Oxygen uptake kinetics during supra-maximal intensity exercise

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Influence of initial metabolic rate on pulmonary O(2) uptake on-kinetics during severe intensity exercise

We hypothesised that the fundamental (Phase II) component of pulmonary oxygen uptake ( [Formula: see text] ) kinetics would be significantly slower when step transitions to severe intensity cycle exercise were initiated from elevated baseline metabolic rates, and that this would be associated with evidence for a greater activation of higher-order (i.e. type II) muscle fibres. Seven male subjects (age 22-34 years) completed repeat step transitions to a severe (S) work rate, estimated to require 100% [Formula: see text] peak, from a baseline of: (1) 3min of unloaded cycling (L-->S); (2) 6min of moderate exercise (M-->S); (3) 6min of heavy exercise (H-->S). Pulmonary gas exchange and the electromyogram (EMG) of the m. vastus lateralis were measured throughout all exercise tests. The Phase II [Formula: see text] kinetics became progressively slower at higher baseline metabolic rates (tau was 37+/-6, 59+/-23, and 93+/-50s for L-->S, M-->S, and H-->S, respectively; PS and H-->S). Both the integrated EMG and the mean power frequency were significantly higher immediately before the step transition to severe exercise when it was initiated from higher metabolic rates. Although indirect, these data suggest that the slower Phase II [Formula: see text] kinetics observed at higher baseline metabolic rates was related to alterations in muscle activation and fibre recruitment patterns

O2 uptake kinetics as a determinant of exercise tolerance

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.EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Influence of endurance training on muscle [PCr] kinetics during high-intensity exercise

We hypothesized that a period of endurance training would result in a speeding of muscle phosphocreatine concentration ([PCr]) kinetics over the fundamental phase of the response and a reduction in the amplitude of the [PCr] slow component during high-intensity exercise. Six male subjects (age 26 ± 5 yr) completed 5 wk of singlelegged knee-extension exercise training with the alternate leg serving as a control. Before and after the intervention period, the subjects completed incremental and high-intensity step exercise tests of 6-min duration with both legs separately inside the bore of a whole-body magnetic resonance spectrometer. The time-to-exhaustion during incremental exercise was not changed in the control leg [preintervention group (PRE): 19.4 ± 2.3 min vs. postintervention group (POST): 19.4 ± 1.9 min] but was significantly increased in the trained leg (PRE: 19.6 ± 1.6 min vs. POST: 22.0 ± 2.2 min; P &lt; 0.05). During step exercise, there were no significant changes in the control leg, but end-exercise pH and [PCr] were higher after vs. before training. The time constant for the [PCr] kinetics over the fundamental exponential region of the response was not significantly altered in either the control leg (PRE: 40 ± 13 s vs. POST: 43 ± 10 s) or the trained leg (PRE: 38 ± 8 s vs. POST: 40 ± 12 s). However, the amplitude of the [PCr] slow component was significantly reduced in the trained leg (PRE: 15 ± 7 vs. POST: 7 ± 7% change in [PCr]; P &lt; 0.05) with there being no change in the control leg (PRE: 13 ± 8 vs. POST: 12 ± 10% change in [PCr]). The attenuation of the [PCr] slow component might be mechanistically linked with enhanced exercise tolerance following endurance training.</p