Stretch-mediated hypertrophy (SMH) is the biggest research revolution from the last years according to many exercise scientists. Stretch-mediated hypertrophy is often defined as the additional muscle growth gained from training muscles at long lengths, such as deep squats, lengthened partials and resisted static stretching protocols, versus shorter-length training. I’ll use that definition here, though as you’ll see, it’s not really clear yet that this growth is directly caused by any stretching effect. Passive tension is a leading candidate growth pathway. In fact, there is a school of thought that SMH is irrelevant, because it only causes temporary muscle lengthening, not thickening. Whether this is correct has major implications for the use of i.a. full ROM training, lengthened partials and weighted stretching, so let’s break down the critique of SMH. The logic is based on the following hypotheses.
PS. If you’re not up-to-date on what SMH is, I recommend you watch this free video excerpt from one of my Online PT Course lectures. Also, if you’re not very serious about evidence-based fitness, I’d just watch that video and skip this article, because this article goes into granular detail.
Hypothesis 1: Emphasizing the stretch causes muscle growth via the addition of sarcomeres in series.
This might be true, but to my knowledge, no human study has ever directly observed sarcomerogenesis in series. In fact, Pincheira et al. (2022) directly refuted it and found that instead of sarcomere addition, the existing sarcomeres lengthen.
Regardless, either makes the muscle fascicle longer, so let’s assume emphasizing the stretch in your training indeed causes muscle lengthening.
Hypothesis 2: All stretch-mediated hypertrophy is due to lengthening.
This goes against the dominant school of thought in science of the past decades. Most muscle growth from training is normally via muscle thickening, not lengthening. Even specifically for SMH, we’ve had direct evidence in animals since the 70s that, purely passive muscle stretching can stimulate robust muscle growth via the addition of sarcomeres in parallel (and in series).
Moreover, I’ve posted 2 studies over the past year showing that purely passive (but extremely brutal) muscle stretching can stimulate strength gains comparable to strength training. Warneke et al. (2023) even found such strength gains in trained individuals when tested at short muscle lengths(!) If all SMH is due to muscle lengthening, how does it increase muscle strength to a similar degree as lifting weights, especially at short muscle lengths? (At long lengths, you could argue for a change in the length-tension relationship.)
Third, multiple human studies have observed significant increases in muscle thickness and cross-sectional area (CSA) from SMH, not just length. However, the critics of SMH have come up with a third hypothesis to counteract this last observation.
Hypothesis 3: The increases in muscle CSA and thickness after SMH are the result of muscle lengthening.
This is highly questionable. Physiological CSA should not logically increase purely as a result of muscle lengthening, as it’s calculated as volume divided by length, so any increases in muscle volume from the muscle being longer should be negated by the increased length.
That said, studies typically measure the simpler anatomical CSA or thickness and these could theoretically increase as a result of muscle lengthening in pennate muscles. Pennate muscles have their muscle fascicles arranged diagonally, so if we increase the length of the fascicles, they could bulge out more, increasing the diameter of the muscle, especially near the middle. However, this assumes that the fascicles are elongated linearly without any resistance and without any changes in the rest of the muscle architecture. How much the muscle’s length and diameter change crucially depends on the orientation of the muscle fibers, which fascicles lengthen, any corresponding changes in tendon length and how the connective tissue keeps the muscle bundled together. As it turns out, multiple human studies have found that even very large increases in muscle fascicle length do not translate into increased physiological cross-sectional area or muscle thickness [2, 3] (which strongly correlates with anatomical cross-sectional area).
I recently made this argument on my Instagram and Paul Carter responded with multiple stories and comments about why he thinks SMH is all just muscle lengthening. His thesis rests on a letter to the editor by Jorgenson & Hornberger (2019). This letter – not a study – contains a model – not actual data – predicting that a 13% increase in fiber length would cause a 52% increase in anatomical CSA. That’s about 10x more muscle growth than we see in a typical strength training study. In contrast, the above human studies have found no significant increases in muscle thickness (and thereby likely ACSA) after increases in muscle fascicle length as great as 22%. Why the difference? Well, the model was applied to the plantaris muscle of anesthetized rats. So perhaps this model is not ideal to explain the results of human strength training studies.
The model also predicts that muscle lengthening increases muscle CSA the most in the middle of the muscle belly, whereas emerging research suggests stretch-mediated hypertrophy occurs primarily in the parts of the muscle closest to the moving joint.
Speaking of Paul Carter, I rarely ever call people out by name, but I believe he’s truly a detriment to the fitness industry. His outlandish claims have been challenged multiple times by some of my evidence-based peers and he has generally responded with name calling and blocking them, 2 things he’s now infamous for. Paul is more intelligent than the average meathead, just smart enough to cite scientific research, but he’s clearly no scientist. Combined with infallible confidence in his own superiority over the rest of the industry and a great physique (which, to his credit, he admits is not natural), he regularly posts pseudoscience that contains just enough truth to confuse people. This is a recipe for success on social media, but as a source of information, it can be worse than no information at all.
Hypothesis 4: Muscle lengthening is finite and therefore not relevant as a long-term driver of muscle growth in trained individuals.
This is another hypothesis that’s untested, but I would say it’s highly plausible and in line with the available data. Muscles can only get so long, as they’re stuck between their origin and insertion. However, it’s worth noting that muscle fascicle lengthening has still been observed in national-level strength athletes near the end of a 6-month training block. So even in the unlikely scenario that muscle lengthening turned out to be the only growth mechanism, it could still be relevant to maximize muscle growth.
In sum, there are 2 ways we can interpret the current literature on stretch-mediated hypertrophy (SMH). The first is the simple and direct way. Multiple studies have shown that emphasizing the lengthened positions – the stretch – of muscles can enhance size and strength gains (depending on how strength is measured), so we should try to take advantage of this in our training. Little to lose, a lot to gain. The alternative viewpoint is that stretch-mediated hypertrophy might be entirely due to muscle lengthening, which somehow also makes you stronger, the animal research of parallel sarcomerogenesis is not representative of humans (but that 1 theoretical model on rat muscles is), the findings of increased muscle thickness in humans could theoretically be the result of muscle lengthening despite multiple studies not observing this, and muscle lengthening is a finite growth pathway; therefore, SMH is irrelevant for trained lifters. Occam’s razor dictates it’s more logical to prefer the simpler explanation. Therefore, my take is: until we have evidence that SMH is not relevant for trained lifters, we should try to take advantage of it.
Thanks to Milo Wolf and Kassem Hanson for peer-reviewing this article!
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