Interpreting O₂ Kinetics in Heavy Exercise

The following is the abstract of the article discussed in the subsequent letter:

	ABSTRACT

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: 1387-1396, 2000.We tested the hypothesis that heavy-exercise phase II oxygen uptake (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 O₂ responses were modeled using two (moderate exercise) or three (heavy exercise) independent exponential terms. Neither moderate- nor heavy-intensity exercise had an effect on the 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 the O₂ response in phase II. Instead, this "speeding" was due to a significant reduction in the amplitude of the O₂ slow component. These results suggest phase II O₂ kinetics are not speeded by prior heavy exercise.

	LETTER

Interpreting O₂ Kinetics in Heavy Exercise

To 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 (O₂) at the onset of two bouts of relatively high-intensity exercise. They observed that the baseline O₂ before the onset of the second bout was elevated, as was 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 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 that 1) the muscle was more "efficient" in bout 2 with a lower net O₂ cost for the same workload and 2) O₂ delivery does not play a role in determining phase II kinetics. In two previous studies reporting similar absolute 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 O₂ adjustment 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-exercise O₂ and the recovery 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 recovery 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 O₂ reflects the recovery of muscle cell homeostasis for electrolyte distribution, high-energy phosphates, metabolite concentrations, and temperature. The elevated O₂ also reflects the recovery of heart rate and ventilation toward baseline. Some excess O₂ might be related to processes such as gluconeogenesis from lactate in the liver. We suggest that, if the elevated O₂ were related to any of these processes that restore muscle homeostasis, then this O₂ would merge with the metabolic demand of the subsequent bout of exercise. That is, 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 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 the 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.

	REFERENCES

1.   Barstow, TJ, Jones AM, Nguyen PH, and Casaburi R. Influence of muscle fiber type and pedal frequency on oxygen uptake kinetics of heavy exercise. J Appl Physiol 81: 1642-1650, 1996[Abstract/Free Full Text].

2.   Burnley, M, Jones AM, Carter H, and Doust JH. Effects of prior heavy exercise on phase II pulmonary oxygen uptake kinetics during heavy exercise. J Appl Physiol 89: 1387-1396, 2000[Abstract/Free Full Text].

3.   Gerbino, A, Ward SA, and Whipp BJ. Effects of prior exercise on pulmonary gas-exchange kinetics during high-intensity exercise in humans. J Appl Physiol 80: 99-107, 1996[Abstract/Free Full Text].

4.   MacDonald, M, Pedersen PK, and Hughson RL. Acceleration of O₂ kinetics in heavy submaximal exercise by hyperoxia and prior high-intensity exercise. J Appl Physiol 83: 1318-1325, 1997[Abstract/Free Full Text].

5.   Tschakovsky, ME, and Hughson RL. Interaction of factors determining oxygen uptake at the onset of exercise. J Appl Physiol 86: 1101-1113, 1999[Abstract/Free Full Text].

Richard L. Hughson, Department of Kinesiology University of Waterloo Waterloo, ON, Canada N2L 3G1 E-mail: hughson{at}uwaterloo.ca

Maureen J. MacDonald, School of Kinesiology McMaster University Hamilton, ON, Canada L8S 4K1 E-mail: macdonmj{at}mcmaster.ca

Michael E. Tschakovsky, School of Physical and Health Education Queen's University Kingston, ON, Canada K7L 3N6 E-mail: mt29{at}post.queensu.ca

	REPLY

To the Editor: We welcome the opportunity to respond to the letter of Hughson et al. regarding our recent paper in this journal (3). Hughson et al.'s fundamental concern appears to be that our "manipulation" of the different baseline 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. 3) has affected our interpretation of the O₂ response. However, this concern is unfounded. Neither our analysis (see results presented in Tables 2 and 3 in Ref. 3) nor our interpretation of the key features of our results was influenced by the differences in baseline O₂ preceding the exercise bouts. This is because, as we make clear in our methods section, our modeling of the O₂ data with two or three exponential terms does not involve subtraction of the baseline O₂. Therefore, our principal findings, i.e., no speeding of phase II O₂ kinetics, a significant increase in the absolute amplitude of the primary O₂ response, and a significant diminution of the O₂ slow component leading to a lower net end-exercise 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-exercise O₂ was similar across the experimental conditions employed in our study. Furthermore, throughout our paper, we emphasize that the elevated baseline O₂ before the second bout of heavy exercise confounds simple interpretation of the O₂ response profiles in both our paper and previous papers (4, 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 O₂ between the first and second bouts of heavy exercise should "be considered" when interpreting the different response profiles.

Our Fig. 4B (Ref. 3), which shows a visual representation of the O₂ responses to heavy exercise when the differences in baseline O₂ were accounted for, was only provided to demonstrate that effects on the amplitude of the O₂ signal can lead to the incorrect interpretation that O₂ kinetics are "speeded" at the onset of heavy exercise. However, we accept that this analysis gives the false impression that absolute end-exercise O₂ and the recovery 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 pulmonary 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-derived O₂ signal from the O₂ signal arising from continued recovery processes would be to extend the recovery period between the two heavy exercise bouts so that baseline O₂ is fully restored but blood lactate concentration remains elevated. We have recently conducted just such a study (2), and our results demonstrate the following: no speeding of phase II O₂ kinetics, a significant increase in both net and absolute O₂ at the end of phase II, a significant reduction in the amplitude of the O₂ slow component, and no change in the absolute end-exercise O₂. These results therefore support our previous study (3) and suggest that the elevation of the primary O₂ response in that study (in absolute terms) was not an artifact of the elevated baseline 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-exercise O₂, are intriguing. However, this response is qualitatively similar to that seen in subjects with a high proportion of type I muscle fibers (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 the O₂ adaptation, but the effect appears to be on the amplitude of the fundamental and slow components of 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 O₂ demonstrate that the O₂ kinetics in phase II are not speeded by prior heavy exercise (2, 3, 6).

We agree with Hughson et al. that the terminology we have adopted from Barstow and colleagues (1) in relation to the modeled parameters of the 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, A_p, _p) are more descriptive, and we hope that they may help unify the language of researchers in this field of study.

	REFERENCES

1.   Barstow, TJ, Jones AM, Nguyen PH, and Casaburi R. Influence of muscle fiber type and pedal frequency on oxygen uptake kinetics of heavy exercise. J Appl Physiol 81: 1642-1650, 1996.

2.   Burnley, M, Doust JH, Carter H, and Jones AM. Effects of prior exercise and recovery duration on oxygen uptake kinetics during heavy exercise in humans. Exp Physiol 86: 417-425, 2001[Abstract].

3.   Burnley, M, Jones AM, Carter H, and Doust JH. Effects of prior heavy exercise on phase II pulmonary oxygen uptake kinetics during heavy exercise. J Appl Physiol 89: 1387-1396, 2000.

4.   Gerbino, A, Ward SA, and Whipp BJ. Effects of prior exercise on pulmonary gas-exchange kinetics during high-intensity exercise in humans. J Appl Physiol 80: 99-107, 1996.

5.   MacDonald, M, Pedersen PK, and Hughson RL. Acceleration of O₂ kinetics in heavy submaximal exercise by hyperoxia and prior high-intensity exercise. J Appl Physiol 83: 1318-1325, 1997.

6.   Scheuermann, BW, Hoelting BD, Noble ML, and Barstow TJ. The slow component of O₂ is not accompanied by changes in EMG during repeated bouts of heavy exercise. J Physiol (Lond) 531: 245-256, 2001[Abstract/Free Full Text].

Andrew M. Jones, Department of Exercise and Sport Science Manchester Metropolitan University Alsager ST7 2HL, United Kingdom E-mail: a.m.jones{at}mmu.ac.uk

Mark Burnley, Chelsea School Research Centre University of Brighton Eastbourne BN20 7SP, United Kingdom E-mail: m.burnley{at}bton.ac.uk

Helen Carter, Jonathan H. Doust, School of Sport, Exercise and Leisure University of Surrey Roehampton London SW15 3SN, United Kingdom E-mail: helen.carter{at}roehampton.ac.uk and j.doust{at}roehampton.ac.uk