Systemic hypoxia affects cardiac autonomic activity and vascular hemodynamic control modulated by physical stimulation.

This study investigates how various hypoxic interventions affect cardiac autonomic activity and hemodynamic control during posture change and the Valsalva maneuver. Ten healthy sedentary men exposed to 12, 15 and 21% O(2) for 1 h in a normobaric hypoxia chamber in a random order. Before and after various O(2) concentrations were administered, subjects performed the sit-up test and Valsalva maneuver, respectively. An impedance plethysmography was utilized to measure blood pressure (BP) and vascular hemodynamics, whereas spectral analysis of heart rate variability (HRV) was performed to determine cardiac autonomic activity. Analytical results can be summarized as follows: while the patient rests in a supine position, exposure to 12% O(2) reduces the ratio of lower to upper extremity systolic BP, which is accompanied by (1) suppressed arterial reactive hyperemia and increased venous flow resistance, as well as (2) decreased total power and high frequency (HF) and increased low frequency (LF) and the ratio of LF to HF. Moreover, the hypoxia-induced changes of time and frequency domains in HRV at resting supine disappear following the sit-up test, whereas this hypoxic exposure attenuates the BP and heart rate responses to the Valsalva maneuver. Conversely, resting and physical stimuli-mediated HRV and vascular hemodynamic values are unaltered by both 15 and 21% O(2) exposures. We conclude that acute hypoxic exposure affects cardiovascular autonomic functions, with reactions determined by the intervening O(2) concentrations. Moreover, the BP and cardiac autonomic responses to 12% O(2), but not 15% O(2), exposure are depressed while performing posture change and the Valsalva maneuver.