The Circadian Rhythm of Core Temperature: Origin and some Implications for Exercise Performance

It has been suggested that a critically high body core temperature may impair central neuromuscular activation and cause fatigue. We investigated the effects of passive hyperthermia on maximal isometric force production (MVC) and voluntary activation (VA) to determine the relative roles of skin (T(sk)) and body core temperature ( T(c)) on these factors. Twenty-two males [VO(2max)=64.2 (8.9) ml x kg(-1) min(-1), body fat=8.2 (3.9)%] were seated in a knee-extension myograph, then passively heated from 37.4 to 39.4 degrees C rectal temperature (T(re)) and then cooled back to 37.4(o)C using a liquid conditioning garment. Voluntary strength and VA (interpolated twitch) were examined during an isometric 10-s MVC at 0.5 degrees C intervals during both heating and cooling. Passive heating to a T(c) of 39.4(o)C reduced VA by 11 (11)% and MVC by 13 (18)% (P<0.05), but rapid skin cooling, with a concomitant reduction in cardiovascular strain [percentage heart rate reserve decreased from 64 (11)% to 29 (11)%] and psychophysical strain did not restore either of these measures to baseline. Only when cooling lowered T(c) back to normal did VA and MVC return to baseline (P<0.05). We conclude that an elevated T(c) reduces VA during isometric MVC, and neither T(sk) nor cardiovascular or psychophysical strain modulates this response. Results are given as mean (SD) unless otherwise stated.

1. Thirty-six subjects in an isolation unit were subjected to time shifts of 12 hr, or of 8 hr in either direction. 2. The rhythms of body temperature and excretion of eight urinary constituents were studied before and after the shift, both on a usual nychthemeral routine and during 24 hr when they remained under constant conditions, awake, engaged in light, mainly sedentary activity, and consuming identical food and fluid every hour. 3. The rhythms on nychthemeral routine were defined by fitting cosine curves. On constant routine the rhythm after the shift was cross-correlated with the original rhythm, either with variable delay (or advance) or with an additive mixture between this variably shifted rhythm and the unshifted or a fully shifted rhythm. The process yielding the highest correlation coefficient was accepted as the best descriptor of the nature of adaptation. 4. A combination of two rhythms was observed more often for urinary sodium, chloride and phosphate than for other variables. 5. Adaptation appeared to have proceeded further after westward than eastward shifts, and this difference was particularly noticeable for urinary potassium, sodium and chloride. 6. Partial adaptation usually involved a phase delay, even after an eastward shift when a cumulative delay of 16 hr would be needed to achieve full adaptation and re-entrainment. 7. Observations under nychthemeral conditions often gave a false idea of the degree of adaptation. In particular, after an eastward shift the phase of the rhythms appeared to shift in the appropriate direction when studied under nychthemeral conditions whereas the endogenous oscillator either showed no consistent behaviour or, in the control of urate excretion, a shift in the wrong direction. 8. The implications for people undergoing time shifts, in the course of shift work or transmeridional flights, are indicated.

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.