L. ANSLEY, G. MARVIN, A. SHARMA, M. J. KENDALL, D. A. JONES, M. W. BRIDGE
School of Psychology and Sport Sciences, Northumbria University, School of Sport & Exercise Sciences, University of Birmingham, Clinical Investigations Unit, Queen Elizabeth Hospital Birmingham, United Kingdom.
Received April 5, 2007, Accepted September 12, 2007, On-line November 30, 2007
The present study investigated the effects of head cooling during endurance cycling on performance and the serotonergic neuroendocrine response to exercise in the heat. Subjects exercised at 75 % VO2max to volitional fatigue on a cycle ergometer at an ambient temperature of 29±1.0 °C, with a relative humidity of approximately 50%. Head cooling resulted in a 51 % (p<0.01) improvement in exercise time to fatigue and Borg Scale ratings of perceived exertion were significantly lower throughout the exercise period with cooling (p<0.01). There were no indications of peripheral mechanisms of fatigue either with, or without, head cooling, indicating the importance of
central mechanisms. Exercise in the heat caused the release of prolactin in response to the rise in rectal temperature. Head cooling largely abolished the prolactin response while having no effect on rectal temperature. Tympanic temperature and sinus skin temperature were reduced by head cooling and remained low throughout the exercise. It is suggested that there is a co-ordinated response to exercise involving thermoregulation, neuroendocrine secretion and behavioural adaptations that may originate in the hypothalamus or associated areas of the brain. Our results are consistent with the effects of head cooling being mediated by both direct cooling of the brain and modified cerebral artery blood flow, but an action of peripheral thermoreceptors cannot be excluded.
Fatigue during sub-maximal endurance exercise is often difficult to attribute to peripheral mechanisms, such as substrate depletion or metabolite accumulation, particularly in the case of fit individuals where the exercise lasts less than 60 min. In such cases the inability to continue exercising may be due to central fatigue mechanisms, whereby a loss of motivation and/or motor cortical activity are the limiting factors (Davis 1995b). The precise mechanism of the central fatigue process is unknown although there has been particular interest in the role of central serotonergic pathways (Davis 1995a, Newsholme and Blomstrand 1995). Raised body temperature, mediated through central mechanisms, may have a role to play limiting endurance exercise (Bruck and Olschewski 1987) and there are several strands of evidence to support this view. The first is the common observation that endurance times are reduced at high ambient temperatures (Galloway and Maughan 1997). It has been suggested that some aspect of body temperature per se may be the limiting factor (Bruck and Olschewski 1987, Nielsen et al. 1993) and this may be more important than circulatory failure or metabolic depletion that have previously been considered to limit this type of exercise (Fink et al. 1975, Kozlowski et al. 1985).