Hyperoxia During Exercise: Impact on Adenosine Plasma Levels and Hemodynamic Data

Abstract

Introduction: Adenosine is an ATP derivative that is strongly implicated in the cardiovascular adaptive response to exercise. In this study, we hypothesized that during exercise the hyperemia, commonly observed during exercise in air, was counteracted by the downregulation of the adenosinergic pathway during hyperoxic exposure.Methods: Ten healthy volunteers performed two randomized sessions including gas exposure (Medical air or Oxygen) at rest and during exercise performed at 40% of maximal intensity, according to the individual fitness of the volunteers. Investigations included the measurement of adenosine plasma level (APL) and the recording of hemodynamic data [i.e., cardiac output (CO) and systemic vascular resistances (SVR) using pulsed Doppler and echocardiography].Results: Hyperoxia significantly decreased APL (from 0.58 ± 0.06 to 0.21 ± 0.05 µmol L −1 , p < 0.001) heart rate and CO and increased SVR in healthy volunteers at rest. During exercise, an increase in APL was recorded in the two sessions when compared with measurements at rest (+0.4 ± 0.4 vs. +0.3 ± 0.2 µmol L −1 for medical air and oxygen exposures, respectively). APL was lower during the exercise performed under hyperoxia when compared with medical air exposure (0.5 ± 0.06 vs. 1.03 ± 0.2 µmol L −1 , respectively p < 0.001). This result could contribute to the hemodynamic differences between the two conditions, such as the increase in SVR and the decrease in both heart rate and CO when exercises were performed during oxygen exposure as compared to medical air.Conclusion: Hyperoxia decreased APLs in healthy volunteers at rest but did not eliminate the increase in APL and the decrease in SVR during low intensity exercise.

Contribution of Adenosine in the Physiological Changes and Injuries Secondary to Exposure to Extreme Oxygen Pressure in Healthy Subjects

“…The vasoconstrictor effect of the decrease in APL was therefore implicated in hemodynamic differences and better tolerance to orthostatic stress during hyperoxic exposure [ 5 ]. These findings were supported by another study in healthy volunteers reporting that breathing pure oxygen at atmospheric pressure can increase peripheral vascular resistance associated with a decrease in APLs compared with the same session in air [ 48 ]. The differences remained significant between the two sessions when a low-intensity exercise was added to each experimental condition.…”

“…The differences remained significant between the two sessions when a low-intensity exercise was added to each experimental condition. Meanwhile, hyperoxia did not suppress the increase in APL and the decrease in peripheral vascular resistance commonly recorded during exercise compared with resting reference [ 48 ]. In addition to various factors such as nitric oxide, prostacyclin (PGI2), and endothelium-derived hyperpolarizing factor [ 49 ], adenosine may be another important contributor involved in muscle hyperemia during exercise [ 50 ].…”

Deletion of CD73 increases exercise power in mice

“…Adenosine is an inter-cellular modulator that signals altered cellular activity and metabolic stress within a tissue by activating adenosine receptors [ 1 ]. Acute exercise increases adenosine levels in human blood [ 2 , 3 ] and the rat brain [ 4 ]. Accordingly, adenosine contributes to exercise-induced vasodilation [ 5 ] and also causes drowsiness and tiredness at rest, being a candidate molecule to signal exercise fatigue [ 6 – 8 ].…”

Incidence of hyperoxia in trauma patients receiving pre-hospital emergency anaesthesia: results of a 5-year retrospective analysis

“…There is compelling evidence that patients exposed to hyperoxia have an increased risk of both short- and long-term mortality [ 17 , 18 ]. This risk is related to both the extent and the duration of hyperoxia patients were exposed to, although recent in-vivo studies have demonstrated that even a short exposure to supra-physiological oxygen levels may result in haemodynamic changes (reduction in cardiac output and an increase in vascular resistance for example) that may contribute to a worse outcome [ 19 ].…”