O2 uptake kinetics as a determinant of exercise tolerance
Bailey, Stephen J.
Date: 21 February 2011
Thesis or dissertation
University of Exeter
PhD in Sport and Health Sciences
Abstract Oxygen uptake ( O2) kinetics determine the magnitude of the O2 deficit and the degree of metabolic perturbation and is considered to be an important determinant of exercise tolerance; however, there is limited empirical evidence to demonstrate that O2 kinetics is a direct determinant of exercise tolerance. The purpose of ...
Abstract Oxygen uptake ( O2) kinetics determine the magnitude of the O2 deficit and the degree of metabolic perturbation and is considered to be an important determinant of exercise tolerance; however, there is limited empirical evidence to demonstrate that O2 kinetics is a direct determinant of exercise tolerance. The purpose of this thesis was to investigate O2 kinetics as a determinant of exercise tolerance and to consider its potential interaction with the maximum O2 ( O2max) and the W′ (the curvature constant of the hyperbolic power-duration relationship) in setting the tolerable duration of exercise. Recreationally-active adult humans volunteered to participate in the investigations presented in this thesis. Pulmonary O2 kinetics was assessed on a breath-by-breath basis and exercise tolerance was assessed by a time-to-exhaustion trial, with exhaustion taken as the inability to maintain the required cadence. A period of repeated sprint training (RST) resulted in faster phase II O2 kinetics (Pre: 29 ± 5, Post: 23 ± 5 s), a reduced O2 slow component (Pre: 0.52 ± 0.19, Post: 0.40 ± 0.17 L•min-1), an increased O2max (Pre: 3.06 ± 0.62, Post: 3.29 ± 0.77 L•min-1) and a 53% improvement in severe exercise tolerance. A reduced O2 slow component and enhanced exercise tolerance was also observed following inspiratory muscle training (Pre: 0.60 ± 0.20, Post: 0.53 ± 0.24 L•min-1; Pre: 765 ± 249, Post: 1061 ± 304 s, respectively), L-arginine (ARG) administration (Placebo: 0.76 ± 0.29 L•min-1 vs. ARG: 0.58 ± 0.23; Placebo: 562 ± 145 s vs. ARG: 707 ± 232 s, respectively) and dietary nitrate supplementation administered as nitrate-rich beetroot juice (BR) (Placebo: 0.74 ± 0.24 vs. BR: 0.57 ± 0.20 L•min-1; Placebo: 583 ± 145 s vs. BR: 675 ± 203, respectively). However, compared to a control condition without prior exercise, the completion of a prior exercise bout at 70% Δ (70% of the difference between the work rate at the gas exchange threshold [GET] and the work rate at the O2max + the work rate at the GET) with 3 minutes recovery (70-3-80) speeded overall O2 kinetics by 41% (Control: 88 ± 22 s, 70-3-80: 52 ± 13 s), but impaired exercise tolerance by 16% (Control: 437 ± 79 s, 70-3-80: 368 ± 48 s) during a subsequent exercise bout. When the recovery duration was extended to 20 minutes (70-20-80) to allow a more complete replenishment of the W′, overall kinetics was speeded to a lesser extent (by 23%; 70-20-80: 68 ± 19 s) whereas exercise performance was enhanced by 15% (70-20-80: 567 ± 125 s) compared to the control condition. In addition, the faster O2 kinetics observed when exercise was initiated with a fast start (FS; 35 ± 6 s), compared to an even start (ES; 41 ± 10 s) and slow start (SS; 55 ± 14 s) pacing strategy, allowed the achievement of O2max in a 3 minute trial and exercise performance was enhanced. Exercise performance was unaffected in a 6 minute trial with a FS, despite faster O2 kinetics, as the O2max was attained in all the variously paced trials. Therefore, the results of this thesis demonstrate that changes in exercise performance cannot be accounted for, purely, by changes in O2 kinetics. Instead, enhanced exercise performance appears to be contingent on the interaction between the factors underpinning O2 kinetics, the O2max and the W′, in support of the proposed ‘triad model’ of exercise performance.
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