Oxygen uptake response to moderate and very heavy intensity exercise: Relationship with muscle creatine kinase and uncoupling protein

Paterson, Nicole (2003) Oxygen uptake response to moderate and very heavy intensity exercise: Relationship with muscle creatine kinase and uncoupling protein. MSc(R) thesis, University of Glasgow.

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Abstract

During a square-wave increase in work rate (WR) there is an immediate and abrupt increase in energy (ATP) demand. The associated phase II kinetics of pulmonary oxygen uptake (VO2) are now known to reflect those of muscle oxidative phosphorylation (QO2). The control of VO2 kinetics remains a topic of intense debate. One of the candidate mechanisms is feedback control via high-energy phosphate status, which is supported by a close matching of the response kinetics of phosphocreatine (PCr) breakdown and VO2 increase following exercise onset. Above the lactate threshold (thetaL) VO2 kinetics become more complex, with a delayed slow component which induces a greater O2 cost which, as work rates exceed the critical power (CP), places VO2 on a trajectory for maximum (or peak) VO2. The mechanism(s) responsible for the VO2 slow component remain conjectural. One recently proposed mechanism might involves mitochondrial uncoupling protein expression. The present study examined phase II VO2 kinetics during moderate and very heavy- intensity cycling exercise with respect to muscle creatine kinase (CK), the enzyme involved in PCr breakdown, whose activity may be important in dictating recruitment of muscle QO2. Second, as mitochondrial uncoupling protein expression (UCP-2 and UCP-3) has been implicated in the compromised oxidative efficiency of the slow component, these kinetics were examined with respect to the degree of UCP expression. Finally, as VO2 kinetics above critical power (CP) are poorly characterised, repeats at two exhausting WRs were used to appropriately characterise VO2 kinetics, placing emphasis on the degree of inter-subject variability, and to examine potential relationships of variability in kinetic parameters with CK activity, UCP expression and aerobic fitness. In six subjects, gas exchange was measured breath-by-breath and VO2 kinetics were modelled using commercially available software. Muscle biopsy samples from the resting quadriceps femoris muscle were analysed for CK activity (gel electrophoresis and spectrophotometry). UCP mRNA was measured (reverse-polymerase chain reaction) and expressed relative to protein content ((beta-actin). Each subject performed an exhausting ramp exercise test for estimation of the lactate threshold (thetaL). Six square- wave exercise tests to 90% of thetaL were then performed on two separate days. The high- intensity power-duration relationship, determined from three to five fatiguing square- wave tests performed on different days, was used to estimate (a) CP (the asymptotic power) and (b) the WRs required to elicit a target duration for fatigue of 12 and 6 minutes. CK activity ranged from 2.38 to 3.11 absorbance.min-1 and tau11 Vo2 for moderate- intensity exercise ranged from 16 to 25s. A significant positive relationship was found between CK activity and tau11 during moderate intensity exercise (p<0.01). For very heavy-intensity exercise (supra-CP), appreciable inter-subject variability was evident for the VO2 kinetics: (a) tau11 ranged from 15-46s and showed a non-significant trend towards a positive association with CK activity; (b) the slow component amplitude (Asc) ranged from 0.47 to 1.02 l.min-1 but this variability did not significantly associate with UCP expression, which ranged from 2.2 to 5.4 O.D for UCP-2 and 1.2 to 3.0 O.D. for UCP-3; and (c) variability in the VO2 kinetic parameters was not significantly correlated with markers of aerobic fitness. This study has shown that the phase II VO2 time constant related to CK activity, although a cause-and-effect relationship could not be determined. Furthermore, the amplitude of the VO2 slow component was not related to UCP mRNA expression (contrary to a recent report) and therefore elucidation of the mechanism causing the slow component awaits further investigation.

Item Type: Thesis (MSc(R))
Qualification Level: Masters
Additional Information: Adviser: Susan Ward
Keywords: Kinesiology, Physiology
Date of Award: 2003
Depositing User: Enlighten Team
Unique ID: glathesis:2003-71038
Copyright: Copyright of this thesis is held by the author.
Date Deposited: 09 May 2019 14:28
Last Modified: 09 May 2019 14:28
URI: http://theses.gla.ac.uk/id/eprint/71038

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