The mechanism(s) underlying the attenuation of the slow component of pulmonary O2 uptake (V̇O2) by prior heavy-intensity exercise is (are) poorly understood but may be ascribed to either an intramuscular-metabolic or a circulatory modification resulting from "priming" exercise. We investigated the effects of altering the circulatory dynamics by delayed vagal withdrawal to the circulation induced by the cold face stimulation (CFS) on the V̇O2 kinetics during repeated bouts of heavy-intensity cycling exercise. Five healthy subjects (aged 21-43 yr) volunteered to participate in this study and initially performed two consecutive 6-min leg cycling exercise bouts (work rate: 50% of the difference between lactate threshold and maximal V̇O2) separated by 6-min baseline rest without CFS as a control (N1 and N2). CFS was then applied separately, by gel-filled cold compresses to the face for 2-min spanning the rest-exercise transition, to each of the first bout (CFS1) or second bout (CFS2) of repeated heavy-intensity exercise. In the control protocol, V̇O 2 responses in N2 showed a facilitated adaptation compared with those in N1, mainly attributable to the reduction of slow component. CFS application successfully slowed and delayed the heart rate (HR) kinetics (P < 0.05) on transition to exercise [HR time constant; N1: 55.6 ± 16.0 (SD) vs. CFS1: 69.0 ± 12.8 s and N2: 55.5 ± 11.8 vs. CFS2: 64.0 ± 17.5 s]; however, it did not affect the "primary" V̇O2 kinetics [V̇O2 time constant; N1: 23.7 ± 7.9 (SD) vs. CFS1: 20.9 ± 3.8 s, and N2: 23.3 ± 10.3 vs. CFS2: 17.4 ± 6.3 s]. In conclusion, increased vagal withdrawal delayed and slowed the circulatory response but did not alter the V̇O2 kinetics at the onset of supra-lactate threshold cycling exercise. As the facilitation of V̇O2 subsequent to prior heavy leg cycling exercise is not attenuated by slowing the central circulation, it seems unlikely that this facilitation is exclusively determined by a blood flow-related mechanism.
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