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Abstract
A central debate in the exercise sciences is the cause of the fatigue that develops
especially during high intensity exercise of short duration. The most popular theory
holds that this form of exercise is limited by a peripherally based, metabolite induced
failure of skeletal muscle contractile function, independent of reduced muscle activation
by the central nervous system; so-called peripheral fatigue. This theory arose originally
from studies undertaken by Nobel Laureate Sir Archibald Vivian Hill and colleagues
in Manchester, UK in the 1920s. In turn, their interpretations were crucially influenced
by the earlier 1907 findings of Sir Frederick Gowland Hopkins, Nobel Laureate for
his discovery of the vitamins, and Walter Morley Fletcher. The original model of Hill
and his colleagues proposed that performance during exercise of high intensity was
limited by skeletal muscle anaerobiosis that developed as the result of a limiting
skeletal muscle blood flow, following the onset of myocardial ischaemia. Such skeletal
muscle anaerobiosis ultimately prevented the neutralization of the lactic acid that,
Hill believed, initiated muscle contraction. The resulting lactic acid accumulation
impaired skeletal muscle relaxation, causing the (involuntary) termination of exercise.
The evolutionary progression of this model led to the "catastrophe theory" of Richard
Edwards, which posits that exercise terminates when the physiological and biochemical
limits of the body are exceeded, causing a catastrophic failure of intracellular homeostasis.
This paper addresses six hallmark physiological requirements that must be correct
if Hill's cardiovascular/ anaerobic/catastrophic model is the exclusive explanation
for the fatigue that develops during maximum exercise to exhaustion. This leads to
a review of the evidence supporting other, related "catastrophe" models that have
been developed to explain fatigue during exercise of lower intensities and longer
durations. It is concluded that there is little published evidence supporting the
theory that fatigue occurs only after physiological homeostasis fails according to
the prediction of these catastrophe models. Rather, it is proposed that fatigue in
any form of exercise may form part of a regulated, anticipatory response co-ordinated
in the subconscious brain. The ultimate goal of this regulation is to preserve homeostasis
in all physiological systems during exercise, regardless of intensity or duration
or the environmental conditions in which it is undertaken.