Effect of short-term high-intensity interval training vs. continuous training on O2 uptake kinetics, muscle deoxygenation, and exercise performance

Abstract

The early time course of adaptation of pulmonary O(2) uptake (Vo(2)(p)) (reflecting muscle O(2) consumption) and muscle deoxygenation kinetics (reflecting the rate of O(2) extraction) were examined during high-intensity interval (HIT) and lower-intensity continuous endurance (END) training. Twelve male volunteers underwent eight sessions of either HIT (8-12 x 1-min intervals at 120% maximal O(2) uptake separated by 1 min of rest) or END (90-120 min at 65% maximal O(2) uptake). Subjects completed step transitions to a moderate-intensity work rate ( approximately 90% estimated lactate threshold) on five occasions throughout training, and ramp incremental and constant-load performance tests were conducted at pre-, mid-, and posttraining periods. Vo(2)(p) was measured breath-by-breath by mass spectrometry and volume turbine. Deoxygenation (change in deoxygenated hemoglobin concentration; Delta[HHb]) of the vastus lateralis muscle was monitored by near-infrared spectroscopy. The fundamental phase II time constants for Vo(2)(p) (tauVo(2)) and deoxygenation kinetics {effective time constant, tau' = (time delay + tau), Delta[HHb]} during moderate-intensity exercise were estimated using nonlinear least-squares regression techniques. The tauVo(2) was reduced by approximately 20% (P < 0.05) after only two training sessions and by approximately 40% (P < 0.05) after eight training sessions (i.e., posttraining), with no differences between HIT and END. The tau'Delta[HHb] ( approximately 20 s) did not change over the course of eight training sessions. These data suggest that faster activation of muscle O(2) utilization is an early adaptive response to both HIT and lower-intensity END training. That Delta[HHb] kinetics (a measure of fractional O(2) extraction) did not change despite faster Vo(2)(p) kinetics suggests that faster kinetics of muscle O(2) utilization were accompanied by adaptations in local muscle (microvascular) blood flow and O(2) delivery, resulting in a similar "matching" of blood flow to O(2) utilization. Thus faster kinetics of Vo(2)(p) during the transition to moderate-intensity exercise occurs after only 2 days HIT and END training and without changes to muscle deoxygenation kinetics, suggesting concurrent adaptations to microvascular perfusion.