The feelings of weakness that lifters experience in the days following exercise are likely underpinned by a range of mechanisms relating to both central and peripheral function, but are NOT primarily attributable to “CNS” fatigue.

Central fatigue, when defined as a decrease in the CNS motor cortex ability to activate muscle to the required level might not be as much of an issue as we previously thought.

You don’t need to exert maximal contractions or achieve high levels of muscle activation to produce CNS fatigue. It occurs readily when performing extended durations of exercise involving very low forces, e.g. aerobic activity.

In the absence of pronounced muscle damage, you recover quickly from the central fatigue that arises over the course of each set in a workout.

Certain training parameters appear to correlate with central fatigue and reduced voluntary activation, but it’s not driven chiefly by the usual suspects (intensity, muscle mass involved etc.). Instead, it appears that muscle damage is a better proxy. More specifically, the process appears to be mediated by the following 3 factors:

1) reductions in motoneuron activity seem to correspond to overall volume and amount of eccentric work performed.

2) Inflammatory cytokines (such as interleukin-1 beta or IL-1b) in the brain have also known to cause sustained fatigue after exercise in animal models. These inflammatory messengers are elicited by muscle-damaging exercise which might affect the motor cortex and its ability to drive the target muscle for up to 48-72 h post-exercise. Increased brain concentrations of this type of cytokines can induce negative behavioural responses and fatigue.

3) Afferent feedback (type III and IV) as this type of signalling could cause CNS fatigue without affecting the size of the initial signal from the motor cortex. Afferent neurons transmit information detected by sensory receptors in various parts of the body to the CNS. Group III and IV afferent neurons are linked to a range of sensory receptors that detect changes in the mechanical loading of muscle fibers and of their metabolic environment.