What is stretch-mediated hypertrophy and how does it work?

Currently, the hive mind of evidence-based fitness influencers is talking about stretch-mediated hypertrophy and how we can maximize it using lengthened partials. So let’s define stretch-mediated hypertrophy and take a look at what the exercise science literature says about it.

If you like this article, you will like my second book (see on Amazon).

What is stretch-mediated hypertrophy?

The wrong definition

In the fitness industry, social media influencers have started to refer to stretch-mediated hypertrophy as the increase in muscle mass that occurs after training with stretched-position exercises. There are a number of problems with using this definition.

Firstly, “hypertrophy” in exercise science refers to an increase in the size of single muscle fibers partly because hypertrophy is an intrinsic process to single muscle fibers and partly because hypertrophy excludes hyperplasia as well as any other change in muscle size that is not mediated by single fiber growth. This distinction is especially relevant in the case of stretch-mediated hypertrophy because many animal models have shown that stretching often produces quite substantial hyperplasia, especially in birds. Other studies have shown that static stretching and eccentric contractions can increase muscle collagen content under certain circumstances. In such cases, substantial increases in muscle mass occur that are not attributable to increases in muscle fiber size. In practice, we need to be careful about what literature we include in any discussion concerning stretch-mediated hypertrophy. We must essentially exclude the hyperplasia literature. And if we do wish to have a conversation that includes references to hyperplasia or collagen addition and how stretch could contribute to increases in muscle mass by means of any such mechanisms, we need to use a more general term like “stretch-mediated muscle growth”.

Secondly, the hypertrophy that occurs after eccentric-only training or training with stretched-position exercises does not arise solely from stretch. Some of the muscle growth arises due to the stretch stimulus and some arises due to the active mechanical tension stimulus that occurs in any strength training exercise because of the muscular contractions that involve actin-myosin crossbridges. Since active mechanical tension created by actin-myosin crossbridge formation shortens the muscle fiber, it cannot be called a stretching force and therefore it cannot ever be a contributor to stretch-mediated hypertrophy. So, there is stretch-mediated hypertrophy in addition to contraction-mediated hypertrophy. Indeed, many studies in the literature have compared the hypertrophy produced by [1] partial range of motion (ROM) or contracted-position exercises and [2] full ROM or stretched-position exercises. Often, the partial ROM or contracted-position exercises cause some muscle growth (contraction-mediated hypertrophy), while full ROM and stretched-position exercise training causes slightly more (both contraction-mediated hypertrophy and stretch-mediated hypertrophy together). When we look at such studies, we can define stretch-mediated hypertrophy as the extra hypertrophy seen in the groups training with full ROM or stretched-position exercises compared to the groups training with partial ROM or contracted-position exercises.

In summary: stretch-mediated hypertrophy only refers to increases in the size of single muscle fibers that are stimulated by stretching them. Also, strength training produces contraction-mediated hypertrophy irrespective of whether it is performed with contracted-position exercises or stretched-position exercises. Therefore, the muscle growth that occurs after training with stretched-position exercises does not solely comprise stretch-mediated hypertrophy.

The right definition

Starting with the fact that the term “hypertrophy” in exercise science always refers to an increase in muscle fiber size and excludes hyperplasia, and acknowledging that we need to separate out the effects of stretch from the stimulating effects of muscular contractions, we can instead define stretch-mediated hypertrophy as an increase in single muscle fiber size that results from a stimulus provided by stretch.

In practice, this means that static stretching studies are far better sources of information regarding stretch-mediated hypertrophy than strength training studies that involve either comparisons between partial and full ROM exercises or that involve comparisons between contracted-position and stretched-position exercises. After all, static stretching only involves the stretch stimulus that produces stretch-mediated hypertrophy, while full ROM and stretched-position exercises always involve both stretch-mediated hypertrophy and contraction-mediated hypertrophy, and it is very difficult to discern which stimulus is responsible for the muscle growth that such types of strength training generate.

Additionally, when looking at static stretching studies, we will learn the most about stretch-mediated hypertrophy by looking at investigations that measure changes in single muscle fibers because hypertrophy is literally defined by reference to changes in single muscle fiber size. If you increase the size of a muscle by changing anything outside of the muscle fiber, such as collagen, extracellular water, or intramuscular fat content then you might be increasing muscle mass but that does not count as hypertrophy. This means that our best opportunities for understanding stretch-mediated hypertrophy are going to come from animal models, which very often measure changes in single muscle fiber size. Human studies rarely do that. Also, when they do take such measurements, the accuracy is very low owing to the inherent limitations of the available techniques and this makes statistical significance difficult to attain.

Finally, this definition is still not without its own problems because some researchers define “hypertrophy” very tightly to refer only to the addition of myofibrils in parallel leading to an increase in muscle fiber diameter. In contrast, others are happy to include both sarcomere addition as well as myofibril addition. This has given rise to parallel terminologies wherein some researchers will describe myofibrillar addition as being hypertrophy and sarcomere addition as sarcomerogenesis, while others will describe myofibrillar addition as being radial hypertrophy and sarcomere addition as being longitudinal hypertrophy. In this article, I will adopt the method of describing myofibrillar addition as being radial or transverse hypertrophy and sarcomere addition as being longitudinal hypertrophy.

In summary: since stretch-mediated hypertrophy involves an increase in the size of single muscle fibers in response to a stimulus provided by stretch, the best studies for understanding the phenomenon are those that actually record changes in the size of single muscle fibers after stretching alone and without the presence of muscular contractions. These studies are all done in animals.

What happens when we passively stretch single muscle fibers?

Introduction

So far, we have defined stretch-mediated hypertrophy as an increase in single muscle fiber size that results from a stimulus provided by stretch. Based on this definition, we established that the most useful information about stretch-mediated hypertrophy is therefore going to come from studies that [1] only involve stretch as a stimulus for muscle growth, and that [2] record changes in single muscle fiber size. Looking for studies that fulfil those criteria, we immediately hit upon animal models. The most common animal models are limb immobilization with casts and distraction (surgical bone lengthening). Even so, other methods have been used quite often such as tissue expanders and tendon transfers, which fulfil the same function as distraction, and daily bouts of static stretching, which basically does the same thing as limb immobilization. Let us now review some of the limb immobilization and distraction literature to see what they can tell us about stretch-mediated hypertrophy.

#1. Limb immobilization

Limb immobilization involves placing a plaster cast upon a limb and leaving it there for a period of time lasting anywhere between a few days and a few weeks. Often, such studies use multiple groups with casts at different joint angles (and therefore at muscle lengths) and with casts placed on the limb for varying durations of time. Often, casts are placed at maximum physiological ranges of motion in order to generate the largest possible adaptation. The effects of limb immobilization can be considered to be physiological because the muscle could be lengthened to that extent in normal day-to-day activities. In practice, we should theoretically be able to create the same kind of adaptations both in animals and in humans by means of static stretching programs, albeit with smaller magnitudes of effect. Here are the key findings of limb immobilization studies.

1. Sarcomerogenesis— studies have shown that when muscles are elongated semi-permanently by being held for days or weeks in a cast in a lengthened position, the individual muscle fibers inside the muscle display very rapid increases in the number of sarcomeres per muscle fiber, which is known as sarcomerogenesis or longitudinal hypertrophy. In contrast, there is relatively little evidence that limb immobilization can cause any increases in single muscle fiber cross-sectional area. The same pattern of results can be observed in the static stretching studies.
2. Sarcomerogenesis is extremely rapid— studies have shown that the addition of sarcomeres (and the increase in muscle mass) occurs very rapidly and there are substantial increases within just a couple of days. This means that sarcomerogenesis is much faster than the addition of myofibrils that causes an increase in muscle fiber cross-sectional area.
3. Change in the length-tension relationship— studies have reported that adding or subtracting sarcomeres corresponds with a change in the length-tension relationship of the immobilized muscle. In other words, adding sarcomeres after immobilization at long muscle lengths causes the muscle fibers of the muscle to exert higher forces at longer muscle lengths, while subtracting sarcomeres as a result of immobilization at short muscle lengths causes the muscle fibers of the muscle to exert higher forces at shorter muscle lengths. The length-tension relationship of the whole muscle reflects the length-tension relationship of single muscle fibers inside that muscle. This is super important because it means that the addition of sarcomeres in series occurs without the muscle fiber changing its termination point within the surrounding muscle fascicle. By doing so, it causes each sarcomere to sit at a shorter resting length and produce its highest forces (on the plateau of the length-tension relationship) at longer muscle lengths. If the muscle fiber added sarcomeres by traveling further up inside the surrounding muscle fascicle and maintaining the resting lengths of the sarcomeres, then neither the length-tension relationship of the muscle fiber nor of the muscle as a whole would change.
4. Motor unit recruitment is not necessary — a subset of studies have explored what happens to denervated muscles when they are placed into casts and immobilized at long muscle lengths. Denervation often creates very rapid atrophy (as does immobilization) so these results can be difficult to interpret. However, there are indications that sarcomere addition still occurs when denervated muscles are stretched, indicating that the stimulus for the adaptation does not require the muscles to be activated at any point in time.

In summary, the animal limb immobilization studies have shown us that stretch causes the very rapid addition of sarcomeres in series, which is known as sarcomerogenesis, but probably does not produce meaningful increases in muscle fiber cross-sectional area. They indicate that the stimulus provided by stretch does not require any muscle fiber activation, as observed by its influence on denervated muscle. And they have shown us that the sarcomere addition does not alter the termination points of the muscle fiber inside the surrounding muscle fascicle because it causes a change in the muscle fiber length-tension relationship, which can be observed in the whole muscle length-tension relationship.

#2. Distraction

Distraction studies involve a type of permanent limb lengthening surgery in animals, for some strange reason most often in rabbits but also in rats. Typically, after the initial surgery, a bone is lengthened gradually over a period of several weeks such that the attached muscle also lengthens gradually. Owing to the way in which muscles bulge away from bones, a relatively small increase in bone length leads to a much larger increase in whole muscle length. This means that the effects of distraction studies are usually very large and can produce very statistically significant effects that are easy to observe in research investigations.

Unfortunately, in contrast to limb immobilization, the effects of distraction are inherently supraphysiological, which means that we cannot extrapolate either the nature or the magnitude of the effects to normal static stretching programs in humans. Even so, the distraction technique is extremely useful because the increase in muscle length is totally under the control of the researchers. Indeed, owing to the way in which the bone is lengthened very gradually, the researchers can produce small increases every day for several weeks and then stop lengthening the bone to see how the muscle responds both to continual lengthening and also to being maintained at a long length. Despite being supraphysiological, distraction studies have nevertheless reported similar findings to limb immobilization trials.

1. Sarcomerogenesis — studies have shown that when muscles are stretched by the underlying bone being lengthened, the individual muscle fibers inside the muscle display very rapid increases in the number of sarcomeres per muscle fiber. The same pattern of results can be observed in tendon release studies. In contrast, there is relatively little evidence that muscle fibers increase meaningfully in diameter as a result of such interventions.
2. Sarcomerogenesis is determined by sarcomere length— likely the most important discovery of the distraction literature is that the extent to which a muscle is stretched does not affect whether sarcomerogenesis happens. It is the sarcomere length that matters. If a muscle is stretched but sarcomeres do not elongate past a certain length (2.7 micrometers in rat muscle), then the muscle fibers do not add additional sarcomeres. Conversely, for as long as the sarcomeres are stretched past this length, sarcomerogenesis occurs.
3. Sarcomerogenesis quickly reaches a plateau — studies have shown that the addition of sarcomeres occurs only while the bone is lengthened continually, day after day. Once the researchers stop lengthening the bone and allow the muscle to remain at the new, longer length, the muscle fibers relatively quickly stop adding sarcomeres. The same pattern of results can be observed with tissue expansion methods.
4. Change in the length-tension relationship— studies have reported that the addition or subtraction of sarcomeres corresponds with a change in the passive length-tension relationship of the stretched muscle. In other words, adding sarcomeres by distraction causes the muscle fibers of the muscle to produce higher forces at longer muscle lengths. This tells us that adding sarcomeres in series occurs without the muscle fiber changing its termination point within the surrounding muscle fascicle. By doing so, it causes each sarcomere to sit at a shorter resting length and produce its highest forces (on the plateau of the length-tension relationship) at longer muscle lengths. If the muscle fiber added sarcomeres by traveling further up inside the surrounding muscle fascicle and maintaining the resting lengths of all of the sarcomeres, then neither the length-tension relationship of the muscle fiber nor of the muscle as a whole would change.

In summary, distraction studies have reported similar findings to the limb immobilization investigations. In addition, they have discovered that the stimulus for sarcomerogenesis is stretching sarcomere lengths (and not muscle lengths) past a certain key threshold, and that sarcomerogenesis will continue for as long as muscle lengths are continually increased from day-to-day. In contrast, when the day-to-day increases in muscle length are discontinued, this causes a very sudden cessation of sarcomere addition. As we will see later in this article, these two observations are closely linked to one another, since it is sarcomerogenesis that is responsible for causing a reduction in sarcomere lengths.

Summary of animal model findings

In summary, the animal model studies have shown us that stretching causes muscle growth without the need for muscle activation and mainly by the addition of sarcomeres in series. They have shown that this type of hypertrophy is very rapid but also quickly reaches a plateau if the muscle length is not continually increased so as to maintain sarcomere lengths longer than a certain, key threshold. And they have clarified that muscle fibers do not change their intrafascicular termination points because we see a clear change in the muscle fiber length-tension relationship that can be related to a change in whole muscle length-tension relationship.

In summary: stretch-mediated hypertrophy predominantly involves adding sarcomeres in series. This adaptation occurs very rapidly when the stretch is initially applied and then displays diminishing returns with plateaus being apparent within just a couple of weeks. The muscle fiber does not change its intrafascicular termination points.

Human studies of static stretching

Static stretching studies have often been performed in humans. The earliest such studies rarely reported hypertrophy. Nevertheless, this is most likely simply due to the lack of sufficient resolution in the measurement methods. Most of the more recent investigations have reported increases in muscle size of statistical significance. Importantly, they have also reported findings that are totally in line with the results observed in animal models.

1. Increases in muscle fascicle length — increases in muscle fascicle length have been reported in static stretching studies as the primary form of hypertrophy that occurs. In animal models, increases in muscle fascicle length occur in tandem with sarcomere addition and there is no reason at all to assume that the same does not occur in humans. Indeed, a recent review paper stated in their opening paragraph that increases in muscle fascicle length are assumed to reflect sarcomere addition in humans, so this is clearly widely-regarded as the default assumption. Therefore, we can assume that sarcomere addition is likely the predominant source of stretch-mediated hypertrophy in humans as well as in animals. If you wish to argue that the muscle fascicle length changes do not reflect sarcomerogenesis, then go ahead but your case must be strong and not simply an appeal to a lack of evidence because the default assumption is that increases in muscle fascicle length do in fact reflect sarcomere addition.
2. Changes in the length-tension relationship — The angle of peak torque changes after programs of static stretching, as evidenced by the fact that the strength gains produced by static stretching training programs occur mainly at long muscle lengths and not at short muscle lengths, which is exactly what we would expect from an increase in sarcomeres in series that changes the resting length of the sarcomere. This tells us that the addition of sarcomeres in series in humans occurs without the muscle fiber changing its intrafascicular termination point. Whenever the intrafascicular termination points are fixed, then the addition of new sarcomeres causes each sarcomere in the muscle fiber to sit at a shorter resting length and therefore produce its highest forces (on the plateau of the length-tension relationship) at longer muscle lengths. Therefore, if you wish to argue that human muscle fibers can change their intrafascicular termination points, you must first provide another explanation for why such changes in the angle of peak torque happen (and it had better be really good because changes in the length-tension relationship due to sarcomere addition are very well-documented).

In summary: stretch-mediated hypertrophy in humans can be observed during static stretching studies in the form of increases in muscle fascicle length. Such increases in muscle fascicle length are assumed to reflect sarcomere addition and are associated with changes in the length-tension relationship, which tells us that the addition of sarcomeres occurs without any changes in the intrafascicular termination points of the growing muscle fibers.

Why does stretching a muscle to a constant length produce diminishing returns in sarcomerogenesis?

Introduction

Studies have shown that stretching a muscle causes rapidly diminishing results in terms of the amount of sarcomere addition that occurs when the muscle is maintained at a fixed long length. In other words, over time, fewer sarcomeres are added in response to the exact same amount of whole muscle stretch. So why does this happen?

Types of mechanical tension

The stimulus for hypertrophy is mechanical tension, which can come from two completely different sources, and which causes two totally different types of muscle fiber growth.

On the one hand, the mechanical tension can be generated by muscular contractions, which is where muscle fiber activation and subsequent excitation-contraction coupling causes the formation of actin-myosin crossbridges which then pull the muscle fiber to shorter lengths. Since this force is pulling the muscle fiber to a shorter length and not to a longer length, we cannot refer to it as a stretch stimulus and any hypertrophy that it stimulates therefore cannot be called “stretch-mediated hypertrophy.” This mechanical tension stimulates the addition of new myofibrils in parallel inside the muscle fiber and thereby causes an increase in muscle fiber cross-sectional area. We can call this type of mechanical tension “active mechanical tension” and we can describe the particular type of muscle growth as “contraction-mediated hypertrophy.” As I have explained in various places previously, the magnitude of this active mechanical tension is determined by the force-velocity relationship, so we need a slow movement speed during the concentric phase of a movement in order to generate enough force to stimulate contraction-mediated muscle growth.

On the other hand, the mechanical tension can be generated by stretching the muscle fiber, which is where an external force pulls the fiber apart. Various studies have been performed to establish what structures inside the muscle fiber produce resistance to this external pulling force. In the beginning, many researchers supposed that the collagen structures were themselves responsible for the resistance to stretch that the muscle fiber produces. However, more recent investigations have revealed that it is the giant molecule titin that provides the resistance. They have shown that in single muscle fibers, removing the collagen wrapping around the muscle fiber has relatively little impact on the resistive force that is generated during a stretch, while limiting the ability of titin to contribute has a very substantial effect. We could describe this type of mechanical tension as “passive mechanical tension” and we obviously already call the related type of muscle growth “stretch-mediated hypertrophy.”

What determines the amount of passive mechanical tension that a muscle fiber experiences during a static stretch?

Titin molecules run longitudinally inside individual sarcomeres and span an entire half sarcomere. The extent to which titin is lengthened and creates passive mechanical tension depends upon the length of individual sarcomeres. Therefore, it is the stretching of individual sarcomeres and hence the stretching of titin that determines the magnitude of the passive mechanical tension stimulus for sarcomerogenesis (and thus also the stretch-mediated hypertrophy). Indeed, this has been confirmed in the animal model studies of titin, which have used breeds of mice with altered titin molecules to make them stiffer. Such mouse breeds display enhanced muscle size due to additional sarcomerogenesis stimulated from muscular contractions performed during normal daily activities.

As we saw in the previous sections discussing limb immobilization, bone distraction, and other animal models such as tissue expansion and tendon transfers, sarcomerogenesis stops happening within just a couple of weeks if whole muscle length is not continually increased. If a muscle is stretched to a particular length and then maintained at that length, then sarcomeres will be added for a couple of weeks (most rapidly at first and progressively more and more slowly) before a plateau in muscle fiber length happens. In contrast, if whole muscle length is continually increased to longer and longer lengths, then sarcomeres are added for as long as this progressive length increase occurs. This makes it very clear that simply reaching a long muscle length is not sufficient to cause sarcomerogenesis. Rather, it is the sarcomere length that matters because this determines the magnitude of the passive mechanical tension provided by titin.

Sarcomerogenesis involves the addition of sarcomeres to a muscle fiber. From our analysis of the changes in the length-tension relationships of muscle fibers and of whole muscles, we know that adding sarcomeres to a muscle fiber does not change its intrafascicular attachment points. This means that adding sarcomeres forces all of the sarcomeres in the muscle fiber to sit at shorter lengths simply so that all of these sarcomeres can occupy space inside the muscle fiber. When each sarcomere sits at a shorter resting length, the titin molecules running through the sarcomeres produce less passive mechanical tension when they are elongated. When the amount of passive mechanical tension drops below a certain threshold, the amount of whole muscle stretch stops stimulating sarcomerogenesis. Rodent studies have shown that when sarcomere length is held below 2.7 micrometers, sarcomerogenesis does not occur. When sarcomere length is held above this threshold, sarcomere addition occurs rapidly. Whether the same threshold is valid in all other animals is unknown but the principle is likely to apply consistently.

Evidently, in practice we can avoid falling below this threshold during static stretching programs if we simply ensure that each static stretching bout involves reaching a longer maximum muscle length corresponding to a larger joint angle ROM. In this way, we can ensure that sarcomerogenesis does not reach a plateau. Training methods that do not involve continual increases in maximum muscle length (such as strength training exercises) cannot circumvent this limitation, however.

In summary: sarcomerogenesis is stimulated whenever the titin molecules inside sarcomeres are stretched and therefore produce passive mechanical tension. Since sarcomere length reduces when new sarcomeres are added, sarcomerogenesis causes a reduction in the amount of passive mechanical tension that titin generates in each sarcomere. This causes diminishing returns over time in the amount of stretch-mediated hypertrophy that is generated by a given amplitude of static stretching.

What happens when we actively stretch single muscle fibers?

Introduction

Having looked at what happens when we passively stretch single muscle fibers, let us now consider what happens when we stretch an activated muscle fiber. Obviously, we have both types of mechanical tension. We have the mechanical tension that involves an internal force pulling muscle fibers to a shorter length by means of muscle fiber activation causing the formation of actin-myosin crossbridges (which we already called active mechanical tension and which causes contraction-mediated hypertrophy). And we have the mechanical tension that involves an external force pulling muscle fibers to a longer length and the resistance to this force by titin molecules inside sarcomeres (which we call passive mechanical tension and which causes stretch-mediated hypertrophy).

It is tempting to assume that we can simply extrapolate the research from the static stretching literature to eccentric contractions and subtract the effects of active mechanical tension stimulating contraction-mediated hypertrophy. However, this is not possible. Indeed, a key feature of static stretching is that muscles are elongated to a maximum muscle length corresponding to a maximum joint angle. Moreover, as explained above, reaching such a maximum muscle length is critical for stimulating the addition of sarcomeres by the production of passive mechanical tension by titin molecules. In stark contrast, neither eccentric-only training nor the eccentric phases of normal strength training reach anything close to such long muscle lengths or their corresponding joint angles. Very often, they simply make use of the normal ranges of motion that we use in daily life. So if we make the assumption that passive mechanical tension functions in exactly the same way in static stretches as in eccentric contractions, then our assumption will be that no meaningful passive mechanical tension is generated. Nevertheless, we know that eccentric contractions can cause stretch-mediated hypertrophy in the form of muscle fascicle length increases in humans without reaching anything close to maximum muscle lengths (the Nordic curl literature is a great example of this happening).

Based on such observations, we can see that passive mechanical tension is generated at shorter muscle lengths during eccentric contractions and that this stimulates stretch-mediated hypertrophy. To understand why this happens, we must look at how the behavior of titin changes in response to muscle fiber activation.

How does titin behave differently during eccentric contractions compared to during static stretching?

Titin is a giant molecule made up of three segments. These segments have technical names but we can call them the compliant segment, the bridge segment, and the stiff segment. When titin is stretched inside an inactive muscle fiber, all three segments are free to move. Obviously, this means that the majority of the lengthening that titin experiences comes from its most compliant segment, and this generates minimal passive mechanical tension. This is why elongating a muscle produces no stimulus for muscle growth in a static stretch until the maximum joint angle ROM is reached. At this point, the compliant segment runs out of capacity to lengthen any further and the stiff segment starts to lengthen instead. As the name suggests, the stiff segment produces a high degree of passive mechanical tension and this is what stimulates sarcomere addition.

(Evidently, if the sarcomere does not lengthen sufficiently because there are too many sarcomeres in series in the muscle fiber, then the stiff segment will never be elongated and minimal passive mechanical tension will be produced and therefore no sarcomerogenesis will be stimulated. This is what happens in the limb immobilization studies after a couple of weeks of holding the muscle at a long length and also what happens in the distraction studies once the bone lengthening process is stopped and the bone is maintained at a new, long length).

In contrast, when titin is stretched inside an activated muscle fiber, only the stiff segment is free to move. Exactly how this happens is a matter of investigation and there are various theories. Even so, it seems likely that the compliant segment is locked down to the nearest actin myofilament by processes that occur during muscle fiber activation. Consequently, the stiff segment starts producing a high degree of passive mechanical tension at a much shorter muscle length than occurs during a static stretch. This is why eccentric contractions produce several times more force per muscle fiber than concentric contractions throughout the whole joint angle ROM. However, the amount of passive mechanical tension still increases with increasing muscle elongation in the eccentric phase because the stiff segment of titin is still being stretched, it is just being stretched from a much shorter length than occurs during a static stretch. This explains why stretched-position exercises produce more stretch-mediated hypertrophy than contracted-position exercises (and this is observed in eccentric-only training programs as well as during normal strength training programs). Additionally, it explains why stretch-mediated hypertrophy is frequently greater after strength training than after static stretching.

It bears repeating that this titin-based mechanism of passive mechanical tension during eccentric contractions is essential for us to display any stretch-mediated hypertrophy during strength training. The static stretch literature and the related animal models show us that we cannot produce any passive mechanical tension for hypertrophy to occur unless we reach extremely long whole muscle lengths. And these studies have shown that we must carry on stretching to longer and longer maximum muscle lengths every session for the adaptation to continue occurring. Strangely, some fitness industry influencers have come to believe that simply holding the lengthened position of an exercise is enough for this to count as a stretch stimulus for a muscle, even though it is not activated. Yet, that exact same position could be reached hundreds of times a day for that muscle in the activities of daily life. The lengthened positions of most strength training exercises are not stretches in the strictest sense of the word because they do not actually involve stretching a muscle. So we need titin for passive mechanical tension to be generated.

In summary: the passive mechanical tension that stimulates stretch-mediated hypertrophy is generated by the elongation of the stiff segment of titin inside sarcomeres. In an inactive muscle fiber, the stiff segment of titin only lengthens once the compliant segment has finished lengthening, which occurs right at the very end of the joint angle range of motion. In an activated muscle fiber, the stiff segment of titin lengthens from a much shorter muscle length because the compliant segment is prevented from lengthening by processes that occur due to muscle activation. In practice, this means that the passive mechanical tension stimulus for stretch-mediated hypertrophy is greater during eccentric contractions than during static stretching.

Human studies of strength training

If you have reached this point in the article, congratuations! We will now start talking about the studies that the hive mind of fitness industry social media influencers believe comprises the stretch-mediated hypertrophy literature, which is the studies comparing stretched-position exercise and contracted-position exercise training, and the studies comparing partial ROM and full ROM exercise training. In addition, we will include studies comparing the effects of concentric-only and eccentric-only training because they are essentially doing exactly the same thing by comparing groups training with [1] active mechanical tension that stimulates only contraction-mediated hypertrophy, and [2] both active mechanical tension that stimulates contraction-mediated hypertrophy and passive mechanical tension that stimulates stretch-mediated hypertrophy. Finally, we will add on studies that have looked at changes in muscle fascicle length over time because increases in muscle fascicle length are widely-assumed to occur as a result of sarcomerogenesis and can be considered to be synonymous with stretch-mediated hypertrophy. Altogether, the human strength training literature shows exactly what we would expect based on the model derived above from the animal model studies.

1. Eccentric-only versus concentric-only studies — these studies have shown that eccentric-only training causes increases in muscle fascicle length while concentric-only training does not. Yet, the total gains in muscle size areonly marginally greater after eccentric-only training. Meanwhile, eccentric-only training produces shifts in the angle of peak torque towards longer muscle lengths that are substantial and clearly far larger than the changes that occur after concentric-only training. Clearly, the obvious interpretation of these results is that the passive mechanical tension produced in eccentric contractions is necessary to create the increases in muscle fascicle length (by sarcomerogenesis, which is evidenced by the shift in the angle of peak torque). Hence, the increase in muscle fascicle length comprises the extra hypertrophy on top of that muscle growth stimulated by active muscular contractions. Therefore, it is synonymous with “stretch-mediated hypertrophy.”
2. Full ROM compared with short ROM (and stretched-position versus contracted-position) studies — these studies have shown that full ROM and stretched-position exercise training causes greater increases in muscle fascicle length than partial ROM and contracted-position exercise training. In this case, the total gains in muscle size are very often greater after full ROM and stretched-position exercise training. In the light of the comparison between eccentric-only and concentric-only training above, the obvious interpretation of these results is that the greater passive mechanical tension produced in the more stretched positions produces greater increases in muscle fascicle length (which obviously again occurs due to sarcomerogenesis, and the increase in muscle fascicle length comprises the extra hypertrophy on top of that muscle growth stimulated by muscular contractions. Therefore, it is synonymous with “stretch-mediated hypertrophy.”
3. Stretched-position versus contracted-position eccentric-only training studies —to date, the only study in this category has shown that stretched-position eccentric-only training causes greater increases in muscle fascicle length in conjunction with a greater change in the angle of peak torque than contracted-position eccentric-only training. This confirms that the greater increases in muscle fascicle length are indeed linked to the sarcomerogenesis that causes the alteration in the muscle length-tension relationship.
4. Increases in muscle fascicle length after strength training — several studies have examined how adaptations in muscle fascicle length occur at different points in a strength training program by taking more than two measurements over time. Such studies have uniformly shown that the increases in muscle fascicle length plateau relatively quickly. This is exactly what we would expect if the muscle fascicle lengths reflected sarcomerogenesis. Sarcomere addition displays rapidly diminishing returns because adding sarcomeres reduces resting sarcomere length and therefore reduces the amount of passive mechanical tension that the stiff segment of titin can generate in a sarcomere for a given amount of whole muscle stretch. This is clearly demonstrated in the animal model studies listed above. Moreover, our understanding of how titin behaves and contributes to the passive mechanical tension stimulus also predicts this outcome. All of the literature fits together exactly as we would expect.

In summary: the human strength training studies fit with the basic physiology derived from animal models. Stretched-position exercises, full ROM exercises, and eccentric-only contractions produce more passive mechanical tension than contracted-position exercises, partial ROM exercises, and concentric-only contractions. This extra passive mechanical tension causes a greater increase in muscle fascicle length due to sarcomerogenesis, which can be observed by the greater increase in the angle of peak torque that indicates a larger change in the length-tension relationship. Even so, the ability to produce increases in muscle fascicle length is limited to a couple of months before a plateau occurs.

What are the practical implications of this different behavior of titin in eccentric contractions compared to during static stretching?

How titin behaves inside an activated muscle fiber and how this is different from how it behaves inside an inactive muscle fiber has huge implications for how stretch-mediated hypertrophy works during strength training because it means that only those muscle fibers that are activated during eccentric phases of strength training exercises are capable of experiencing the stimulus that causes the addition of sarcomeres. Obviously, the above section has shown the fundamental findings. Nevertheless, we can add a few more implications that follow inevitably from the physiology.

1. Limited motor unit recruitment — Since the eccentric phases of normal strength training exercises involve much lower levels of motor unit recruitment even at muscular failure, this limits the number of muscle fibers that can experience the stimulus for stretch-mediated hypertrophy. We can estimate the level of muscle activation by considering the difference between muscle fiber force in concentric and eccentric contractions, since the larger the relative force in the eccentric phase the lower the required level of muscle activation. Since the residual force enhancement effect means that single muscle fibers can produce 80% more force in the eccentric phase than in a concentric phase, the number of muscle fibers that are activated will never really be higher than 55% of the level in the early repetitions of the concentric phase (it is the early repetitions that count since eccentric contractions do not experience fatigue in the same way as concentric contractions). The majority of these muscle fibers are slow twitch muscle fibers that do not have the ability to grow substantially after strength training and quickly reach a plateau due to the size principle of striated muscle.
2. Defining stretched-position exercises — Since muscle fibers must be activated in order for titin to behave in this unique way and provide passive mechanical tension despite the muscle not actually being stretched to a maximum length, this affects our definition of a stretched position exercise. It means that a stretched position exercise must be an exercise that involves the peak level of effort at a long muscle length (for example, a preacher curl). An exercise that involves reaching a long muscle length but which does not involve much effort at that long length (for example, an incline bench biceps curl) will not produce the same amount of passive mechanical tension since the muscle fibers of the muscle are minimally activated. We cannot compensate for the lack of muscle fiber activation unless the muscle fibers are lengthened to the same extent as they would be during a static stretch.
3. Which muscles can experience stretch-mediated hypertrophy in any given exercise — since muscle fibers must be activated in order for titin to behave in this unique way and provide passive mechanical tension despite the muscle not actually being stretched to a maximum length, this determines whether a stretched position exercise can actually work a muscle group. Indeed, the principle of neuromechanical matching tells us that muscles receive a proportion of the available central motor command according to their leverage during the exercise. This means that when muscles have poor leverage in the stretched position of an exercise, they will not experience passive mechanical tension despite being lengthened to relatively long length. For example, the glutes do not have good leverage when the hip is flexed so do not experience as high levels of muscle activation as the adductor magnus in stretched positions. Thus, despite reaching a long muscle length in full squats, they will not display substantial stretch-mediated hypertrophy. Similarly, the latissimus dorsi has poor leverage when the shoulder is flexed in the sagittal plane during pull-downs, pull-ups, or pull-overs. Therefore, it is not strongly activated in the stretched position and will not not display substantial stretch-mediated hypertrophy. We cannot make up for the low muscle activation with passive mechanical tension because we are not reaching the truly maximum muscle lengths that would qualify as a static stretch and thereby reach the critical threshold for sarcomere lengths that would be required in muscle fibers that are not activated.

In summary: stretch-mediated hypertrophy occurs during strength training only in those muscle fibers that are activated because the passive mechanical tension that stimulates the extra muscle growth is dependent upon a change in titin’s behavior that is caused by muscle fiber activation. Thus, it cannot easily be produced in muscles that are not strongly activated in the stretched position of an exercise even if they are in fact stretched, such as the gluteus maximus in squats and the latissimus dorsi in narrow grip pull-ups and pull-overs.

Why do some muscles more readily experience stretch-mediated hypertrophy than others?

Sarcomere operating lengths

In the above sections, we saw how the magnitude of passive mechanical tension that titin produces during an eccentric contraction depends upon the resting sarcomere length at the start of the contraction. We also saw how programs of static stretching or eccentric-only training or strength training with stretched-position exercises cause an increase in the number of sarcomeres (by means of sarcomerogenesis) and that this makes each of the sarcomeres shift to shorter resting lengths so that they can all fit into the same muscle fiber length as before.

Obviously, when a sarcomere has a shorter resting length, it must also have a shorter maximum length at a given maximum joint angle ROM (assuming that this maximum joint angle ROM does not increase). When we collect information about the starting and finishing lengths of the sarcomere over the whole physiological joint angle ROM, we can describe what we call the “sarcomere operating lengths” as relate to the length-tension relationship. The length-tension relationship is basically a set of thresholds that tell us at what sarcomere length a sarcomere displays certain features. For example, it tells us that sarcomeres cannot form actin-myosin crossbridges when they are shorter than a certain length (this is called “active insufficiency”). It tells us that sarcomeres produce a maximum number of crossbridges when they are between two moderate lengths (this is called the “plateau of the length-tension relationship”). And it tells us that sarcomeres will start to exert passive mechanical tension when they exceed a certain sarcomere length (this is the “descending limb of the length-tension relationship”).

When a muscle fiber adds sarcomeres in series during a static stretching or strength training program, the resting sarcomere length is reduced and this also changes the sarcomere operating lengths such that the sarcomere now reaches the start of the descending limb where passive mechanical tension is generated at a longer muscle length. Indeed, this is what causes the shift in the angle of peak torque because the point at which the plateau of the length-tension relationship is reached also shifts to a longer muscle length. After a certain number of sarcomeres are added and the resting sarcomere length is shifted sufficiently, the sarcomeres now do not reach far enough down the descending limb for enough passive mechanical tension to be generated to stimulate sarcomerogenesis.

Even so, not all muscles have the same resting sarcomere lengths and therefore they do not have the same sarcomere operating lengths. In practice, this means that some muscles do not have sarcomeres that reach far enough down the descending limb so as to cause sarcomere addition even before starting a static stretching or strength training program. Several studies have measured sarcomere operating lengths over the normal joint angle ROM and they have shown that they vary greatly between muscles. Some muscles contain fibers that have sarcomere operating lengths that reach the descending limb and others do not. For example, the quadriceps muscles have sarcomere operating lengths that reach the very end of the descending limb. In contrast, the triceps brachii have sarcomere operating lengths that do not even reach the start of the descending limb. In line with this, the quadriceps muscles typically grow more and display greater increases in muscle fascicle length after being trained with stretched-position exercises, while the triceps brachii usually do not display any differences between stretched and contracted-position exercises and never display any increases in muscle fascicle length.

In practice, there are various muscle groups that very likely have long resting sarcomere lengths and therefore respond easily to the stretch stimulus during strength training. The gluteus maximus, hamstrings, quadriceps, and pectoralis major are definitely in this category. There are a number of other muscle groups that definitely do not respond to the stretch stimulus during strength training. The biceps brachii and triceps brachii are definitely in this category. Other muscles are less easy to pin down to one category or another.

In summary: sarcomere operating lengths vary between muscles and this means that some muscles easily experience stretch-mediated hypertrophy while others do not. The gluteus maximus, hamstrings, quadriceps, and pectoralis major definitely respond to the stretch stimulus, while the biceps brachii and triceps brachii definitely do not.

How does fatigue differ between stretched position and contracted position exercises?

Introduction

Fatigue is defined as a temporary and reversible reduction in exercise performance as a result of previous bout of exercise. This reduction in exercise performance is often measured by a reduction in strength. Fatigue is produced by a range of mechanisms inside the central nervous system (CNS) and inside the muscle. Some of these local muscular mechanisms are long-lasting and cause fatigue to occur for days after a workout. Other local muscular mechanisms are much less long-lasting and the fatigue dissipates quickly after the workout ends. The long-lasting local muscular mechanisms involve calcium ion accumulation and are known to interfere with our ability to produce active and passive mechanical tension during strength training. The less long-lasting local muscular mechanisms involve metabolite accumulation.

If you want a much more detailed understanding of fatigue (particularly in relation to the calcium ion mechanisms), please read my other blog.

Calcium ion-related fatigue

Calcium ion-related fatigue mechanisms include a series of processes that stop actin-myosin crossbridges from forming. This makes them different from metabolite-related fatigue mechanisms, which largely just slow down the formation of crossbridges rather than preventing them from occurring. This means that calcium ion-related fatigue mechanisms impair our ability to generate mechanical tension. For this reason, if we still have some of these types of fatigue mechanism present in a muscle from a previous workout, our current workout will stimulate less hypertrophy.

Eccentric-only training is very well-known to produce far more calcium ion-related fatigue than concentric-only training. In exactly the same way, stretched-position exercise training causes much more calcium ion-related fatigue than contracted-position exercise training. In both cases, stretching the muscle fiber causes the opening of stretch-activated ion channels from the outside of the muscle fiber to the inside of the muscle fiber and this allows the influx of additional calcium ions. Once these extra calcium ions accumulate, they cause a very rapid development of calcium ion-related fatigue mechanisms, including muscle damage. Consequently, there are downsides to training with stretched-position exercises that are relatively similar to the downsides of eccentric-only training. Obviously, using a partial range of motion that involves only the stretched-position range of motion will only exacerbate this particular problem.

In summary: stretching a muscle while it is activated causes the opening of calcium ion channels between the inside and the outside of a muscle fiber and this leads to an increase in calcium ion accumulation in stretched-position exercises compared to in contracted-position exercises, which in turn causes much more post-workout fatigue.

What does this mean in practice?

Using static stretching for hypertrophy

Static stretching produces stretch-mediated hypertrophy, which involves the addition of new sarcomeres. This adaptation happens in order to keep resting sarcomere lengths at their optimal lengths. Thus, when being used for producing stretch-mediated hypertrophy, static stretching programs must treat maximum joint angle range of motion as the measurement of progressive overload. If range of motion is increasing, then a passive mechanical tension stimulus is being applied to the muscle fibers in each successive stretching session. Yet, if range of motion stops increasing, then the passive mechanical tension stimulus will stop being applied within a couple of weeks and stretch-mediated hypertrophy will plateau.

Using strength training for hypertrophy

Stretched-position exercises stimulate stretch-mediated hypertrophy but only in certain muscle groups that have long resting sarcomere lengths, and then only for a very limited period of time because the maximum joint angle range of motion used in the exercise is not increased from workout to workout. While lengthened partials will cause such adaptations to occur more rapidly, they will not cause them to occur for a longer period of time than would otherwise happen because the resting sarcomere length is the limitation. Nevertheless, stretched-position exercises cause more fatigue in the post-workout period than contracted-position exercises and we would predict that lengthened partials will cause even more of this type of fatigue owing the longer time spent while the stretch-activated ion channels are opened. Therefore, we can see that once sarcomerogenesis has plateaued and there is no more scope for stretch-mediated hypertrophy (or in those muscles that cannot experience sarcomerogenesis anyway), exercises that involve peak forces elsewhere in the joint angle ROM probably possess a better stimulus-to-fatigue ratio and are more useful for maximizing the overall hypertrophy effect of a strength training program.

If you like this article, you will like my second book (see on Amazon).