White, Matthew D.

The purpose of the present study was to develop and validate a new compact, portable end-tidal forcing (ETF) system capable of reliably controlling end-tidal gases. The system consists of compressed gas sources (air, N 2 and CO 2) that are connected via three solenoid valves to a humidification chamber and an inspiratory reservoir bag from which the participant breathes. This computer-controlled system compares actual end-tidal gas partial pressures with target pressures and mixes the gases on a breath-by-breath basis. This leaves no unused exhaust gas and keeps gas requirements to a minimum. Eight participants underwent two different 30-min protocols that included each possible combination of end-tidal O 2 partial pressure ( PE T O 2 ) and end-tidal CO 2 partial pressure ( PE T C O 2 ) control at two different levels ( PE T O 2 at 55 and 75 mmHg; and PE T C O 2 at 4 and 7 mmHg above resting). The ETF system maintained the mean PE T C O 2 at 0.13 mmHg from the target values, with a pooled S.D. across conditions of ±0.91 mmHg and a 95% confidence interval (CI) of ±0.63 mmHg. The mean PE T O 2 was held at 0.49 mmHg from its target values, with a pooled S.D. across conditions of ±1.31 mmHg and a 95% CI of ±0.91 mmHg. To demonstrate suitability of this system for measuring chemosensitivity to hypoxia, hypoxic ventilatory response (HVR) tests were conducted in a subset of five participants. During a 20-min HVR test both PE T C O 2 and PE T O 2 were not significantly different from their target values. These data demonstrate the performance of a portable, compact, economical system that controls PE T C O 2 within 1 mmHg and PE T O 2 within 2 mmHg of their respective target values.

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 −37.5 mmHg, LBPP at +37.5 mmHg and to ambient pressure (LBAP) at 0 mmHg. Blood pressure, expired gases and haemoglobin O2 saturation were continuously recorded. Hypoxia was administered in a single step to a of 50 mmHg for 20 min. For all tests was maintained at the pre-hypoxic resting level. Results The peak ventilation was significantly greater during LBNP (36.0 ± 10.8 L min−1) than during ambient pressure (29.4 ± 8.1 L min−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 37.5 mmHg 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.