Speeding of oxygen uptake kinetics is not different following low-intensity blood-flow-restricted and high-intensity interval training.

Abstract

What is the central question of this study? Can interval blood-flow-restricted (BFR) cycling training, undertaken at a low intensity, promote a similar adaptation to oxygen uptake ( ) kinetics to high-intensity interval training? What is the main finding and its importance? Speeding of pulmonary on-kinetics in healthy young subjects was not different between low-intensity interval BFR training and traditional high-intensity interval training. Given that very low workloads are well tolerated during BFR cycle training and speed on-kinetics, this training method could be used when high mechanical loads are contraindicated. Low-intensity blood-flow-restricted (BFR) endurance training is effective to increase aerobic capacity. Whether it speeds pulmonary oxygen uptake ( ), CO2 output ( ) and ventilatory ( ) kinetics has not been examined. We hypothesized that low-intensity BFR training would reduce the phase2 time constant (τp ) of , and by a similar magnitude to traditional high-intensity interval training (HIT). Low-intensity interval training with BFR served as a control. Twenty-four participants (25±6years old; maximal 46±6mlkg-1 min-1 ) were assigned to one of the following: low-intensity BFR interval training (BFR; n=8); low-intensity interval training without BFR (LOW; n=7); or high-intensity interval training without BFR (HIT; n=9). Training was 12 sessions of two sets of five to eight×2min cycling and 1min resting intervals. LOW and BFR were conducted at 30% of peak incremental power (Ppeak ), and HIT was at ∼103% Ppeak . For BFR, cuffs were inflated on both thighs (140-200mmHg) during exercise and deflated during rest intervals. Six moderate-intensity step transitions (30% Ppeak ) were averaged for analysis of pulmonary on-kinetics. Both BFR (pre- versus post-training τp =18.3±3.2 versus 14.5±3.4s; effect size=1.14) and HIT (τp =20.3±4.0 versus 13.1±2.9s; effect size=1.75) reduced the τp (P<0.05). As expected, there was no change in LOW ( τp =17.9±6.2 versus 17.7±4.3s; P=0.9). The kinetics of and were speeded only after HIT (38.5±10.6%, P<0.001 and 31.2±24.7%, P=0.004, respectively). Both HIT and low-intensity BFR training were effective in speeding moderate-intensity kinetics. These data support the findings of others that low-intensity cycling training with BFR increases muscle oxidative capacity.