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

Abstract

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 (V̇normalO2) kinetics to high‐intensity interval training? What is the main finding and its importance? Speeding of pulmonary V̇normalO2 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 V̇normalO2 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 (V̇O2normalp), CO2 output (V̇normalCO2normalp) and ventilatory (V̇ Ep ) kinetics has not been examined. We hypothesized that low‐intensity BFR training would reduce the phase 2 time constant (τp) of V̇O2normalp, V̇normalCO2normalp and V̇ Ep 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 V̇normalO2 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 (Ppeak), and HIT was at ∼103% Ppeak. For BFR, cuffs were inflated on both thighs (140–200 mmHg) 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 ± 3.4 s; effect size = 1.14) and HIT (τp = 20.3 ± 4.0 versus 13.1 ± 2.9 s; effect size = 1.75) reduced the V̇O2normalp τp (P < 0.05). As expected, there was no change in LOW (V̇O2normalp τp = 17.9 ± 6.2 versus 17.7 ± 4.3 s; P = 0.9). The kinetics of V̇normalCO2normalp and V̇ Ep 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 V̇O2normalp kinetics. These data support the findings of others that low‐intensity cycling training with BFR increases muscle oxidative capacity.

Influence of blood flow restriction training on the aerobic capacity: a systematic review and meta-analysis

“…According to the PRISMA reporting guidelines, 13 trials were included in the analysis [12,14,15,[18][19][20][21][22][23][24][25][26]. Fig.…”

The Effect of Endurance Training on Pulmonary V˙O2 Kinetics in Solid Organs Transplanted Recipients

“…Is it well known that endurance training (ET) elicits favorable adaptations at cardiovascular [ 21 ] and muscular [ 22 ] levels, speeding O 2p kinetics, and reducing SC amp [ 7 , 23 ]. However, small muscle mass ET (i.e., SL or leg-kicking exercise) seems to be more effective than DL if one aims to improve the oxidative capacity of the skeletal muscle [ 24 ].…”

Blood flow restriction accelerates aerobic training-induced adaptation of VO2 kinetics at the onset of moderate-intensity exercise

“…Although low-intensity aerobic training does not alter V ． O2 kinetics at the onset of exercise 19 , moderate-intensity aerobic training (the American College of Sports Medicine 20 defines 40-59% V…”