Effect of short-term HIIT vs. LSD
Posted: Mon Jul 13, 2009 11:55 pm
Effect of short-term high-intensity interval training vs. continuous training on O2 uptake kinetics, muscle deoxygenation, and exercise performance
The early time course of adaptation of pulmonary O2 uptake (VO2p) (reflecting muscle O2 consumption) and muscle deoxygenation kinetics (reflecting the rate of O2 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 O2 uptake separated by 1 min of rest) or END (90–120 min at 65% maximal O2 uptake). Subjects completed step transitions to a moderate-intensity work rate (~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. VO2p 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 VO2p ({tau}VO2) 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}VO2 was reduced by ~20% (P < 0.05) after only two training sessions and by ~40% (P < 0.05) after eight training sessions (i.e., posttraining), with no differences between HIT and END. The {tau}'{Delta}[HHb] (~20 s) did not change over the course of eight training sessions. These data suggest that faster activation of muscle O2 utilization is an early adaptive response to both HIT and lower-intensity END training. That {Delta}[HHb] kinetics (a measure of fractional O2 extraction) did not change despite faster VO2p kinetics suggests that faster kinetics of muscle O2 utilization were accompanied by adaptations in local muscle (microvascular) blood flow and O2 delivery, resulting in a similar "matching" of blood flow to O2 utilization. Thus faster kinetics of VO2p 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.
The early time course of adaptation of pulmonary O2 uptake (VO2p) (reflecting muscle O2 consumption) and muscle deoxygenation kinetics (reflecting the rate of O2 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 O2 uptake separated by 1 min of rest) or END (90–120 min at 65% maximal O2 uptake). Subjects completed step transitions to a moderate-intensity work rate (~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. VO2p 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 VO2p ({tau}VO2) 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}VO2 was reduced by ~20% (P < 0.05) after only two training sessions and by ~40% (P < 0.05) after eight training sessions (i.e., posttraining), with no differences between HIT and END. The {tau}'{Delta}[HHb] (~20 s) did not change over the course of eight training sessions. These data suggest that faster activation of muscle O2 utilization is an early adaptive response to both HIT and lower-intensity END training. That {Delta}[HHb] kinetics (a measure of fractional O2 extraction) did not change despite faster VO2p kinetics suggests that faster kinetics of muscle O2 utilization were accompanied by adaptations in local muscle (microvascular) blood flow and O2 delivery, resulting in a similar "matching" of blood flow to O2 utilization. Thus faster kinetics of VO2p 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.