The aim of the present thesis was to experimentally test hypotheses originally forwarded by Burnley and Jones (2007): that the kinetics interact with an individual’s capacity for substrate-level phosphorylation and maximal oxygen uptake to determine the power-duration relationship. Experiments were designed to manipulate the kinetics, the “anaerobic capacity,” and/or the maximal oxygen uptake, and determine the effect of these manipulations on the power-duration relationship. Prior high-intensity exercise was used to investigate the classic priming effect during subsequent high-intensity exercise. Both heavy- and severe-intensity exercise ‘primed’ the kinetics (i.e., increased primary amplitude, reduced the slow component trajectory and amplitude). Following 10 min recovery, prior heavy-intensity exercise increased exercise tolerance as a result of an increase in W (C: 16.0 4.8 vs. PHE: 18.7 4.8 kJ; 95% CI, 0.3, 5.2 kJ). In contrast, following the same recovery period, no difference was seen in performance or the power-duration relationship after prior severe-intensity exercise. It was considered that the accumulation of H+ ions (thereby reducing pH) during high-intensity exercise may be implicated in the fatigue process. Sodium bicarbonate ingestion was used to increase the buffering capacity of the blood. This intervention had no effect on the kinetics or , but increased CO2 production, , and blood [lactate] at exhaustion. Despite these results, no overall difference was seen in exercise tolerance between conditions; however, CP was reduced (Pl: 303 ± 48 vs. Na: 296 ± 53 W; 95% CI, 0,14 W) and W increased (Pl: 19.5 ± 8.6 vs. Na: 22.4 ± 9.2 kJ; 95% CI, -5.2, -0.7 kJ), following alkalosis. The final two studies were designed to reduce muscle O2 availability by lowering the O2 carrying capacity of the blood (Blood donation), or through a reduction in perfusion pressure (Supine exercise). Each of these interventions has similar effects on the kinetics: a reduction in the primary amplitude (and a longer time constant; supine only); no change in the slow component trajectory; and a reduction in its amplitude and . Blood donation reduced exercise tolerance, and supine exercise was performed at the same relative intensity, so no difference was seen in time to exhaustion. Each of these interventions reduced CP for blood donation and supine exercise (C: 259 ± 54; vs. BD: 246 ± 42 W; 95% CI: 2, 26W) and (UP: 275 ± 36 vs. SUP: 216 ± 13 W; 95% CI, 40, 78 W), while W was unchanged following each intervention. The experiments conducted in the current programme of research demonstrate that manipulating the kinetics, , or the parameters of the power-duration relationship have predictable effects on exercise tolerance. Hence, these data support the notion that the interaction between the kinetics, the maximal oxygen uptake, and substrate-level phosphorylation determines exercise tolerance and therefore shapes the power-duration relationship.
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