O2 uptake kinetics during exercise at peak O2 uptake.

Abstract

Compared with moderate- and heavy-intensity exercise, the adjustment of O2 uptake (VO2) to exercise intensities that elicit peak VO2 has received relatively little attention. This study examined the VO2 response of 21 young, healthy subjects (25 +/- 6 yr; mean +/- SD) during cycle ergometer exercise to step transitions in work rate (WR) corresponding to 90, 100, and 110% of the peak WR achieved during a preliminary ramp protocol (15-30 W/min). Gas exchange was measured breath by breath and interpolated to 1-s values. VO2 kinetics were determined by use of a two- or three-component exponential model to isolate the time constant (tau2) as representative of VO2 kinetics and the amplitude (Amp) of the primary fast component independent of the appearance of any VO2 slow component. No difference in VO2 kinetics was observed between WRs (tau90 = 24.7 +/- 9.0; tau100 = 22.8 +/- 6.7; tau110 = 21.5 +/- 9.2 s, where subscripts denote percent of peak WR; P > 0.05); nor in a subgroup of eight subjects was tau2 different from the value for moderate-intensity (<lactate threshold) exercise (tau2 = 25 +/- 12 s, P > 0.05). As expected, the Amp increased with increasing WRs (Amp90 = 2,089 +/- 548; Amp100 = 2,165 +/- 517; Amp110 = 2,225 +/- 559 ml/min; Amp90 vs. Amp110, P < 0.05). However, the gain (G) of the VO2 response (deltaVO2/deltaWR) decreased with increasing WRs (G90 = 8.5 +/- 0.6; G100 = 7.9 +/- 0.6; G110 = 7.3 +/- 0.6 ml.min-1.W-1; P < 0.05). The Amp of the primary component approximated 85, 88, and 89% of peak Vo2 during 90, 100, and 110% WR transitions, respectively. The results of the present study demonstrate that, compared with moderate- and heavy-intensity exercise, the gain of the Vo2 response (as deltaVO2/DeltaWR) is reduced for exercise transitions in the severe-intensity domain, but the approach to this gain is well described by a common time constant that is invariant across work intensities. The lower deltaVO2/deltaWR may be due to an insufficient adjustment of the cardiovascular and/or pulmonary systems that determine O2 delivery to the exercising muscles or due to recruitment of motor units with lower oxidative capacity, after the onset of exercise in the severe-intensity domain.