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

New Findings 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. Abstract Low‐intensity blood‐flow‐restricted (BFR) endurance training is effective to increase aerobic capacity. Whether it speeds pulmonary oxygen uptake ( ), CO 2 output ( ) and ventilatory ( ) kinetics has not been examined. We hypothesized that low‐intensity BFR training would reduce the phase 2 time constant (τ p ) 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 ± 6 years old; maximal 46 ± 6 ml kg −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 × 2 min cycling and 1 min resting intervals. LOW and BFR were conducted at 30% of peak incremental power ( P peak ), and HIT was at ∼103% P peak . For BFR, cuffs were inflated on both thighs (140–200 mmHg) during exercise and deflated during rest intervals. Six moderate‐intensity step transitions (30% P peak ) were averaged for analysis of pulmonary on‐kinetics. Both BFR (pre‐ versus post‐training τ p = 18.3 ± 3.2 versus 14.5 ± 3.4 s; effect size = 1.14) and HIT (τ p = 20.3 ± 4.0 versus 13.1 ± 2.9 s; effect size = 1.75) reduced the τ p ( P < 0.05). As expected, there was no change in LOW ( τ p = 17.9 ± 6.2 versus 17.7 ± 4.3 s; 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.