Contrasting effects of hypoxia and hypercapnia on ventilation and sympathetic activity in humans

Abstract

We compared the effects of isocapnic hypoxia (IHO) and hyperoxic hypercapnia (HC) on sympathetic nerve activity (SNA) recorded from a peroneal nerve in 13 normal subjects. HC caused greater increases in blood pressure (BP), minute ventilation (VE), and SNA [53 +/- 14% (SE) during HC vs. 21 +/- 7% during IHO; P less than 0.05]. Even at equivalent levels of VE, HC still elicited greater SNA than IHO. However, apnea during HC caused a lesser (P less than 0.05) increase in SNA (91 +/- 26% compared with apnea on room air) than apnea during IHO (173 +/- 50%). Hypercapnic hypoxia resulted in a greater absolute increase in VE (23.6 +/- 2.8 l/min) than the additive increases due to HC alone plus IHO alone (18.0 +/- 1.8 l/min, P less than 0.05). SNA also increased synergistically by 108 +/- 23% with the combined stimulus compared with the additive effect of HC alone plus IHO alone (68 +/- 19%; P less than 0.05). We conclude that 1) HC causes greater increases in VE and SNA than does hypoxia; 2) for the same increase in VE, hypercapnia still causes a greater increase in SNA than hypoxia; however, during apnea, hypoxia causes a much greater increase in SNA than hypercapnia; 3) the inhibitory influence of ventilation on SNA is greater during hypoxia (i.e., predominantly peripheral chemoreceptor stimulation) than hypercapnia (i.e., predominantly central chemoreceptor stimulation); and 4) combined hypoxia and hypercapnia have a synergistic effect on SNA as well as on VE.

Respiratory modulation of cardiovagal baroreflex sensitivity

“…While our data from healthy humans do not disqualify this theory, they point to a possible need to reexamine this hypothesis in patient groups where the slow breathing method of enhancing BRS may have therapeutic benefit. Of note, replication of our findings in clinical cohorts would suggest that the clinical efficacy of slow, deep breathing on chemoreflex and sympathetic activity might involve neural factors beyond baroreflex function (1,26).…”

Cardiorespiratory parameters during submaximal exercise under acute exposure to normobaric and hypobaric hypoxia

“…The absence of changes in HRV at NH conditions at rest confirms previous findings, 32 reporting no changes at a simulated altitude of 3500 m, but contrasts with another recent study describing changes in HF power at 4800 m above sea level. 19 The level of simulated altitude exposure could be an important factor affecting these differences, since in NH exposure a threshold of around 10% O 2 (the subjects in our study were submitted to an equivalent of 14% O 2 ) is considered necessary to achieve discernible modifications of muscle sympathetic nerve activity, 33 a parameter that correlates closely with some HRV indices. 34 Apart from these differences in HRV, another finding showed discordance between the two simulated altitude systems used in this study: the correlation between the areas of the spectral peaks (LF%, HF% and the LF/HF ratio) in normoxia and in HH (Fig.…”

Exercise-induced respiratory muscle fatigue: implications for performance

“…These include an inhibitory effect of lung stretch (27,107) and an excitatory effect of carotid chemoreceptor stimulation (115,122). In addition, we assume that the reduction in limb blood flow with fatiguing respiratory muscle work is directed toward the respiratory muscles, but it is unclear whether the respiratory muscle vasculature also vasoconstricts in response to global sympathetic outflow.…”