The development of fatigue has been an area of interest to athletes and scientists alike for many years. Often, particularly during prolonged exercise in the heat, there is no obvious peripheral reason for fatigue and the central nervous system is cited as the source. The mechanisms and potential manipulations of this fatigue remain largely unclear. Chapters Three and Four attempted to reduce the transport of the serotonin precursor tryptophan into the brain in order to reduce or delay serotonin synthesis and therefore increase exercise capacity. In Chapter Three branched-chain amino acid drinks were fed before and during prolonged cycling to exhaustion in the heat on two occasions and control drinks were fed on two other occasions. There was no effect of the branched-chain amino acids on exercise capacity and the intra-individual variability in seven of the eight participants was small. One participant did appear to cycle for longer on the branched-chain amino acid trials compared to the control trials. In Chapter Four a 104 g bolus of amino acids, designed to deplete plasma tryptophan concentration, was fed seven hours before a prolonged cycle to exhaustion in the heat. There was no difference in exercise capacity between the tryptophan depletion trial and the control trial in which tryptophan was also ingested. These findings suggest that the delivery of tryptophan to the central nervous system is not the only factor influencing the onset of fatigue. The investigation undertaken in Chapter Five looked at the serotonin transporter density on the blood platelets of current and retired international level athletes competing in either endurance or sprint running events and a sedentary control group. Using the platelet as an accessible and reliable model for the serotonergic neuron, the maximum number of binding sites was assessed using the radio-labelled serotonin reuptake inhibitor [3H]Paroxetine. Those currently training for endurance events had a greater number of binding sites than any of the other groups. This supports previous findings and suggests that endurance training can increase the number of serotonin transporters on blood platelet membranes. During resting heat exposure in Chapter Six, the application of a 1 % menthol solution to the skin of the forearms, back and forehead elicited a warming sensation in some individuals and a cooling sensation in other individuals, but never any change in skin or core temperature nor skin blood flow. A small proportion of individuals did not perceive any change in skin thermal sensation. Chapter Seven applied these findings to a pre-loaded twenty minute exercise performance test in the heat. It was hypothesised that those who perceived a warming effect may perform worse when a menthol solution was applied compared to a control solution and conversely, those who perceived a cooling sensation may perform better with a menthol solution than with a control solution. There was no difference in exercise performance between those who felt a warming sensation and those who felt a cooling sensation. Those who felt a warming sensation felt significantly warmer on the menthol trial than the control trial but this did not affect their performance. However, those who reported a cooling sensation tended to feel cooler on the menthol trial than the control trial, and there was a tendency for an improvement in performance on the menthol trial compared to the control trial. Due to the experimental protocols adopted in this thesis it was possible to assess the reliability of an exercise capacity test compared to an exercise performance test. Chapter Three showed a coefficient of variation of 11.0 ± 11.2 % and Chapter Four showed a 11.5 ± 12.4 % variability for exercise capacity tests. Chapter Seven showed a coefficient of variation in a pre-loaded time-trial exercise performance test of 3.9 ± 9.6 % suggesting that an exercise performance test may be more reliable than an exercise capacity test. However, the aims of an investigation are still likely to be the main factor influencing the choice of protocol. It seems likely that no single mechanism will be responsible for the cessation of exercise. The investigations undertaken in this thesis also highlight many avenues for future exploration.
| Identifer | oai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:544482 |
| Date | January 2010 |
| Creators | Hobson, Ruth M. |
| Publisher | Loughborough University |
| Source Sets | Ethos UK |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
| Source | https://dspace.lboro.ac.uk/2134/6975 |
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