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The determinants of exercise intolerance are vital as they impinge on all individuals and are applicable across the whole spectrum of physical abili.ties. Key in this regard is the rate at which pulmonary oxygen uptake (Vo2 ) adapts to meet the energetic requirement at exercise onset, with this dependent on both the limit (i.e. v02 max) and the contour (i.e. v02 kinetics) of the v02 response. The purpose of this research was. to better understand the mechanisms. controlling v02 kinetics, and also to investigate the mechanisms determining high-intensity exercise tolerance, with specific reference to the hyperbolic power-duration (P-t) relationship. Three studies were conducted: 1. The role of 02 delivery in the control of v02 kinetics during moderate-intensity cycle ergometry. The presence of a delayed increase in deoxygenated [haemoglobin] in the region of muscle interrogation suggests that, during this delay phase, there is a dynamic balance between capillary perfusion and O2 consumption. Hence, it was \. concluded that 02 delivery is not a primary determinant of v02 kinetics, although its potential contribution under certain conditions is acknowledged. 2. Effects of supra-critical power (CP) 'priming' exercise on the profile and parameters of the P-t relationship (i.e. CP and W'J and parameters of aerobic function (i.e. the v02 time constant (rVo2 ), functional gain, lactate threshold (BJ .and Va] maJ during subsequent supra-CP exercise performed to the tolerable limit. 't vo2 , functional gain, SL, CP, v02 max were unaffected, but WI was decreased such that exercise tolerance was reduced as a predictable function of the re-define'd P-t relationship. It was concluded that WI is a key parameter of high-intensity exercise tolerance. 3. The kinetics of w' recovery, relative to ·those of v02 and blood [Lactate]. WI recovery was clearly dissociated both from that of metabolic rate and blood [Lactate], being slower compared to the former but more rapid relative to the latter. Consistent with the results of Chapter 4, exercise tolerance was reduced as a predictable function of the re-defined P-t relationship, supporting the notion that WI 'depletion' shapes high intensity exercise tolerance. Furthermore, doubt is cast on the current view that WI simply reflects a fixed 'store' of energy; rather, accumulation of fatigue-related metabolites instead may be important in defining the physiological constructs ofthis parameter.

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Several aspects of cardio-respiratory control during exercise in humans are not yet understood. One such question is how the autonomic outflow to the circulation is calibrated to provide accurate regulation of arterial pressure (AP) during dynamic exercise. One hypothesis is that the calibration can be 'learnt' through feedback from the arterial baroreceptors arising over multiple trials of exercise. ro test this hypothesis, we paired bouts of submaximal exercise with neck suction to overstimulate the carotid baroreceptors during the course of a 7-day training protocol (study presented in chapter three). The study showed a reduction in systolic AP (but not mean AP) following the training protocol which suggests the presence of some plasticity within the autonomic response consistent with this hypothesis. Eight hours of exposure to hypoxia result in a progressive elevation of ventilation, a lowering of end-tidal Peo2 (PETeo2)' a progressive pulmonary vasoconstriction and an elevation of pulmonary arterial pressure. These effects persist for some time after return to air-breathing conditions. However, little has been known of the effect of preconditioning with 8 hours of hypoxia on the ventilatory and pulmonary vascular response to air-breathing exercise. The study presented in chapter four demonstrated that preconditioning with 8 hours of hypoxia (but not euoxic control) significantly reduced air-breathing PETeo2 at rest, and that this reduction was maintained nearly constant throughout an air-breathing incremental exercise test. This indicates that the increment in ventilation following 8 hours of hypoxia is proportional to the rise in metabolic rate associated with exercise, thus defending the lowered PETe02. The maximum pressure gradient during systole across the tricuspid valve (~Pmax, measured by Doppler ultrasound) can be used as an index of pulmonary arterial pressure. The study presented in c~apter five found that preconditioning with 8 hours of hypoxia (but not euoxic control) significantly increased ~Pmax both at rest and during exercise and increased the sensitivity of ~Pmax to air-breathing exercise. This suggests that the pulmonary vasculature remains in' a somewhat constricted state during air-breathing exercise following 8 hours of hypoxia.