Diet, acid-base status and the metabolic response to high intensity exercise
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.