| Summary: | The hyperbolic power duration relationship for high intensity exercise is defined by two parameters: a power asymptote (critical power; CP) and a curvature constant (W′) which have been associated with sustainable, and non-sustainable metabolism, respectively. Conventionally, the power duration relationship is derived from a series of constant work-rate (CWR) prediction trials. However, it may be advantageous to establish this relationship using the 3 min all out test, or a series of time trial (TT) tests. The validity, plasticity and applicability of the power duration relationship derived using these different protocols has not been experimentally verified. Moreover, although the CP has been shown to represent a threshold in muscle metabolic and neuromuscular responses during single legged knee extension exercise, it is unclear whether this is also the case during whole body exercise. The purpose of this thesis, therefore, was to: 1) evaluate the predictive validity of the laboratory based 3-min all out test; 2) investigate the plasticity and applicability of the power-duration relationship; 3) elucidate the mechanistic bases for fatigue during whole body exercise above and below CP. In study 1, the CP (r=-0.83, P < 0.001) derived from the 3 min all out test was more strongly associated with 16.1-km road cycling TT performance than; maximum oxygen uptake (V̇O2max) (r=-0.60, P > 0.05); gas exchange threshold (GET), (r= 0.60, P > 0.05); and, respiratory compensation point (RCP), (r=-0.68, P < 0.05). In study 2, the power duration relationship derived from CWR prediction trials overestimated ramp incremental exercise performance by 2.9 ± 2.4%, and the predictive error was associated with the magnitude of the W′ (r= 0.56; P < 0.05). Study 3 demonstrated that the CP derived from a series of self paced TTs (265 ± 44 W) was greater (P < 0.05) than the CP derived from CWR prediction trials (250 ± 47 W), while W′ was not different between the protocols (TT: 18.1 ± 5.7 kJ, CWR: 20.6 ± 7.4 kJ), and the increase in CP was associated (r=0.88, P < 0.05, n=20) with faster mean response time of pulmonary O2 uptake during the TTs (TT: 34 ± 16 s, CWR: 39 ± 19 s, P < 0.05). In study 4, muscle biopsies revealed a similar (P > 0.05) muscle metabolic milieu (i.e., low pH, low [PCr] and high [lactate]) at the limit of tolerance (Tlim) for all severe intensity ( > CP) work rates irrespective of duration (~2-14 min). The muscle metabolic perturbation was greater at Tlim following severe-intensity exercise compared to exercise heavy intensity exercise (< CP, > GET), and also following severe and heavy intensity exercise compared to moderate intensity exercise (< CP, < GET) (all P < 0.05). Moreover, the rates of change in M-wave amplitude and neural drive were significantly correlated with changes in muscle metabolic ([PCr], [lactate]) and blood ionic/acid base status ([lactate], [K+]) during severe and heavy intensity exercise (all P < 0.05), but not during moderate intensity exercise (P > 0.05). Finally, study 5 found no differences in muscle carnosine content or the power duration relationship following 4 weeks of beta-alanine (BA) supplementation (6.4 g.d-1). Therefore, the results of this thesis demonstrate that the CP model is a powerful predictor of exercise performance, but only when the work rate forcing function of the prediction trials is closely matched to the performance trial. Furthermore, this thesis provides novel insights into the underlying mechanisms that characterise the power-duration relationship during whole-body exercise which explains the plasticity and thus applicability of the power duration relationship.
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