David Low, Alison Purvis, Thomas Reilly and N. Tim Cable
Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, 15–21 Webster Street, Liverpool L3 2ET, UK. School of Sport and Leisure Management, Sheffield Hallam University, Sheffield, SH10 2BP, UK.
The aim of this study was to compare the prolactin and blood pressure responses at identical core temperatures during active and passive heat stresses, using prolactin as an indirect marker of central fatigue. Twelve male subjects cycled to exhaustion at 60% maximal oxygen uptake (VO2peak) in a room maintained at 33◦C (active). In a second trial they were passively heated (passive) in a water bath (41.56 ± 1.65◦C) until core temperature was equal to the core temperature observed at exhaustion during the active trial. Blood samples were taken from an indwelling venous cannula for the determination of serum prolactin during active heating and at corresponding core temperatures during passive heating. Core temperature was not significantly different between the two methods of heating and averaged 38.81 ± 0.53 and 38.82 ± 0.70◦C (data expressed as means ± S.D.) at exhaustion during active heating and at the end of passive heating, respectively (P > 0.05). Mean arterial blood pressure was significantly lower throughout passive heating (active, 73 ± 9 mmHg; passive, 62 ± 12 mmHg; P < 0.01). Despite the significantly reduced blood pressure responses during passive heating, during both forms of heating the prolactin response was the same (active, 14.9 ± 12.6 ng ml−1; passive, 13.3 ± 9.6 ng ml−1; n.s.). These results suggest that thermoregulatory, i.e. core temperature, and not cardiovascular afferents provide the key stimulus for the release of prolactin, an indirect marker of central fatigue, during exercise in the heat.
The capacity for prolonged exercise is diminished in hot environments relative to normothermic conditions (Galloway & Maughan, 1997; Parkin et al. 1999). The precise mechanism(s) for this decreased endurance capacity during exercise in the heat is unknown. However, possible causes include an intolerable thermoregulatory strain, cerebral perturbations, central nervous system disturbances, high cardiovascular strain and altered skeletal muscle function (Febbraio, 2000; Cheung & Sleivert, 2004). Support for the proposal that an intolerable thermoregulatory strain mediates fatigue during prolonged exercise in the heat comes from studies in which subjects reached the point of voluntary fatigue at similar core temperatures despite various manipulations to alter the baseline core temperature and/or the rate of increase in core temperature (Nielsen et al. 1993; Cheung & McLellan, 1998; Gonzalez-Alonso et al. 1999; Gregson et al. 2002). It is thought that the fatigue that ensues at an intolerable core temperature is mediated byareflex inhibition within the central nervous system, characterized by an increased reluctance of subjects to continue exercise, which acts as a safety brake to stop exercise and thus prevent any further increases in core and brain temperature (Bruck & Olschewski, 1987; Nielsen & Nybo, 2003). Furthermore, it has also been proposed that this reflex inhibition possibly occurs via alterations in\ central serotonergic and dopaminergic activity (Pitsiladis et al. 2002; Bridge et al. 2003).