We examined whether lactic acidemia-induced hyperemia at the onset of high-intensity leg exercise contributed to the speeding of pulmonary O2 uptake (VO2) after prior heavy exercise of the same muscle group or a different muscle group (i.e., arm). Six healthy male subjects performed two protocols that consisted of two consecutive 6-min exercise bouts separated by a 6-min baseline at 0 W: 1) both bouts of heavy (work rate: 50% of lactate threshold to maximal VO2) leg cycling (L1-ex to L2-ex) and 2) heavy arm cranking followed by identical heavy leg cycling bout (A1-ex to A2-ex). Blood lactate concentrations before L1-ex, L2-ex, and A2-ex averaged 1.7 ± 0.3, 5.6 ± 0.9, and 6.7 ± 1.4 meq/l, respectively. An "effective" time constant (τ) of VO2 with the use of the monoexponential model in L2-ex (τ: 36.8 ± 4.3 s) was significantly faster than that in L1-ex (τ: 52.3 ± 8.2 s). Warm-up arm cranking did not facilitate the VO2 kinetics for the following A2-ex [τ: 51.7 ± 9.7 s]. The double-exponential model revealed no significant change of primary τ (phase II) VO2 kinetics. Instead, the speeding seen in the effective τ during L2-ex was mainly due to a reduction of the VO2 slow component. Near-infrared spectroscopy indicated that the degree of hyperemia in working leg muscles was significantly higher at the onset of L2-ex than A2-ex. In conclusion, facilitation of VO2 kinetics during heavy exercise preceded by an intense warm-up exercise was caused principally by a reduction in the slow component, and it appears unlikely that this could be ascribed exclusively to systemic lactic acidosis.
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