Central circulatory and peripheral O2 extraction changes as interactive facilitators of pulmonary O2 uptake during a repeated high-intensity exercise protocol in humans

Abstract

It has frequently been demonstrated that prior high-intensity exercise facilitates pulmonary oxygen uptake [Formula: see text] response at the onset of subsequent identical exercise. To clarify the roles of central O(2) delivery and/or peripheral O(2) extraction in determining this phenomenon, we investigated the relative contributions of cardiac output (CO) and arteriovenous O(2) content difference [Formula: see text] to the [Formula: see text] transient during repeated bouts of high-intensity knee extension (KE) exercise. Nine healthy subjects volunteered to participate in this study. The protocol consisted of two consecutive 6-min KE exercise bouts in a supine position (work rate 70-75% of peak power) separated by 6 min of rest. Throughout the protocol, continuous-wave Doppler ultrasound was used to measure beat-by-beat CO (i.e., via simultaneous measurement of stroke volume and the diameter of the arterial aorta). The phase II [Formula: see text] response was significantly faster and the slow component (phase III) was significantly attenuated during the second KE bout compared to the first. This was a result of increased CO during the first 30 s of exercise: CO contributing to 100 and 56% of the [Formula: see text] speeding at 10 and 30 s, respectively. After this, the contribution of [Formula: see text] became increasingly more predominant: being responsible to an estimated 64% of the [Formula: see text] speeding at 90 s, which rose to 100% by 180 s. This suggests that, while both CO and [Formula: see text] clearly interact to determine the [Formula: see text] response, the speeding of [Formula: see text] kinetics by prior high-intensity KE exercise is predominantly attributable to increases in [Formula: see text].

Relationship between changes in pulmonary kinetics and autonomic regulation of blood flow

“…This is the first study to investigate the relationship between cardiac vagal activity, kinetics, and kinetics within the same participants, the aim of which was to provide further insight into the mechanism(s) responsible for regulating kinetics (Grassi, ; Hughson et al., ; Grassi, ; Hughson, ). This work extends those previous studies that have assessed the relationship between kinetics and either or HR (De Cort et al., ; Fukuba et al., ) or only the relationship between vagal withdrawal and HR kinetics (Javorka et al., ; Ricardo et al., ).…”

“…Fukuba et al. () reported a similar contribution of to the response, accounting for 100% of the initial rise in 10 s after the step transition and 56% of the rise in 30 s after the step transition. Despite these values being similar to our findings, caution is required when interpreting the findings of Fukuba et al.…”

Remote ischemic preconditioning accelerates systemic O2 dynamics and enhances endurance during work-to-work cycling exercise

“…Accelerated systemic O 2 dynamics during exercise is associated with enhanced cardiovascular functions . Previous studies have reported that RIPC can enhance cardiac contractile capacity .…”

“…These previous findings suggest that the beneficial effect of RIPC on exercise performance may be associated with increased contractile capacity of the cardiac muscle. This enhanced cardiac contractile capacity may lead to the acceleration of systemic O 2 dynamics during whole‐body exercise . Furthermore, enhancement of whole‐body exercise performance is associated not only with the acceleration of local muscle O 2 dynamics but also with that of systemic O 2 dynamics .…”

Exercise Transients

“…Among these, increased muscle oxygen delivery may play a crucial role for its potentially direct effect (DeLorey et al 2007;Endo et al 2005;Faisal et al 2009), although enhanced activity of muscle oxidative enzymes and alterations of motor unit recruitment patterns have also been considered (for a review of these alternative hypotheses, see Poole and Jones 2012). According to Faisal et al (2009), greater oxygen delivery with increased leg blood flow after prior heavy exercise (Fukuba et al 2007), or an elevation in pyruvate dehydrogenase and intracellular lactate and acetyl CoA concentrations (Gurd et al 2006), may generate an increase in PO 2 following elevated oxygen delivery.…”