There’s no strong evidence on the importance and fact of O2 level differences as having much of an effect on body size.

One of the theories onto why we increase ROM over time is due to the addition of sarcomeres added in series. This review goes over factors likely increasing ROM:.

Some data on sEMG changes with different loads:.

One of my favorite papers that shows just imagining doing max effort exercises but not actually activating the muscle or moving joints produces strength gains almost as much as the group that did the exercises!.

Passive tension by muscle fibers is affected by lengthening velocity?.

Those claims, in my opinion, are a bit deceptive. They haven't conducted research comparing the scaling of single fibers against entire muscles, though, and they don't have any data on load bearing!

Really good work from @chenglabyorku on CWI for recovery. However, it seems hardly conclusive as it is plausible that the intervention is not that fatiguing and the CWI is not warranted as a recovery treatment!.

Many speculate that the addition of serial sarcomere number is a mechanism of the REB. This really interesting paper from @Geoff_A_Power show it might not (at least in the initial stage).

Compression garments may aid in recovery from muscle damage?.

Greta papers on muscle soreness:.

Muscle fiber elongation (not whole muscle) is likely a cause for sarcomerogenesis.

Through imaging biceps muscles via three noninvasive methods, stroke patients had fewer sarcomeres along the length of the muscle fiber, resulting in a shorter overall muscle structure. Great work from @wendymmurrayphd .

The synchronization of motor unit discharge times does not increase muscle force.

Latissimus dorsi works as a lateral flexor, at high levels during maximally resisted lateral flexion. However, it is only active at minimal to low levels during low load tasks such as in standing.

Maximally activated, single-skinned rat muscle fibres behave like linear springs across almost the entire working range. As a result, muscle forces up to 2.5 times the maximum isometric force can be generated.

Are you convinced from any of these reasons? Which sounds the most sound or are you skeptical with any?.

3.) This paper provides fair insight into the physiology behind this understanding where ampk would impede on the progression of concentric force but not necessarily eccentric force as eccentrics don’t use as much energy.

2.) However, other work shows that some of the cross-bridges do not cycle but are continuously pulled backward preventing the myosin heads from rotating forward, keeping the actin and myosin bound (Stauber, 1989):.

1.) Herzog uses Huxley’s model to show cross-bridges attach more “securely” as there’s more cross-bridge attachments and each force per cross-bridge is higher.

Why are we stronger during eccentric contractions? Below I’ll give 3 reasons I’m aware of. I’d love to hear which reason sounds the most sound!.