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

Abstract

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.

Effect of acute systemic hypoxia on human cutaneous microcirculation and endothelial, sympathetic and myogenic activity

“…Other explanation of skin blood flows increase could be due to systemic hemodynamic changes (Table 4) which could be caused by sympatho-vagal tonus impact to heart (Table 2). It is known that acute systemic hypoxia, either direct or as a result of reflex hyperventilation, stimulates the chemoreceptors, which in turn activate the sympatho-adrenergic axis (Marshall 1998, Povea et al 2005 in such kind of way acute hypoxic exposure affects cardiovascular autonomic functions (Huang et al 2009). During exposure to hypoxic environments, such us high altitudes or artificial hypoxia, RR variability in heart rate is reduced with a relative increase in the low-frequency component, indicating changed cardiac autonomic activity of the sinus node in response to hypoxic stimulation (Huang et al 2009).…”

“…It is known that acute systemic hypoxia, either direct or as a result of reflex hyperventilation, stimulates the chemoreceptors, which in turn activate the sympatho-adrenergic axis (Marshall 1998, Povea et al 2005 in such kind of way acute hypoxic exposure affects cardiovascular autonomic functions (Huang et al 2009). During exposure to hypoxic environments, such us high altitudes or artificial hypoxia, RR variability in heart rate is reduced with a relative increase in the low-frequency component, indicating changed cardiac autonomic activity of the sinus node in response to hypoxic stimulation (Huang et al 2009). This response is observed in our study (Table 2), and is supported by earlier observations that acute systemic hypoxia causes decrease of total power of high frequency (HF) and increase of total power of low frequency (LF) and the ratio of LF/HF.…”

“…Polar S810i is a valid method to record RR interval and to obtain a valid analysis of HRV (Parrodo et al 2010). Analysis of HRV measurements were conducted with the aid of Kubios HRV Analysis Software 2.1 (MATLAB, the Biomedical Signal Analysis Group, University of Kuopio, Kuopio, Finland) and data interpretation was M A N U S C R I P T ACCEPTED MANUSCRIPT made on basis of previous researches (Huang et al 2009;Wang & Huang 2012). To simulate systemic hypoxia (normobaric hypoxia), a hypoxicator (GO2Altidude, Biomedtech, Melbourne, Australia) which has an air separation system employing semi-permeable membrane technology (Spurling et al, 2011) was used, continuously pumping air at a flow rate of 20 l*min −1 into an air bag which was connected to a facial mask to deliver lower atmospheric O 2 concentration to the subjects (GO2Altitude, Biomedtech, Melbourne, Australia).…”

Effects of normoxic and hypoxic exercise regimens on cardiac, muscular, and cerebral hemodynamics suppressed by severe hypoxia in humans

“…Hence, a possible explanation for the different findings in hematological parameters from chronic continuous hypoxia is that the relatively short episode (30 min/day for 4 wk) of moderate hypoxia (15% O 2 ) with exercise may fail to cause sustained accelerated erythropoiesis. One the other hand, our recent study (21) indicated that both exposures to 12-15% O 2 decreased total power and highfrequency power and increased low-frequency power and the ratio of low-frequency to high-frequency power, indicating changed cardiac autonomic activity of the sinus node in response to acute hypoxic stimulation. However, only exposure to 12% O 2 , but not 15% O 2 , downregulates autonomic responses to physical stresses.…”

“…Probes were attached to a plastic spacer with an optode distance of 3.5-4.5 cm and secured to the skin using doublesided tape, and the lower extremities were elevated to a 30°angle from the examination couch. The subdiastolic occlusion pressure in the left lower leg was set at 60 mmHg to measure basal arterial blood flow (21). This occlusion procedure was conducted three times with Table 3.…”