The effect of low-level normobaric hypoxia on orthostatic responses

Altitude-induced hypoxia is believed to decrease tolerance to orthostasis. This preliminary investigation assesses the interaction between low-level normobaric hypoxia and the cardiovascular responses to orthostasis.

We hypothesize that low-level hypoxia at simulated altitudes up to 3350 m adversely affects cardiovascular responses to orthostasis.

Six women and eight men underwent + 75 degrees head-up tilt (HUT) at 3 simulated altitudes (115 m (377 ft), 1680 m (5500 ft) and 3350 m (11,000 ft)). Minute ventilation (VE), tidal volume (VT), breathing frequency (f), heart rate (HR), and arterial blood pressure (BP) were measured non-invasively. Ventilatory parameters (VE, VT, and f) were measured during the control period to assess the respiratory response to hypoxia. Cardiovascular variables (HR and BP) during HUT were compared and analyzed by calculating the deviation from control (pre-tilt) values.

Respiratory data showed no significant hypoxic ventilatory response. The average HR deviation significantly decreased (p < 0.05) with HUT from 13 +/- 2 bpm (115 m) to 9 +/- 2 bpm (3350 m). The pattern of mean arterial BP deviation with HUT was similar across the three altitudes (-6.6 +/- 2.9 mm Hg at 115 m to -6.8 +/- 2.4 mm Hg at 3350 m), with no significant differences.

Changes in HR and arterial BP are fundamental aspects of the cardiovascular response to orthostatic stress. Although there were no significant changes in the BP response to orthostasis with hypoxia, the HR changes seen in this study suggest that the ability to modulate HR under orthostatic stress is reduced with exposure to low-level normobaric hypoxia.