The aim of these experiments was to investigate the influence that dietary manipulation has upon acid-base balance and substrate availability at rest and during high intensity exercise. It was hoped to identify some of the mechanisms that may control the utilisation of energy substrate and influence the onset of fatigue during high intensity exercise. A pattern of dietary and exercise manipulation intended to alter carbohydrate (CHO) and fat availability was undertaken during the first two experiments. In addition to influencing energy substrate availability, the diet and exercise regimen also significantly influenced resting acid-base balance and high intensity exercise capacity. The reduction in exercise performance afer administration of a low CHO, high fat, high protein diet may have been due to the diet-induced acidosis produced by this diet. However, it is also probable that glycogen availability was influencing exercise performance in this situation. A fixed period of exercise under the same experimental conditions indicates that a higher than normal muscle glycogen content may dictate the pattern of substrate utilisation during high intensity exercise. In a second series of experiments it was demonstrated that dietary manipulation alone will influence acid-base balance and exercise capacity. A high fat, high protein diet will produce a metabolic acidosis but will not influence total muscle glycogen content. In this situation, it is unlikely that a reduction in high intensity exercise performance can be attributed to the availability of muscle glycogen. It is possible that a change in fat availability, rather than muscle glycogen content, will influence the pattern of substrate utilisation during high intensity exercise. However, it is unlikely that a change in fat availability will be responsible for the reduction in exercise capacity recorded after a high fat, high protein diet. The reduction in exercise capacity may be the result of a diet-induced acidosis. Although it is unlikely that dietary acidosis will influence H+ efflux from muscle it may influence pre-exercise muscle buffering capacity. The resulting greater decline in muscle pH during exercise after a high fat, high protein diet may influence muscle function: firstly, by inhibiting the activation of muscle contraction which is due possibly to a reduction in the release of Ca2+ from the sarcoplasmic reticulum and a reduction in the affinity of the myofilaments to Ca2+. Secondly, by inhibiting muscle relaxation which is thought to result from a disruption in actin-myosin corss-bridge separation and a reduction in the rate of Ca2+ removal from the myofibril cytoplasm. Thirdly, by inhibiting muscle glycolysis at the point of PFK. Finally, there is some evidence to suggest that the rate of muscle lactate efflux and/or the metabolic fate of lactate produced during high intensity exercise are different from normal after a period of dietary manipulation.

Within the context of a metabolic model of fatigue, formulated from a review of the literature, a decrease in intramuscular pH was identified as a potential limiting factor to the performance of high intensity exercise (HIE). This suggested a role for skeletal muscle buffering (B) in retarding the intramuscular acidosis typically incurred during HIE. Previous studies on human muscle, were largely unable to confirm this role, partly due to the lack of a clearly defined and consistently utilised method of measurement of B. The validity of the procedures currently employed in the determination of B was therefore investigated, revealing that many of the individual differences in B, previously attributed physiological significance, may have originated from inappropriate methodology. In a cross-sectional examination of the vastus lateralis muscle of young, active individuals, low correlations (p<0.05) between the muscle carnosine concentration ([CAR]) and in the 'in vitro B' (Bvit) (r=0.30), and between either [CAR] or Bvit and the % type II fibre area were observed. An elevated Bvit was shown to be of importance in minimising the decrement in pH during HIE, but did not per se permit the accumulation of a higher muscle lactate concentration, or allow for an enhanced HIE performance; these factors were more dependent on the % type II fibre area. The muscle pH, following dynamic HIE was highly variable between individuals, and showed a significant (p<0.05) negative correlation with the % type II fibre area. 16 weeks of isokinetic training of the quadriceps resulted in significant improvements (p<0.05) in dynamic HIE performance with no concomitant improvements in [CAR] or Bvit. The data suggest that the muscle buffer value per se, is not a major limiting factor to HIE, and that rather, the glycolytic capacity and pH tolerance of the muscle may be the more important factors to consider.

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The strength model of self-control suggests that self-regulation and self-control processes are governed by finite internal energy resources. However, this perspective has recently come under scrutiny suggesting that self-control processes are not solely constrained to limited resources and may also be guided by motivational-cognitive processing. Self-efficacy theory and control theory are two theoretical views of self-regulation that also suggest self-regulation failures are dependent on motivational-cognitive processes; however the potential role of limited resources has not been evaluated in the context of these theoretical views. This dissertation sought to advance our understanding of self-regulation and self-control of exercise behaviour by integrating the three theoretical perspectives discussed above. Study 1 showed that self-control depletion leads to reductions in task self-efficacy mediating the self-control depletion – negative performance change relationship. Overall, findings are consistent with self-efficacy theory. However the results are limited as the mechanism(s) leading to reduced self-efficacy following self-control depletion remain unclear. Study 2 explored a sequential (serial) mediation model investigating the idea that exerting self-control leads to an altered psychophysiological state increasing subjective fatigue, which in turn, leads to reduced self-efficacy to exert self-control and reductions in physical self-control performance. Findings supported the proposed sequential mediation model. However, it remains unclear to what extent that self-efficacy plays a passive or active role guiding self-controlled behaviour following self-control depletion. Study 3 explored the independent and interactive effects of self-control depletion and normative performance feedback on self-efficacy and physical self-control. Findings showed an interaction between self-control depletion and feedback. Findings support predictions of control theory when self-control resources are intact, but suggest feedback information is processed differently when self-control strength is depleted. Overall, results show that when self-efficacy is manipulated by feedback the effects of self-control depletion on performance are no longer evident supporting self-efficacy’s role as an active causal mechanism determining behaviour. / Dissertation / Doctor of Philosophy (PhD) / Self-control failures are at the heart of many societal problems. A dominant theoretical view suggests self-control is governed by a limited internal resource. However, this perspective has recently been opposed by theorizing and evidence suggesting that people experience self-control failures due to shifts in motivational-cognitive processes. This thesis integrated three theories of self-control (i.e., strength model of self-control, control theory, and self-efficacy theory) in an attempt to provide a more complete understanding of why self-control failures occur for people performing demanding physical exercise. Findings suggest that each theoretical perspective provides complementary explanations for why self-control failures occur and how they can be overcome through shifts in cognitive processing. Specifically, self-control exertion leads to subjective fatigue, which decreases self-efficacy to exert self-control, and in turn reduces self-control performance. Furthermore, after self-control exertion, positive normative performance feedback increases self-efficacy and subsequent self-control performance whereas negative feedback drastically reduces self-efficacy and performance.