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Updated: Jun 13, 2026

Normothermic Negative Pressure Ventilation Ex Situ Lung Perfusion: Evaluation of Lung Function and Metabolism
Published on: February 14, 2022
The effects of lower body positive and negative pressure on the hypoxic ventilatory decline
Michael S Koehle1, Luisa V Giles, Michael L Walsh
1Laboratory for Exercise and Environmental Physiology, 8888 University Drive, Department of Biomedical Physiology and Kinesiology, Simon Fraser University, Burnaby, British Columbia, Canada, V5A 1S6.
Purpose:
Lower body negative pressure (LBNP) augments the acute hypoxic ventilatory response (AHVR) in humans, presumably through altered central integration of baro- and chemoreceptor afferents. This study investigated the effects of LBNP and lower body positive pressure (LBPP) on hypoxic ventilatory decline (HVD) in humans.
Methods:
Nine individuals (4 females and 5 males) were tested in a supine position with the lower body supported inside a hypo/hyperbaric chamber. During each test the participant was exposed in a random order to LBNP at -37.5mmHg, LBPP at +37.5mmHg and to ambient pressure (LBAP) at 0mmHg. Blood pressure, expired gases and haemoglobin O(2) saturation were continuously recorded. Hypoxia was administered in a single step to a PET O₂ of 50mmHg for 20min. For all tests PET CO₂ was maintained at the pre-hypoxic resting level.
Results:
The peak ventilation was significantly greater during LBNP (36.0+/-10.8Lmin(-1)) than during ambient pressure (29.4+/-8.1Lmin(-1); p=0.032). However, peak ventilation was not significantly different between LBPP and ambient pressure. The HVD was not significantly different across the three conditions (p=0.144). Both mean arterial pressure and pulse pressure were not affected by 37.5mmHg of either LBPP (p=0.941) or LBNP (p=0.275). Baroreflex slope was decreased by both hypoxia and LBNP.
Conclusion:
These data suggest that LBNP increases AHVR through an effect on the baroreflex, while LBPP has no effect on AHVR. Since LBNP increases AHVR without affecting HVD, these findings support that the mechanism accounting for the HVD includes afferent output originating from the peripheral rather than the central chemosensitive tissues.
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