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

McKay BR, Paterson DH, Kowalchuk JM. Effect of short-term high-intensity interval training vs. continuous training on O-2 uptake kinetics, muscle deoxygenation, and exercise performance. J Appl Physiol 107: 128-138, 2009. First published May 14, 2009; doi: 10.1152/japplphysiol. 90828.2008.-The early time course of adaptation of pulmonary O-2 uptake (<(V)over dot>(O2p)) (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 (similar to 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. <(V)over dot>(O2p) 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 nearinfrared spectroscopy. The fundamental phase II time constants for <(V)over dot>(O2p) (tau<(V)over dot>(O2)) 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 tau<(V)over dot>(O2) was reduced by similar to 20% (P < 0.05) after only two training sessions and by similar to 40% (P < 0.05) after eight training sessions (i. e., posttraining), with no differences between HIT and END. The tau'Delta[HHb] (similar to 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 lowerintensity END training. That Delta[HHb] kinetics (a measure of fractional O-2 extraction) did not change despite faster <(V)over dot>(O2p) 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 <(V)over dot>(O2p) during the transition to moderateintensity exercise occurs after only 2 days HIT and END training and without changes to muscle deoxygenation kinetics, suggesting concurrent adaptations to microvascular perfusion.