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Sarcomeres are added when muscle fibers receive a very specific stimulus, which is different from the stimulus that causes myofibrillar addition. See more in the weekly free Patreon article.

In contrast to the lack of effect in young people, dietary leucine may help slow or partially prevent the losses in muscle mass that occur during limb immobilization.

When the very short-term effects of eccentric-only training and static stretching on flexibility and stretch tolerance are compared, they are statistically similar. However, the magnitudes of the effects produced by eccentric-only training are larger.

AAS stop exogenous glucocorticoids from elevating muscle protein breakdown rate (which causes muscle atrophy or reduces muscle hypertrophy). We might expect AAS to have similar positive effects on stress-induced glucocorticoids as occur during sleep restriction.

Leucine supplementation may have interesting applications when stressors are causing muscle atrophy by means of an increase in muscle protein breakdown rates. Read more in the weekly free Patreon article.

When young humans experience limb immobilization, there is pretty much no way of stopping muscle atrophy from happening. This study tested high-dose dietary leucine and found no effect.

Eccentric-only training substantially increases flexibility. Longer training programs cause greater increases in flexibility, which indicates that the effect is not limited to the first couple of weeks of the training program.

AAS cause hypertrophy through signaling in the mTOR pathway, in the same way as mechanical tension. mTOR is a very widely-used signaling pathway and is involved in sarcomerogenesis and muscle damage repair as well as hypertrophy.

Currently, many fitness influencers are making big claims about plyometrics causing increases in tendon stiffness. The reality is that plyometrics are really not best-placed to produce that particular adaptation. They are much better at increasing stretch-shortening cycle function through another mechanism.

One of the most persistent myths in the fitness industry is the idea that we can reach maximal levels of motor unit recruitment in any exercise, so long as we train to muscular failure. For more details and citations, see the weekly free Patreon article.

AAS enhance the rate of healing from skin injury by accelerating the rate of collagen deposition, which can be prevented by applying an anti-androgenic. This shows that the AAS mediate these effects by acting on androgen receptors.

Stressors slow the rate of post-workout recovery by interferring with the secondary muscle damage effect. This allows us to explain the negative effects of any non-exercise intervention without resorting to the general adaptation syndrome.

AAS increase extracellular matrix collagen deposition after non-exercise injury, most likely by increasing rates of collagen synthesis.

Sprinting does not automatically benefit from stiffer tendons. In fact, most data suggest the opposite due to the way in which the stretch-shortening cycle works. For more details and citations, see the weekly free Patreon article.

While AAS seem to interfere with the repair processes in tendons (leading to an increased injury risk), they are more likely to produce accelerated repair in muscles, causing faster recovery from fatigue.

Exactly this

It is easy to see that "active recovery" is not going to produce a faster rate of post-workout recovery when we have a clearly described physiological model of fatigue. The active recovery workout will only ever add more fatigue on top of the pre-existing fatigue.

The maintenance literature routinely shows that 3-4 sets, once per week can only maintain net hypertrophy across the week. In contrast, 1 set twice per week causes growth. This shows that atrophy happens within a training week and that frequency is important.

How many stimulating reps are there in a set to failure? For more details and citations, see the weekly free Patreon article.

Faster running speeds are associated with MORE tendon lengthening and shortening and LESS muscle fascicle lengthening and shortening. In this way, the stretch-shortening cycle does more during a faster running gait cycle than during a slower running gait cycle, despite the greater forces being exerted on the ground.