UBC Theses and Dissertations
Physiology of extreme breath-holding Bain, Anthony R.
The practice of competitive breath-hold (apnea) diving has provided a gateway for studying the physiologic limits of severe hypoxemia and hypercapnia beyond otherwise possible in healthy humans. In elite apnea competitors, the broad objectives of this Thesis were to, a) quantify the impact of peripheral and central chemoreception, and lung volume on the elite dry-land apnea breakpoint, and b) examine the consequences of prolonged apnea on the cerebral metabolic functioning. These objectives were achieved in four experimental studies. Study 1 explored the impact of peripheral chemoreflex silencing with low-dose dopamine. Here, compared to placebo, dopamine blunted the ventilatory response to hypercapnic-hypoxia by ~27%; however, maximal apnea duration was only increased by ~5%. At the breakpoint, arterial hypoxemia was identical with dopamine compared to placebo, indicating that the apnea termination may largely be determined by a threshold level of hypoxemia to maintain consciousness. To eliminate the influence of hypoxia, Study 2 assessed the main determinants of an apnea breakpoint following hyperoxic pre-breathing. Here, the apnea duration was related to the individual forced vital capacity, and unrelated to the central chemoreflex. Respiratory muscle fatigue and pending atelectasis likely determined the capacity of a maximal hyperoxic apnea. Study 3 quantified the cerebral metabolism during apnea. The cerebral metabolic rate of oxygen, measured from the product of cerebral blood flow and the radial artery-jugular venous oxygen content difference, was reduced by ~29% at the termination of apnea. However, there was no change in the cerebral non-oxidative metabolism, calculated from the ratio of oxygen and carbohydrate metabolism. Study 4 examined the cerebral metabolic response in three apneas eliciting separate levels of hypoxemia and hypercapnia. Apneas generating the most severe hypercapnia, irrespective of hypoxia, elicited the largest reduction in the cerebral metabolic rate of oxygen. Moreover, apneas generating the most severe hypoxia, irrespective of hypercapnia, caused a cerebral net release of lactate, suggesting astrocyte glycogenolysis. Together, the findings of this thesis provide new insight into the determinants of an extreme apnea breaking point, and the observations of hypercapnic-induced reduction in oxidative cerebral metabolism provides a tenable mechanism for cerebral protection against prolonged apnea.
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