MATTHEW WAKEFIELD BRIDGE
A thesis submitted to The University of Birmingham For the degree of DOCTOR OF PHILOSOPHY. School of Sport and Exercise Sciences The University of Birmingham October 2002.
Increase in body temperature is a major factor limiting endurance performance in the heat and it is shown in this thesis that the effects of raised body temperature on performance, perception and neuroendocrine response to exercise are mediated by an interaction of body temperatures. Prolactin has been used as an indicator of hypothalamic activity and the pathways regulating its release have been investigated using pindolol as a 5-HT1A antagonist. The prolactin response to a buspirone challenge has been shown to be approximately 50% serotonergic and 50% dopaminergic, but with a wide inter-subject variation. Passive heating is a potent stimulus for prolactin release and it was shown that 5-HT1A stimulation plays virtually no part in this process, raising the possibility that prolactin release during hyperthermic exercise may also be largely due to withdrawal of dopamine inhibition. A comparison of exercise tolerance in the heat and the sensitivity of central serotonergic and dopaminergic pathways further indicates the importance of dopamine in central fatigue. The action of caffeine in enhancing endurance performance has been shown not to involve the hypothalamus and this draws attention to other pathways that may be involved in central fatigue including the basal ganglia and limbic system.
Fatigue is defined in the Oxford English dictionary as; a) Lassitude or weariness resulting from either bodily or mental exertion; b) a condition of muscles, organs, or cells characterized by a temporary reduction in power or sensitivity following a period of prolonged activity or stimulation. These two definitions correspond quite well with what, in the physiological world, have come to be known respectively as, central and peripheral fatigue. Another term sometimes used is ‘objective fatigue’ (Layzer, 1998) which is seen as a deterioration of performance, either during a specific type of competition or as a task is repeated from one day to another. Edwards (Edwards, 1983) described the major possible causes of fatigue in relation to the chain of command for voluntary muscle activations (Figure 1.1). The separation of these possible causes into peripheral and central effects occurs at the level of the motoneurone. A failure of transmission along the peripheral nerve, at the neuromuscular junction or within the muscle itself is therefore considered peripheral fatigue and is the main problem during short duration high intensity exercise. Many studies have addressed the biochemical mechanisms of peripheral fatigue and while the details have yet to be elucidated, there is broad agreement that the loss of force and power is due to decreased calcium release and slowing of cross bridge cycling consequent upon metabolic changes within the muscle fibre (Allen et al., 1995; Jones, 1999).