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, thetaL). For a 10:20s 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 (30s:60 s exercise) or rising progressively (60s:120s, 90s: 180s 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- thetaL 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.