Role of cortisol and/or adrenaline in the VO2 per breath

[Sasha Pachev]

I have a hypothesis that properly functioning adrenal glands will reduce runner's respiratory rate of a well-trained runner at the same pace by increasing the amount of oxygen inhaled per breath. However, I do not know the science behind it. Comments?

[Dallen]

Differential chemoreceptor reflex responses of adrenal preganglionic neurons
Wei-Hua Cao and Shaun F. Morrison

Abstract:
Adrenal sympathetic preganglionic neurons (ADR SPNs) regulating the chromaffin cell release of epinephrine (Epi ADR SPNs) and those controlling norepinephrine (NE ADR SPNs) secretion have been distinguished on the basis of their responses to stimulation in the rostral ventrolateral medulla, to glucopenia produced by 2-deoxyglucose, and to activation of the baroreceptor reflex. In this study, we examined the effects of arterial chemoreceptor reflex activation, produced by inhalation of 100% N2 or intravenous injection of sodium cyanide, on these two groups of ADR SPNs, identified antidromically in urethane-anesthetized, artificially ventilated rats. The mean spontaneous discharge rates of 38 NE ADR SPNs and 51 Epi ADR SPNs were 4.4 ± 0.4 and 5.6 ± 0.4 spikes/s at mean arterial pressures of 98 ± 3 and 97 ± 3 mmHg, respectively. Ventilation with 100% N2 for 10 s markedly excited all NE ADR SPNs (+222 ± 23% control, n = 36). In contrast, the majority (40/48; 83%) of Epi ADR SPNs were unaffected or slightly inhibited by ventilation with 100% N2 (population response: +6 ± 10% control, n = 48). Similar results were obtained after injection of sodium cyanide. These observations suggest that the network controlling the spontaneous discharge of NE ADR SPNs is more sensitive to brief arterial chemoreceptor reflex activation than is that regulating the activity of Epi ADR SPNs. The differential responsiveness to activation of the arterial chemoreceptor reflex of the populations of ADR SPNs regulating epinephrine and norepinephrine secretion suggests that their primary excitatory inputs arise from separate populations of sympathetic premotor neurons and that a fall in arterial oxygen tension is not a major stimulus for reflex-mediated adrenal epinephrine secretion.



This is the best that I could find. If I'm interpreting this correctly, these people had the same hypothesis as you, but the evidence wasn't there.

[Dallen]

I have an alternate similar theory. Endorphins, our natural opioid friends. Opioids severely depress respiratory drive. Maybe endorphins do the same. That part makes sense to me, but I don't know whether a well trained runner makes more or less endorphins, and whether the respiratory supression effect is significant compared to its other effects.