Intermittent supra-maximal cycling of varying work: recovery durations was used to explore the kinetics of respiratory compensation for the metabolic acidosis of high-intensity exercise (> lactate threshold, θl). For a 10:20 s duty-cycle, blood [lactate] ([L−]) was not increased, and there was no evidence of respiratory compensation (RC); i.e, no increase in the ventilation (Ve)-CO2 output (Vco2) slope, nor fall in end-tidal PCO2 (PETCO2). For longer duty-cycles, [L−] was elevated, stabilizing (30 s:60 s exercise) or rising progressively (60 s:120 s, 90 s:180 s exercise). In addition, Vco2 and Ve now oscillated with WR, with evidence of delayed RC (progressive increase in Ve — Vco2 slope; decrease in PETCO2) being more marked with longer duty-cycles. These results, which extend earlier findings with supra- θl step and ramp exercise, are not consistent with an appreciable contribution to RC from zero-order central command or peripheral neurogenesis. The reasons for the slow RC kinetics are unclear, but may reflect in part the H+-signal transduction properties of carotid chemoreceptors.
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Cathcart, A.J., Turner, A.P., Butterworth, C., Parker, M., Wilson, J., Ward, S.A. (2008). Ventilatory Control during Intermittent High-Intensity Exercise in Humans. In: Poulin, M.J., Wilson, R.J.A. (eds) Integration in Respiratory Control. Advances in Experimental Medicine and Biology, vol 605. Springer, New York, NY. https://doi.org/10.1007/978-0-387-73693-8_35
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