Fatigue mechanisms
Evidence: contested
Fatigue has both peripheral (muscle) and central (nervous-system) causes. Whether a protective brain ‘governor’ sets the limit, or sensory feedback from the muscle does, is genuinely unsettled. The balance shifts with the task.
Fatigue is the decline in the ability to produce force or hold a pace. It has two broad sources. Peripheral fatigue happens inside the muscle, where the chemistry of contraction degrades. Central fatigue happens upstream, where the nervous system sends less drive to the muscle. Both occur in every hard effort. The argument is over which one sets the limit, and that argument is not resolved (Weir et al. 2006).
Peripheral fatigue
Peripheral fatigue is the better understood half. During intense contraction, inorganic phosphate accumulates in the muscle fibre and impairs calcium handling in the sarcoplasmic reticulum, so each contraction produces less force (Allen, Lamb & Westerblad 2008). Hydrogen ions, long blamed as the main cause of ‘the burn’, now look like a smaller contributor than the older lactic-acid story claimed (Allen, Lamb & Westerblad 2008). This is a real, measurable decline that happens within the muscle whether or not the brain is involved.
Central fatigue and the central governor
The peripheral picture is incomplete, because runners almost never recruit all their muscle at the point they stop, and a motivated athlete can often push harder when exhausted. This is the opening for central explanations.
Tim Noakes pressed the strongest version, the central governor model. It holds that the brain regulates pace in anticipation, reading feedback on fuel, heat and effort, and holds motor recruitment in reserve so that exhaustion arrives before the muscle actually fails, protecting the body from harm (Noakes 2012). On this view fatigue is closer to an emotion than a mechanical failure, and the finishing kick is proof that reserve was held back all along.
Why it is contested
Critics argue the central governor routes all fatigue through one unproven mechanism and leans on surface EMG that is hard to interpret. They favour task dependency: central and peripheral factors both contribute, and their balance shifts with the type, intensity and duration of the effort, rather than one governor deciding everything (Weir et al. 2006).
A middle ground
The most useful position links the two halves rather than choosing between them. Sensory nerves in working muscle, the group III and IV afferents, feed back to the central nervous system and inhibit motor drive once peripheral fatigue reaches an individual ceiling (Amann 2011). Block that feedback and runners push past their usual limit but finish with more peripheral fatigue than they would normally tolerate (Amann 2011). This gives a concrete mechanism for a centrally set limit without needing a single governor, and it explains why the limit feels protective: the brain reads the muscle and reins in drive before damage occurs.
What dominates, and when
The honest summary is that the balance depends on the task (Weir et al. 2006). In short, very intense efforts, peripheral metabolic disturbance dominates and the muscle genuinely runs down (Allen, Lamb & Westerblad 2008). In long, lower-intensity efforts, central regulation, pacing and the integration of afferent feedback carry more weight (Amann 2011). Where exactly the line sits, and how much of the everyday sense of fatigue is protective regulation versus true failure, remains open.