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1 School of Kinesiology, University of Western Ontario, London, Ontario, Canada
2 Canadian Centre for Activity and Aging, London, Ontario, Canada; School of Kinesiology, University of Western Ontario, London, Ontario, Canada; Department of Physiology and Pharmacology, University of Western Ontario, London, Ontario, Canada
3 Canadian Centre for Activity and Aging, London, Ontario, Canada; School of Kinesiology, University of Western Ontario, London, Ontario, Canada
* To whom correspondence should be addressed. E-mail: dpaterso{at}uwo.ca.
The effects of prior heavy-intensity exercise on oxygen uptake (VO2) kinetics of a second heavy
exercise have been suggested to be due to vasodilation (associated with metabolic acidosis) and improved muscle blood flow. The purpose of the present study was to examine the effect of prior heavy-intensity exercise on femoral artery blood flow (Qleg) and its relationship with VO2 kinetics. Five young subjects completed 5 to 8 repeats of two 6-min bouts of heavy-intensity
(80%VO2peak) one-legged, knee-extension exercise separated by 6-min of loadless exercise.
VO2 was measured breath-by-breath. Pulsed-wave Doppler ultrasound was used to measure femoral artery blood velocity (MBV), and to image the vessel diameter to allow calculation of blood flow. VO2 and MBV data were interpolated, time-aligned and ensemble averaged then fit using a monoexponential model to identify the time periods of phase II and phase III components
and estimate the response amplitudes and time constants (
). Phase II VO2 kinetics were speeded
on the second heavy-intensity exercise (mean (SD), 29 (10) s to 24 (10) s, p<0.05) with no change in the phase II amplitude or phase III slow component amplitude. Qleg was elevated prior to the second exercise (1.55 (0.34) L.min-1 to 1.90 (0.25) L.min-1, p<0.05) but the amplitude and time course (, 25 (13) s to 35 (13) s) were not changed, such that throughout the transient the Qleg (and 
Qleg/VO2) did not differ from the prior heavy exercise. Thus, VO2 kinetics
were accelerated on the second exercise bout, but the faster kinetics were not associated with changes in femoral artery blood flow throughout the exercise. Thus, limb blood flow appears not to limit VO2 kinetics during single-leg heavy-intensity exercise, nor be the mechanism of the altered VO2 response following the heavy-intensity prior exercise.
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