VO2 kinetics in heavy exercise is not altered by prior exercise with a different muscle group

We examined whether lactic acidemia-induced hyperemia at the onset of high-intensity leg exercise contributed to the speeding of pulmonary O-2 uptake ((V) over dot O-2) 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 (V) over dot O-2) 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 (tau) of (V) over dot O-2 with the use of the monoexponential model in L2-ex (tau: 36.8 +/- 4.3 s) was significantly faster than that in L1-ex (tau: 52.3 +/- 8.2 s). Warm-up arm cranking did not facilitate the (V) over dot O-2 kinetics for the following A2-ex [tau: 51.7 +/- 9.7 s]. The double-exponential model revealed no significant change of primary tau (phase II) (V) over dot O-2 kinetics. Instead, the speeding seen in the effective tau during L2-ex was mainly due to a reduction of the (V) over do O-2 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 (V) over dot O-2 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.