step. Future research should examine other muscles and manipulate stretching duration and intensity to see just how much stretching is required to provide an adequate stimulus for muscle growth. Finally, we’re still a long way from fully understanding stretch-mediated hypertrophy. We can observe its effects, and we’ve now established its underlying assumption (stretch per se can independently contribute to hypertrophy in humans), but there’s a lot of work left to do before we understand the mechanistic underpinnings of this phenomenon.

Note: This article was published in partnership with MASS Research Review. Full versions of Research Spotlight breakdowns are originally published in MASS Research Review. Subscribe to MASS to get a monthly publication with breakdowns of recent exercise and nutrition studies.

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