Aggravated hypoxia during breath-holds after prolonged exercise

Hyperventilation prior to breath-hold diving increases the risk of syncope as a result of hypoxia. Recently, a number of cases of near-drownings in which the swimmers did not hyperventilate before breath-hold diving have come to our attention. These individuals had engaged in prolonged exercise prior to breath-hold diving and it is known that such exercise enhances lipid metabolism relative to carbohydrate metabolism, resulting in a lower production Of CO(2) per amount Of O(2) consumed. Therefore, our hypothesis was that an exercise-induced increase in lipid metabolism and the associated reduction in the amount Of CO(2) produced would cause the urge to breathe to develop at a lower PO(2), thereby increasing the risk of syncope due to hypoxia. Eight experienced breath-hold divers performed 5 or 6 breath-holds at rest in the supine position and then 5 or 6 additional breath-holds during intermittent light ergometer exercise with simultaneous apnoea (dynamic apnoea, DA) on two different days: control (C) and post prolonged sub-maximal exercise (PPE), when the breathholds were performed 30 min after 2 h of sub-maximal exercise. After C and before the prolonged submaximal exercise subjects were put on a carbohydrate-free diet for 18 h to start the depletion of glycogen. The respiratory exchange ratio (RER) and end-tidal PCO(2), PO(2), and SaO(2) values were determined and the data were presented as means (SD). The RER prior to breath-holding under control conditions was 0.83 (0.09), whereas the corresponding value after exercise was 0.70 (0.05) (P < 0.01). When the three apnoeas of the longest duration for each subject were analysed, the average duration of the dynamic apnoeas was 96 (14) s under control conditions and 96 (17) s following exercise. Both PO(2) and PCO(2) were higher during the control dynamic apnoeas than after PPE [PO(2) 6.9 (1.0) kPa vs 6.2 (1.2) kPa, P < 0.01; P CO(2) 7.8 (0.5) kPa vs 6.7 (0.4) kPa, P<0.001; ANOVA testing]. A similar pattern was observed after breath-holding under resting conditions, i.e., a lower end-tidal PO(2) and PCO(2) after exercise (PPE) compared to control conditions. Our findings demonstrate that under the conditions of a relatively low RER following prolonged exercise, breath-holding is terminated at a lower PO(2) and a lower PCO(2) than under normal conditions. This suggests that elevated lipid metabolism may constitute a risk factor in connection with breath-holding during swimming and diving.