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Nielsen et al. [120] were among the first to detail that participants terminate exercise at a core temperature close to 40 °C and that a high core temperature per se is the critical factor for exercise termination in the heat. In the study of Nielsen et al. [120], participants voluntarily stopped exercising close to a rectal temperature of 40 °C on successive exercise trials (9 to 12) despite gradual heat acclimation. These findings were replicated in a subsequent heat acclimation study, whereby the authors [124] observed that participants were able to exercise for longer (pre-acclimation 44.6 ± 2.8 min; post-acclimation 52 ± 1.9 min) in hot humid environmental conditions (35 °C, 87% RH) at 45% V̇O2max but terminated at similar rectal temperatures of

39.9 ± 0.1 °C and 39.9 ± 0.1 °C, respectively. Furthermore, González-Alonso et al. [108] also reported that voluntary fatigue occurred at an oesophageal temperature around 40 °C, irrespective of initial body temperature (36, 37, 38 °C) which was manipulated by water immersion. These studies suggest that exhaustion during exercise in hot environments coincides with the attainment of a critical core temperature that is independent of the intensity of exercise, rate of heat storage, state of acclimation, initial core temperature or skin temperature. This limited body of evidence, has led to the assertion that a high body temperature and not cardiovascular or metabolic challenges is the main factor underlying fatigue during prolonged exercise in the heat. This critical core temperature, deemed to be around 40 °C, is postulated to reduce voluntary central nervous system activation [125, 126], thus termed central fatigue. That is, a 'safety switch' or mechanism is proposed to prevent catastrophic systemic damage from hyperthermia [127].

Advancing earlier work, suggestive of a critical core temperature, Nybo and Nielsen [128] demonstrated that when participants were hyperthermic (40 °C) compared to

'normothermic' (38 °C), after 50 and 60 min cycling at 60% V̇O2max they had less ability

to produce knee extensor force over a 2-min sustained isometric action, despite an equal potential for electrically-invoked superimposed twitch force. The authors were unable to replicate this finding in a trial whereby they asked participants to produce maximal force in a 2-s effort with 5-s recovery repeated 40 times. The authors postulated that brain temperature was a key regulator of motor unit activation, but they were unable to establish whether exercise was terminated because of central fatigue per se, nor were they able to elucidate why sustained but not repeated muscular activity was impaired. A limitation of this study was the failure to isolate core temperature from skin temperature. That is, skin temperature was also high in these studies; thus the observed decrease in voluntary force production cannot necessarily be ascribed to a critical core temperature alone, since there were concomitant increases in skin temperature which present cardiovascular challenges. Furthermore, there are no data concerning the time- course of fatigue throughout the exercise trial since assessments of force production were only conducted immediately after reaching a threshold temperature or fatigue from a preliminary trial. Morrison et al. [129] sought to isolate core temperature independently from skin temperature and cardiovascular strain using passive heating as well as determining the time course of fatigue. Using a water-perfused suit, the investigators heated the skin surface to raise both skin and core temperature, at 0.5 °C increments from rest until 39.5 °C; at each interval they assessed voluntary activation of knee extensor force and electrically-evoked twitch force. The authors observed a progressive decline in mean maximal voluntary activation of the knee-extensors and knee extensor torque (Nm) as rectal temperature increased to 39.5 °C. At this point knee-extensor force was statistically (P < 0.05) less than knee extensor force at 37.5 °C; these findings were observed both with a high core temperature and high skin

temperature. At a core temperature of 39.5 °C the authors cooled the participants, so that skin temperature declined rapidly while core temperature remained at 39.5 °C. Despite the reduction in skin temperature and a return of heart rate reserve to near resting levels there was not an immediate statistically significant recovery in voluntary activation or force production. The authors concluded that a high core temperature impairs force production, independent of skin temperature. However, whether a meaningful decline in knee extensor force occurred is unclear. The standardised mean difference ± 95% confidence limits for baseline (37.5 °C) and peak core temperature (39.5 °C) peak isometric knee extensor force was -0.53 (-1.19 to 0.14). As the effect size confidence interval spans positive and negative effects the interpretation of force should not be that it is significantly impaired, because there might be a beneficial (albeit trivial) effect of heating on force production.

In another study by Nybo and Nielsen [130] it was demonstrated that exercise was terminated at 40 °C oesophagal temperature and that middle cerebral artery velocity, an index of blood flow, was impaired due to hyperthermia when compared with the control trial. The authors noted that cerebral blood flow was probably impaired by a decreased cardiac output but concluded that fatigue seems to coincide with a critical core temperature that might influence central nervous system drive. However, this assertion seems secondary to cardiovascular challenges imposed by hyperthermia, i.e. a reduced cerebral artery velocity. Indeed, no study has demonstrated that a critical core temperature independently induces fatigue, in an emergency break like manner, since neuromuscular function is impaired transiently (but perhaps not meaningfully) with an increase in core temperature and skin temperature. Additionally, the choice of neuromuscular assessment is also important to consider. A maximal effort is an assessment of performance and is influenced by perceived exertion. When participants

are hot and uncomfortable, their thermal perception feeds forward to perceived exertion and performance is regulated to achieve the task goal. To isolate the influence of critical core temperature on performance, researchers also need to isolate the effect of thermal perception and perceived exertion if an assessment involves the choice to produce force. A fixed-intensity protocol would likely alleviate the impact of perceptual influences.

There is insufficient evidence to suggest that there is a critical core temperature at which exercise is terminated [131]. Since it has not been clearly demonstrated that a critical core temperature alone limits exercise capacity during fixed intensity exercise, it is unlikely that a critical core temperature would limit performance in self-paced exercise. Indeed, core temperature exceeding 40 °C is observable in highly motivated athletes during performance in hot environments [132] and with dopamine reuptake inhibition, using bupropion which increases extracellular adrenergic neurotransmitters improving central nervous system function [133]. Conversely, moderately-trained participants voluntarily terminate exercise at core temperatures (38.5 °C). Thus, using a critical core temperature threshold to explain fatigue in the heat is too simple and ignores the complexity physiological processes involved in determining exercise capacity and performance.