The present study tested the hypothesis that motion sickness affects thermoregulatory responses to cooling in humans. Ten healthy male volunteers underwent three separate head‐out immersions in 28 °C water after different preparatory procedures. In the ‘control’ procedure immersion was preceded by a rest period. In the ‘motion sickness’ procedure immersion was preceded by provocation of motion sickness in a human centrifuge. This comprised rapid and repeated alterations of the gravitational (G‐) stress in the head‐to‐foot direction, plus a standardized regimen of head movements at increased G‐stress. In the ‘G‐control’ procedure, the subjects were exposed to similar G‐stress, but without the motion sickness provocation. During immersion mean skin temperature, rectal temperature, the difference in temperature between the forearm and 3rd digit of the right hand (ΔTforearm‐fingertip), oxygen uptake and heart rate were recorded. Subjects provided ratings of temperature perception, thermal comfort and level of motion sickness discomfort at regular intervals. No differences were observed in any of the variables between control and G‐control procedures. In the motion sickness procedure, the ΔTforearm‐fingertip response was significantly attenuated, indicating a blunted vasoconstrictor response, and rectal temperature decreased at a faster rate. No other differences were observed. Motion sickness attenuates the vasoconstrictor response to skin and core cooling, thereby enhancing heat loss and the magnitude of the fall in deep body temperature. Motion sickness may predispose individuals to hypothermia, and have significant implications for survival time in maritime accidents.
To simulate pressure effects and experience thoracic compression while breath-hold diving in a relatively safe environment, competitive breath-hold divers exhale to residual volume before diving in a swimming pool, thus compressing the chest even at depth of only 3-6 m. The study was undertaken to investigate whether such diving could cause pulmonary edema and hemoptysis. Eleven volunteer breath-hold divers who regularly dive on full exhalation performed repeated dives to 6 m during a 20-min period. The subjects were studied with dynamic spirometry, video-fibernasolaryngoscopy, and single-breath diffusion capacity of carbon monoxide (Dl(CO)). The duration of dives with empty lungs ranged from 30 to 120 s. Postdiving forced vital capacity (FVC) was reduced from mean (SD) 6.57 +/- 0.88 to 6.23 +/- 1.02 liters (P < 0.05), and forced expiratory volume during the first second (FEV(1.0)) was reduced from 5.09 +/- 0.64 to 4.59 +/- 0.72 liters (P < 0.001) (n = 11). FEV(1.0)/FVC was 0.78 +/- 0.05 prediving and 0.74 +/- 0.05 postdiving (P < 0.001) (n = 11). All subjects reported a (reversible) change in their voice after diving, irritation, and slight congestion in the larynx. Fresh blood that originated from somewhere below the vocal cords was found by laryngoscopy in two subjects. Dl(CO)/alveolar ventilation (Va) was 1.56 +/- 0.17 mmol.kPa(-1).min(-1).l(-1) before diving. After diving, the Dl(CO)/Va increased to 1.72 +/- 0.24 (P = 0.001), but 20 min later it was indistinguishable from the predive value: 1.57 +/- 0.20 (n = 11). Breath-hold diving with empty lungs to shallow depths can induce hemoptysis in healthy subjects. Edema was possibly present in the lower airways, as suggested by reduced dynamic spirometry.
Breath-hold diving is an activity that humans have engaged in since antiquity to forage for resources, provide sustenance and to support military campaigns. In modern times, breath-hold diving continues to gain popularity and recognition as both a competitive and recreational sport. The continued progression of world records is somewhat remarkable, particularly given the extreme hypoxaemic and hypercapnic conditions, and hydrostatic pressures these athletes endure. However, there is abundant literature to suggest a large inter-individual variation in the apnoeic capabilities that is thus far not fully understood. In this review, we explore developments in apnoea physiology and delineate the traits and mechanisms that potentially underpin this variation. In addition, we sought to highlight the physiological (mal)adaptations associated with consistent breath-hold training. Breath-hold divers (BHDs) are evidenced to exhibit a more pronounced diving-response than non-divers, while elite BHDs (EBHDs) also display beneficial adaptations in both blood and skeletal muscle. Importantly, these physiological characteristics are documented to be primarily influenced by training-induced stimuli. BHDs are exposed to unique physiological and environmental stressors, and as such possess an ability to withstand acute cerebrovascular and neuronal strains. Whether these characteristics are also a result of training-induced adaptations or genetic predisposition is less certain. Although the long-term effects of regular breath-hold diving activity are yet to be holistically established, preliminary evidence has posed considerations for cognitive, neurological, renal and bone health in BHDs. These areas should be explored further in longitudinal studies to more confidently ascertain the long-term health implications of extreme breath-holding activity.
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 P O(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 breath-holds 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 P CO(2), P O(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 P O(2) and P CO(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 P O(2) and P CO(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 P O(2) and a lower P CO(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.
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