Interpreting V˙o 2 Kinetics in Heavy Exercise

Abstract

LETTERS TO THE EDITORInterpreting V˙o 2 Kinetics in Heavy ExerciseRichard L. Hughson, Maureen J. MacDonald, and Michael E. TschakovskyRichard L. Hughson, Maureen J. MacDonald, and Michael E. TschakovskyPublished Online:01 Jul 2001https://doi.org/10.1152/jappl.2001.91.1.530MoreSectionsPDF (85 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmail Interpreting V˙o2 Kinetics in Heavy ExerciseTo the Editor: Burnley et al. (2) reported on a carefully conducted study designed to examine the time course of change in whole body oxygen uptake (V˙o2) at the onset of two bouts of relatively high-intensity exercise. They observed that the baselineV˙o2 before the onset of the second bout was elevated, as was V˙o2 throughout the major adaptive phase (phase II). However, the phase II time constant was not different. In their analysis, they decided that the “correct interpretation” (p. 1395 of Ref. 2) required subtraction of the baseline (see Fig. 4B in Ref. 2) to determine whether adjustment in V˙o2 was different in bout 1 vs. bout 2. This manipulation revealed the amplitude of phase II in the second bout to be equal to the first bout, whereas the magnitude of the slow component (phase III) appeared to be reduced. The authors suggest this as evidence that1) the muscle was more “efficient” in bout 2with a lower net O2 cost for the same workload and2) O2 delivery does not play a role in determining phase II kinetics. In two previous studies reporting similar absolute V˙o2 responses, neither Gerbino et al. (3) nor MacDonald et al. (4) felt that a subtraction of the baseline difference between the first and second bout of high-intensity exercise was warranted. Instead, these authors suggested that V˙o2adjustment in the second bout improved because residual vasodilation from the first bout provided for increased availability of O2 at the onset of the second bout.The analysis of Burnley et al. (2) leads to a fundamentally different interpretation of the data, yet an appropriate rationale is not given. We believe that there are a number of physiological reasons for questioning the baseline subtraction applied by Burnley et al.In the study of Burnley et al. (2), the end-exerciseV˙o2 and the recoveryV˙o2 were identical in both exercise bouts (see Fig. 4A in Ref. 2). Thus, by subtracting a “lingering” baseline component, the authors had to explain improved “efficiency” and should have explained an apparently lower recoveryV˙o2 (see Fig. 4B in Ref.2).To justify the baseline subtraction, the elevated baseline must be due to O2 cost that is totally independent of muscle contraction. It has been considered extensively in previous research that the excess postexercise V˙o2 reflects the recovery of muscle cell homeostasis for electrolyte distribution, high-energy phosphates, metabolite concentrations, and temperature. The elevated V˙o2 also reflects the recovery of heart rate and ventilation toward baseline. Some excessV˙o2 might be related to processes such as gluconeogenesis from lactate in the liver. We suggest that, if the elevated V˙o2 were related to any of these processes that restore muscle homeostasis, then thisV˙o2 would merge with the metabolic demand of the subsequent bout of exercise. That is,V˙o2 reflected the elevated oxidative supply of ATP for exercise.Burnley et al. (2) concluded that O2 was not rate limiting in bout 1; however, in bout 2, they speculated that more O2 was available and that this provided for tighter coupling of oxidative phosphorylation accounting for reduced lactate production. As considered previously (5), it is impossible to have tighter coupling without simultaneously affecting V˙o2 adaptation because of the interaction of regulatory factors related to O2 supply and establishment of mitochondrial redox potential and phosphorylation potential that drive ATP production.Finally, we have a plea to any other researchers who follow this topic. Although the model of Barstow et al. (1) adopted by Burnley et al. (2) for fitting theV˙o2 response during heavy exercise is the best presented to date, the terminology obscures physiology. Let us revert to calling the parameters associated with each phase by the appropriate subscripts so we have phase I labeled as 1 rather than 0.REFERENCES1 Barstow TJ, Jones AM, Nguyen PH, Casaburi R.Influence of muscle fiber type and pedal frequency on oxygen uptake kinetics of heavy exercise.J Appl Physiol81199616421650Link | ISI | Google Scholar2 Burnley M, Jones AM, Carter H, Doust JH.Effects of prior heavy exercise on phase II pulmonary oxygen uptake kinetics during heavy exercise.J Appl Physiol89200013871396Link | ISI | Google Scholar3 Gerbino A, Ward SA, Whipp BJ.Effects of prior exercise on pulmonary gas-exchange kinetics during high-intensity exercise in humans.J Appl Physiol80199699107Link | ISI | Google Scholar4 MacDonald M, Pedersen PK, Hughson RL.Acceleration of V˙o2 kinetics in heavy submaximal exercise by hyperoxia and prior high-intensity exercise.J Appl Physiol83199713181325Link | ISI | Google Scholar5 Tschakovsky ME, Hughson RL.Interaction of factors determining oxygen uptake at the onset of exercise.J Appl Physiol86199911011113Link | ISI | Google ScholarjapjapJAPPLPHYSIOLJournal of Applied PhysiologyJ Appl Physiol1522-16018750-7587American Physiological SocietyBethesda, MDjapjapJAPPLPHYSIOLJournal of Applied PhysiologyJ Appl Physiol1522-16018750-7587American Physiological SocietyBethesda, MDLETTERS TO THE EDITOR Andrew M. Jones, Mark Burnley, Helen Carter, and Jonathan H. Doust 1 Department of Exercise and Sport Science 2 Manchester Metropolitan University 3 Alsager ST7 2HL, United Kingdom 4 E-mail: a.m.[email protected]ac.uk 5 Chelsea School Research Centre 6 University of Brighton 7 Eastbourne BN20 7SP, United Kingdom 8 E-mail: m.[email protected]ac.uk 9 School of Sport, Exercise and Leisure 10 University of Surrey Roehampton 11 London SW15 3SN, United Kingdom 12 E-mail: helen.[email protected]ac.uk andj.[email protected]ac.uk 172001911530532Copyright © 2001 the American Physiological Society2001LETTERS TO THE EDITOR 172001911530532Copyright © 2001 the American Physiological Society2001REPLYTo the Editor: We welcome the opportunity to respond to the letter of Hughson et al. regarding our recent paper in this journal (1-3). Hughson et al.'s fundamental concern appears to be that our “manipulation” of the different baselineV˙o2 values observed in the second compared with the first of two bouts of heavy exercise (see our Fig. 4,A and B, in Ref. 1-3) has affected our interpretation of the V˙o2 response. However, this concern is unfounded. Neither our analysis (see results presented in Tables 2 and 3 in Ref. 1-3) nor our interpretation of the key features of our results was influenced by the differences in baseline V˙o2 preceding the exercise bouts. This is because, as we make clear in our methods section, our modeling of the V˙o2 data with two or three exponential terms does not involve subtraction of the baseline V˙o2. Therefore, our principal findings, i.e., no speeding of phase IIV˙o2 kinetics, a significant increase in the absolute amplitude of the primary V˙o2response, and a significant diminution of theV˙o2 slow component leading to a lower net end-exercise V˙o2, are correct and are explicitly stated. At no point in our paper do we suggest that muscle efficiency was improved by prior heavy exercise, and we clearly state in both the results and discussion that the absolute end-exerciseV˙o2 was similar across the experimental conditions employed in our study. Furthermore, throughout our paper, we emphasize that the elevated baseline V˙o2before the second bout of heavy exercise confounds simple interpretation of the V˙o2 response profiles in both our paper and previous papers (1-4, 1-5). We did not state, as Hughson et al. suggest, that “the correct interpretation of the response required subtraction of the baseline”; rather, we stated that differences in baseline V˙o2 between the first and second bouts of heavy exercise should “be considered” when interpreting the different response profiles.Our Fig. 4B (Ref. 1-3), which shows a visual representation of the V˙o2 responses to heavy exercise when the differences in baseline V˙o2 were accounted for, was only provided to demonstrate that effects on the amplitude of the V˙o2 signal can lead to the incorrect interpretation that V˙o2kinetics are “speeded” at the onset of heavy exercise. However, we accept that this analysis gives the false impression that absolute end-exercise V˙o2 and the recoveryV˙o2 response were different between the two bouts of heavy exercise. From this analysis, it is interesting to note that the elevated metabolism before the second bout of heavy exercise is no longer evident at the end of the 6 min of exercise. This suggests that there are two sources to the pulmonaryV˙o2 signal measured during the second bout of heavy exercise: one arising predominantly from aerobic ATP resynthesis in the contracting muscle and one arising from recovery processes in muscle and other organs subsequent to the first heavy exercise bout. These signals will be additive, but the oxygen cost of the latter will tend to fall as exercise proceeds, thereby obscuring simple interpretation of the response profile.One way to disentangle the exercise-derivedV˙o2 signal from theV˙o2 signal arising from continued recovery processes would be to extend the recovery period between the two heavy exercise bouts so that baselineV˙o2 is fully restored but blood lactate concentration remains elevated. We have recently conducted just such a study (1-2), and our results demonstrate the following: no speeding of phase II V˙o2 kinetics, a significant increase in both net and absolute V˙o2 at the end of phase II, a significant reduction in the amplitude of theV˙o2 slow component, and no change in the absolute end-exercise V˙o2. These results therefore support our previous study (1-3) and suggest that the elevation of the primary V˙o2 response in that study (in absolute terms) was not an artifact of the elevated baselineV˙o2. The altered response profiles in the second of two heavy exercise bouts, i.e., an increased amplitude of the primary component (without a speeding of this phase) and a decreased amplitude of the slow component leading to the same end-exerciseV˙o2, are intriguing. However, this response is qualitatively similar to that seen in subjects with a high proportion of type I muscle fibers (1-1), which leads us to suggest that the differences may be related to an altered motor unit recruitment profile in the second exercise bout. In our earlier paper, we also speculated that additional O2 availability in the second bout, consequent to residual vasodilation, might have led to the establishment of a tighter metabolic control early in exercise and influenced the blood lactate response and motor unit recruitment strategy later in exercise. We agree with Hughson et al. that a tighter coupling of oxidative phosphorylation, if present, would influence theV˙o2 adaptation, but the effect appears to be on the amplitude of the fundamental and slow components ofV˙o2 and not on the phase II time constant. Several studies utilizing repeat exercise transitions and modeling procedures that discriminate the primary component from the slow component of V˙o2 demonstrate that the V˙o2 kinetics in phase II are not speeded by prior heavy exercise (1-2, 1-3, 1-6).We agree with Hughson et al. that the terminology we have adopted from Barstow and colleagues (1-1) in relation to the modeled parameters of theV˙o2 response to exercise is somewhat esoteric. Our group has recently taken to annotating parameters associated with phase I, phase II, and phase III with the subscripts c (for cardiodynamic), p (for primary), and s (for slow component), respectively. These terms (for example, Ap, τp) are more descriptive, and we hope that they may help unify the language of researchers in this field of study. The following is the abstract of the article discussed in the subsequent letter:Burnley, Mark, Andrew M. Jones, Helen Carter, and Jonathan H. Doust. Effects of prior heavy exercise on phase II pulmonary oxygen uptake kinetics during heavy exercise. J Appl Physiol 89: , 2000.—We tested the hypothesis that heavy-exercise phase II oxygen uptake (V˙o2) kinetics could be speeded by prior heavy exercise. Ten subjects performed four protocols involving 6-min exercise bouts on a cycle ergometer separated by 6 min of recovery: 1) moderate followed by moderate exercise; 2) moderate followed by heavy exercise;3) heavy followed by moderate exercise; and 4) heavy followed by heavy exercise. The V˙o2responses were modeled using two (moderate exercise) or three (heavy exercise) independent exponential terms. Neither moderate- nor heavy-intensity exercise had an effect on theV˙o2 kinetic response to subsequent moderate exercise. Although heavy-intensity exercise significantly reduced the mean response time in the second heavy exercise bout (from 65.2 ± 4.1 to 47.0 ± 3.1 s; P < 0.05), it had no significant effect on either the amplitude or the time constant (from 23.9 ± 1.9 to 25.3 ± 2.9 s) of theV˙o2 response in phase II. Instead, this “speeding” was due to a significant reduction in the amplitude of the V˙o2 slow component. These results suggest phase II V˙o2 kinetics are not speeded by prior heavy exercise.REFERENCES1-1. Barstow TJ, Jones AM, Nguyen PH, Casaburi R.Influence of muscle fiber type and pedal frequency on oxygen uptake kinetics of heavy exercise.J Appl Physiol81199616421650 Link | ISI | Google Scholar1-2. Burnley M, Doust JH, Carter H, Jones AM.Effects of prior exercise and recovery duration on oxygen uptake kinetics during heavy exercise in humans.Exp Physiol862001417425 Crossref | ISI | Google Scholar1-3. Burnley M, Jones AM, Carter H, Doust JH.Effects of prior heavy exercise on phase II pulmonary oxygen uptake kinetics during heavy exercise.J Appl Physiol89200013871396 Link | ISI | Google Scholar1-4. Gerbino A, Ward SA, Whipp BJ.Effects of prior exercise on pulmonary gas-exchange kinetics during high-intensity exercise in humans.J Appl Physiol80199699107 Link | ISI | Google Scholar1-5. MacDonald M, Pedersen PK, Hughson RL.Acceleration of V˙o2 kinetics in heavy submaximal exercise by hyperoxia and prior high-intensity exercise.J Appl Physiol83199713181325 Link | ISI | Google Scholar1-6. Scheuermann BW, Hoelting BD, Noble ML, Barstow TJ.The slow component of O2 is not accompanied by changes in EMG during repeated bouts of heavy exercise.J Physiol (Lond)5312001245256 Crossref | Google Scholar Previous Back to Top FiguresReferencesRelatedInformationRelated articlesEffects of prior heavy exercise on phase II pulmonary oxygen uptake kinetics during heavy exercise 01 Oct 2000Journal of Applied Physiology More from this issue > Volume 91Issue 1July 2001Pages 530-532 Copyright & PermissionsCopyright © 2001 the American Physiological Societyhttps://doi.org/10.1152/jappl.2001.91.1.530History Published online 1 July 2001 Published in print 1 July 2001 PDF download Metrics Downloaded 101 times