Abstract

Background: We aimed to investigate the effect of a priming ischemia-reperfusion (IR) model on the kinetics of pulmonary oxygen uptake (VO2) and cardiopulmonary parameters after high-intensity exercise. Our primary outcome was the overall VO2 kinetics and secondary outcomes were heart rate (HR) and O2 pulse kinetics. We hypothesized that the IR model would accelerate VO2 and cardiopulmonary kinetics during the exercise.Methods: 10 recreationally active men (25.7 ± 4.7 years; 79.3 ± 10.8 kg; 177 ± 5 cm; 44.5 ± 6.2 mL kg−1 min−1) performed a maximal incremental ramp test and four constant load sessions at the midpoint between ventilatory threshold and VO2 max on separate days: two without IR (CON) and two with IR (IR). The IR model consisted of a thigh bi-lateral occlusion for 15 min at a pressure of 250 mmHg, followed by 3 min off, before high-intensity exercise bouts.Results: There were no significant differences for any VO2 kinetics parameters (VO2 base 1.08 ± 0.08 vs. 1.12 ± 0.06 L min−1; P = 0.30; τ = 50.1 ± 7.0 vs. 47.9 ± 6.4 s; P = 0.47), as well as for HR (MRT180s 67.3 ± 6.0 vs. 71.3 ± 6.1 s; P = 0.54) and O2 pulse kinetics (MRT180s 40.9 ± 3.9 vs. 48.2 ± 5.6 s; P = 0.31) between IR and CON conditions, respectively.Conclusion: We concluded that the priming IR model used in this study had no influence on VO2, HR, and O2 pulse kinetics during high-intensity cycling exercise.

Highlights

  • Pulmonary oxygen uptake (VO2) kinetics plays a role in the oxidative metabolism during constant load exercise (Poole et al, 2008)

  • There were no significant differences for any VO2 kinetics parameters (VO2 base 1.08 ± 0.08 vs. 1.12 ± 0.06 L min−1; P = 0.30; τ = 50.1 ± 7.0 vs. 47.9 ± 6.4 s; P = 0.47), as well as for heart rate (HR) (MRT180s 67.3 ± 6.0 vs. 71.3 ± 6.1 s; P = 0.54) and O2 pulse kinetics (MRT180s 40.9 ± 3.9 vs. 48.2 ± 5.6 s; P = 0.31) between IR and CON conditions, respectively

  • We concluded that the priming IR model used in this study had no influence on VO2, HR, and O2 pulse kinetics during high-intensity cycling exercise

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Summary

Introduction

Pulmonary oxygen uptake (VO2) kinetics plays a role in the oxidative metabolism during constant load exercise (Poole et al, 2008). An increase in vascular dilation (Enko et al, 2011), a potential increase in local blood flow, O2 muscle saturation and cardiac function (Daly and Bondurant, 1962; Faisal et al, 2010) is expected, which may accelerate VO2 kinetics by improving O2 delivery and availability. The blood flow restriction (e.g., increases in ADP, Pi, etc.,) may affect the VO2 time course through spin-off manifestations, likely improvements in the mitochondrial oxidation activity through the increases in ADP and Pi concentrations (Boushel et al, 1998; Walsh et al, 2002). We aimed to investigate the effect of a priming ischemia-reperfusion (IR) model on the kinetics of pulmonary oxygen uptake (VO2) and cardiopulmonary parameters after high-intensity exercise. We hypothesized that the IR model would accelerate VO2 and cardiopulmonary kinetics during the exercise

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