Hyperthermia: a failure of the motor cortex and the muscle

Authors


Corresponding author S. C. Gandevia: Prince of Wales Medical Research Institute, Barker Street, Randwick, NSW 2031, Australia.  Email: s.gandevia@unsw.edu.au

Abstract

Fatigue is increased during hyperthermia, and torque declines more rapidly in sustained maximal voluntary contractions (MVCs). This can be caused by a greater decline in voluntary activation of muscle (i.e. ‘central fatigue’). The present study aimed to localize the site of failure of voluntary drive during hyperthermia. Seven subjects made brief (2–3 s) and sustained (2 min) MVCs of elbow flexor muscles in two experiments. Core temperature was normal (∼37°C) in the first experiment, and elevated (∼38.5°C) by passive heating in the second. During some MVCs, transcranial magnetic stimulation of the motor cortex (TMS) was delivered, and the evoked torque (superimposed twitch) and EMG responses were measured. During hyperthermia, voluntary torque was reduced by ∼2.4% during brief MVCs (P= 0.03), and decreased further (∼12%) during sustained MVCs (P= 0.01). The superimposed twitch amplitude in the sustained MVC was ∼50% larger (P= 0.01). Thus, the ability to drive the muscle maximally in a sustained fashion was decreased, and some motor cortical output, which could have increased torque, remained untapped by voluntary drive. The additional central fatigue was not associated with altered motor cortical ‘excitability’, as EMG responses produced by TMS were similar at the two temperatures. However, the peak relaxation rate of muscle increased by ∼20% (P= 0.005) during hyperthermia. Hence, faster motor unit firing rates would be required to produce fusion of force. The increased central fatigue during hyperthermia may represent a failure of descending voluntary drive to compensate for changed muscle properties, despite the availability of additional cortical output.

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