Oxygen Uptake Kinetics as a Determinant of ­Exercise Intensity Domains

Response to Professor Cross’s Letter to the Editor:

We would like to thank Dr. Cross and Dr. Sabapathy for their interest in our recent study [8] describing the VO₂ kinetics above and below the respiratory compensation point (RCP) in swimmers. Their comments on RCP as a determinant of O₂ uptake kinetics are very interesting and add value to the debate. However, we would like to clarify some points that could have been misinterpreted.

Cross and Sabapathy [3] stated that if the incremental stage is longer than 4–5 min, respiratory compensation (RCP) for metabolic acidosis is observed at the first work rate performed above the gas-exchange threshold (GET) (i. e., GET≈RCP). However, there is a substantial body of evidence showing that GET and RCP are not influenced by stage duration of the incremental test, for stages of at least 1, 3 and 5 min [7] [10]. In our study [8], the 300-m intervals used as increments lasted around 3.5 min (i. e., 4.1–3.2 min). Although exercise intensity domains are narrow in swimming [6], we have checked whether GET and RCP were ­different and they were (GET: 41.1±7.2 mL.kg^− 1.min^− 1, 70.5±8.0% VO₂max; RCP: 49.8±5.5 mL.kg^− 1.min^− 1, 85.9±4.8% VO₂max).

Another concern of Cross and Sabapathy [3] is the use of RCP as a “physiological boundary” demarcating the heavy from the severe exercise intensity domain for constant-load exercise. As stated in our study, exercise intensity domains have been defined based on VO₂ and blood lactate responses measured during constant work rate exercise [5]. Although during an exercise performed at a heavy intensity, a slow component from the VO₂ kinetics is superimposed upon the rapid response, a steady state remains observed after 15–20 min of exercise [5]. Indeed, as stated by Cross and Sabapathy, Poole et al. [9] have evidenced a respiratory compensation (i. e., decline in the end-tidal partial pressure of CO₂) during exercise performed at critical power (CP; the boundary between heavy and severe intensity domains). However, Poole et al. [9] also reported a delayed steady state in the VO₂ response (see Fig. 2, in Poole et al. [9]) at the same exercise intensity. Similar data (i. e., increased minute ventilation and decreased arterial carbon dioxide pressure alongside a VO₂ steady state) was observed by Baron et al. [1] during an exercise performed at maximal lactate steady state (i. e., heavy intensity domain). This demonstrates that it is possible to observe a VO₂ stabilization and compensatory hyperventilation during constant-load exercise of heavy intensity (above GET but below CP). However, it is important to note that in the present study [8] , the variable used to define the exercise intensity domain was pulmonary oxygen uptake, and not respiratory (VE, PETO₂, PETCO₂) and blood acid-base (pH, PCO₂) parameters. Thus, we are confident that the RCP obtained during our 300-m incremental swimming protocol represents a physiological boundary around which VO₂ kinetics can be studied in swimming.

Finally, it is worth bearing in mind that our study was not specifically performed to investigate if RCP and CP could be determined by shared putative physiological mechanisms. However, Dekerle et al. [4] have verified that RCP obtained during incremental exercise test was similar to CP in cycling. Moreover, Cross et al. [2] have recently verified during constant-load exercise that VO₂max was only attained when exercising above RCP.

• References

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