Why is longitudinal hypertrophy after strength training more limited than transverse hypertrophy?
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Strength coaches and bodybuilders often make use of strength training exercises with peak forces in stretched positions and/or full ranges of motion with the goal of maximizing hypertrophy. But does this apply equally in all populations, or are more advanced lifters less able to generate longitudinal (stretch-mediated) hypertrophy compared to beginners? Let’s look at the physiology and see what it says.
What is the difference between transverse and longitudinal hypertrophy?
Strength training causes muscle fibers to increase in size, and these changes can involve increases in fiber diameter (by increases in the number of myofibrils in parallel) and increases in fiber length (by increases in the number of sarcomeres in series). While they are different, both of these changes contribute to increases in overall muscle volume (in addition to increases in maximum strength).
An increase in muscle fiber diameter is stimulated by active mechanical tension (by the formation of crossbridges). When the crossbridges create an active force that pulls the two cytoskeletal disks towards each other, this transmits force through the costameres into the endomysium. Subsequently, the mechanoreceptors (which are likely located close to the costameres), detect these forces and subsequently start signaling cascades that cause the number of myofibrils inside the muscle fiber cytoplasm to increase in number. In contrast, an increase in muscle fiber length is stimulated by passive mechanical tension (by the stretching of the stiff segment of titin). When the stiff segment of titin is stretched, it creates a passive force that is detected by titin itself. Titin then commences signaling cascades that cause the number of sarcomeres inside the muscle fiber to increase in number.
Consequently, while muscle fibers will increase in fiber diameter after most strength training exercises that involve a relatively high effort and a slow bar speed (since this will always involve a high active force being generated by the crossbridges), they tend only to increase in fiber length after strength training exercise that involves either  a relatively high effort in the eccentric phase (like eccentric training), or  a long maximum muscle length (such as full range of motion strength training), since these types of exercise are necessary for the stiff segment of titin to produce high passive forces (of course, muscle fibers also increase in length after static stretching).
How do transverse and longitudinal hypertrophy each affect future adaptations?
When active mechanical tension causes an increase in the number of myofibrils inside a muscle fiber, the muscle fiber increases in diameter, and it also increases the amount of active mechanical tension it can produce during a muscular contraction at the same shortening velocity. Theoretically, this might therefore mean that the stimulus for transverse hypertrophy could be increased in future workouts, since the amount of active mechanical tension detected by the costameres is probably higher during subsequent workouts in comparison with the previous workouts. Yet, this does not seem to occur, which suggests that either  the stimulus provided by active mechanical tension is in fact normalized to muscle fiber cross-sectional area, or that  the decreased capability for growth of the larger muscle fiber counteracts the increased capacity for generating active mechanical tension.
In contrast, when passive mechanical tension causes an increase in the number of sarcomeres inside a muscle fiber, the muscle fiber increases in length, and this actually decreases the amount of passive mechanical tension it can produce  when the muscle fiber experiences a static stretch to a given muscle length, and  when the muscle fiber is actively lengthened, as in an eccentric contraction. The amount of passive mechanical tension is reduced because the addition of sarcomeres in series means that the maximum length of each sarcomere (and therefore the maximum length of each stiff segment of titin) is shorter when the muscle fiber reaches its longest length during the static stretch or during the eccentric contraction. Consequently, the stimulus for longitudinal hypertrophy is decreased in future workouts, since the amount of passive mechanical tension detected by titin is lower during subsequent workouts in comparison with the previous workouts.
Essentially, this means that while we tend to expect rapidly diminishing returns in terms of hypertrophy from successive strength training workouts, the diminishing returns from passive mechanical tension are likely vastly more pronounced in comparison with the diminishing returns from active mechanical tension. While active mechanical tension might stop producing meaningful (transverse) hypertrophy in a muscle after many years of strength training, passive tension may well stop producing meaningful (longitudinal) hypertrophy after several months.
Do the rapidly diminishing returns differ between static stretching and strength training?
Importantly, there are key differences between static stretching and strength training, and they relate to the nature of the range of motion used during each rep. Static stretching uses  a maximal range of motion, and  this range of motion increases over time, as we improve our stretch tolerance. In contrast, strength training exercises do not typically use a maximal range of motion and this range of motion is typically also fixed over time (which is useful, because it means that we can track progressive overload accurately).
Consequently, strength training exercises that cause sarcomerogenesis are likely to add sarcomeres in series until the muscle fibers are so long that they no longer produce very much passive force when they are lengthened to the end of the exercise range of motion. For this reason, they likely cease creating longitudinal (stretch-mediated) hypertrophy at a certain point, even though they use a full range of motion. This means that there will likely be little difference in the amount of hypertrophy caused by a full range of motion and a partial range of motion exercise. In contrast, while static stretches also cause sarcomerogenesis, they gradually increase the maximum muscle length that is used in every training session, such that the increase in sarcomere length is compensated for by the increase in the end of the exercise range of motion. For this reason, they can probably continue generating longitudinal (stretch-mediated) hypertrophy even when full range of motion exercises cannot. In practice, they may therefore be very useful for more advanced lifters, for whom full range of motion strength training exercises are no longer providing the additional benefits as they were previously.
What does this mean in practice?
Strength training causes muscle fibers to increase in diameter by adding myofibrils (as a result of active mechanical tension) and in length by adding sarcomeres (as a result of passive mechanical tension). Importantly, these adaptations differ quite fundamentally, because an increase in muscle fiber diameter does not reduce the stimulus for increasing muscle fiber diameter in subsequent workouts, while an increase in muscle fiber length does reduce the stimulus for increasing muscle fiber length in future workouts. For this reason, the ability to create longitudinal (stretch-mediated) hypertrophy by increasing muscle fiber length is likely much more limited than the ability to create transverse hypertrophy. More advanced lifters may actually not be able to cause very much longitudinal (stretch-mediated) hypertrophy at all using normal strength training methods. Nevertheless, since static stretching allows us to compensate for the effects of increased sarcomere lengths by stretching a muscle to longer lengths, it may still be a viable option for more experienced bodybuilders to achieve longitudinal (stretch-mediated) hypertrophy.
If you enjoy this article, you will like my second book (see on Amazon).