Lessons from the sea for medicine.
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Several personality attributes were hypothesized to account for a part of the performance variability in continuous repetitive and real-stress situations. A Personality Inventory For Divers (PIFD) was administered to 518 divers and non-divers. Cross sectional and longitudinal studies supported the validity of the PIFD (p less than 0.05). Some implications of the results are discussed.
In hyperbaric environments, comfortable ambient temperatures are necessarily higher than normal room temperature, and high levels of humidity are also common. These conditions are stressful and even hazardous for an exercising diver. We monitored the heart rates and core temperatures of divers participating in deep experimental dives to pressures up to 300 msw. Accelerated heart rates (100 to 180 beats/min) and elevated core temperatures (+0.4 to 0.9 degrees C) were registered. The increase in heart rate can be explained by the rise in core temperature. Formulas are presented for the relationships between heart rate and duration of activity, between core temperature and duration of activity, and between heart rate and core temperature. These formulas allow the estimation of core temperature from the diver's pulse, and serve to prevent excessive heat stress which could lead to an accident.
Isolated inner ear decompression sickness (DCS) is recognized in deep diving involving breathing of helium-oxygen mixtures, particularly when breathing gas is switched to a nitrogen-rich mixture during decompression. The biophysical basis for this selective vulnerability of the inner ear to DCS has not been established. A compartmental model of inert gas kinetics in the human inner ear was constructed from anatomical and physiological parameters described in the literature and used to simulate inert gas tensions in the inner ear during deep dives and breathing-gas substitutions that have been reported to cause inner ear DCS. The model predicts considerable supersaturation, and therefore possible bubble formation, during the initial phase of a conventional decompression. Counterdiffusion of helium and nitrogen from the perilymph may produce supersaturation in the membranous labyrinth and endolymph after switching to a nitrogen-rich breathing mixture even without decompression. Conventional decompression algorithms may result in inadequate decompression for the inner ear for deep dives. Breathing-gas switches should be scheduled deep or shallow to avoid the period of maximum supersaturation resulting from decompression.
Using a breathing medium of 40 kPa oxygen, remainder helium, 18 volunteer subjects participated in a series of 15 exposures to pressures equivalent to depths of 180-540 m s.w. The time of exposure at these pressures was mostly 2 days, except for the 540 m s.w. exposure, when 6 days were spent at full pressure. Compression procedures, based upon placing 'stages' at 60 m s.w. intervals, evolved with experience and proved to be a highly successful way of achieving acceptable pressure-time courses. Decompression combined slow linear release of pressure with overnight halts for sleep. On one occasion a depth of 660 m s.w. was reached by breathing 40 kPa oxygen, 10% nitrogen, remainder helium. Throughout all exposures, teams of investigators followed the changes in cardiovascular, respiratory, haematological, neurophysiological and metabolic status, and mental performance of the volunteers. Some major findings were that the neurophysiological and behavioural changes could be assigned to the motor, or vestibular, or cerebral, or autonomic systems, and were mainly first observed during compression. The subjects suffered, apparently from severe nitrogen narcosis, when breathing 10% (by volume) nitrogen in oxygen-helium at 420 m s.w. Lung ventilation was remarkably adaptable to the oxygen requirements of exercise at all depths, but cardiac output was adversely affected at 540 m s.w., particularly for heavier workloads. Ventilatory responses to carbon dioxide were significantly elevated after diving. Thermal balance was seen to be precarious, but nevertheless it was achieved by the normal subjective assessments of comfort. Water loss was affected by diminished evaporation from the skin. Skin temperature sensitivity was changed and took many days after the dives to return to normal. Energy requirements increased for work purposes, but basal metabolic rate was undisturbed. Body chemistry altered at pressures in excess of 300 m s.w., for example thyroid hormone and nitrogen balances were affected. No decompression sickness was encountered until the pressures were low, but marked haematological changes could occur during decompression. Every change that occurred during these dives reverted to normal, mostly before the end of the decompression. It is concluded that diving with oxygen-helium breathing mixtures to depths as great as 540 m s.w. can be effective and safe. An attempt is made to assess the physiological significance of the principal findings.
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Noxious stimulation of the nasal mucosa evokes a nasotrigeminal reflex (diving response), consisting of apnoea, bradycardia and vasoconstriction. However, the central mechanisms underlying the respiratory component remain unclear. Here, we describe the influence of nasotrigeminal stimulation (NS) on different types of ventral medullary respiratory neurones and upper airway patency in the rat. In an arterially perfused working heart-brainstem preparation (WHBP), NS was induced by either irrigation of the nasal passage with cold saline (100-200 microl) or electrical stimulation of the trigeminal ethmoidal nerve (EN5, 20 Hz, 10 s, 100 micros, 0.5-2 V). Both stimuli evoked apnoea, bradycardia, a pressor response, persistent discharge in the recurrent laryngeal nerve and marked glottal adduction (P<0.001). NS evoked a distinct pattern of response in respiratory neurones: inspiratory (I) neurones ceased firing and hyperpolarized (n=19), while postinspiratory neurones depolarized (n=10) and discharged persistently. The latency of EN5-evoked synaptic responses (excitatory to postinspiratory neurones 12.3+/-2.8 ms, n=10; inhibitory to inspiratory neurones 11.8+/-1.9 ms; n=19) was comparable. During the NS-evoked apnoea burst discharges were superimposed on a maintained level of tonic activity recorded from both the recurrent laryngeal nerve (n=4) and some postinspiratory neurones (n=7). The physiological significance of these "apnoeic rhythms" is discussed. We conclude that the cardiorespiratory components of the diving response are mediated by activation of distinct sets of postinspiratory respiratory neurones.
INTRODUCTION: In a previous study we reported that Korean female breath-hold divers (BHD) with life-long experience of diving in cold water (10-12 degrees C in winter and 25-27 degrees C in summer) had reduced muscle fiber size and increased capillary density. The hypothesis tested in the present study was whether prolonged habitual diving at a moderate water temperature (MWT, 29-30 degrees C all year round) similarly caused a reduction in muscle fiber size. METHODS: The subjects were 14 Indonesian BHDs with long experience of diving at MWT, and a control group of 10 age-matched non-diving Indonesian men (CON), selected from the same tribe among which the BHDs lived. Muscle samples obtained from the middle portion of the vastus lateralis muscle were analyzed for muscle morphology by histochemical analysis and the levels of vascular endothelial growth factor (VEGF) protein by Western blotting. RESULTS: Muscle fiber type composition was identical in both groups, and no difference in cross-sectional area (CSA), VEGF protein, or capillarity between the BHD and the CON was observed. CONCLUSION: The present study demonstrated that prolonged habitual breath-hold diving at MWT does not cause any alteration in muscle fiber composition, fiber size, or capillarity.
Fifteen divers performed five tasks in water of temperatures 20 degrees C and 5 degrees C, using standard scuba equipment. A significant deterioration of performance occurred under the colder condition in: simple arithmetic 13%; logical reasoning 17%; word recall 37%; word recognition 11%; and manual dexterity 17%. Throughout each dive, rectal and five skin temperatures were monitored. Average fall in rectal temperature was 0.5 degrees C during 20 degrees C dives and 1.1 degrees C during 5 degrees C dives. Average body surface temperature fell by 5 degrees C and 12.5 degrees C respectively. Average heat losses calculated from the data were 95 kcal.m(-2).hr(-1) (20 degrees C dives) and 245 kcal.m(-2).hr(-1) (5 degrees C dives). The impairment in word recognition was significantly correlated with the fall in rectal temperature for the 5 degrees C dives. For other tests, the deterioration did not appear to be correlated with body-temperature changes, but rather, occurred rapidly upon cold water immersion. The significance of these findings is discussed in relation to current understanding of the mechanisms by which cold is thought to influence performance underwater.
Ascorbic acid and glutathione (GSH) are antioxidants and free radical scavengers that provide the first line of defense against oxidative damage in the CNS. Using HPLC with electrochemical detection, we determined tissue contents of these antioxidants in brain and spinal cord in species with varying abilities to tolerate anoxia, including anoxia-tolerant pond and box turtles, moderately tolerant garter snakes, anoxia-intolerant clawed frogs (Xenopus laevis), and intolerant Long-Evans hooded rats. These data were compared with ascorbate and GSH levels in selected regions of guinea pig CNS, human cortex, and values from the literature. Ascorbate levels in turtles were typically 100% higher than those in rat. Cortex, olfactory bulb, and dorsal ventricular ridge had the highest content in turtle, 5-6 mumol g-1 of tissue wet weight, which was twice that in rat cortex (2.82 +/- 0.05 mumol g-1) and threefold greater than in guinea pig cortex (1.71 +/- 0.03 mumol g-1). Regionally distinct levels (2-4 mumol g-1) were found in turtle cerebellum, optic lobe, brainstem, and spinal cord, with a decreasing anterior-to-posterior gradient. Ascorbate was lowest in white matter (optic nerve) in each species. Snake cortex and brainstem had significantly higher ascorbate levels than in rat or guinea pig, although other regions had comparable or lower levels. Frog ascorbate was generally in an intermediate range between that in rat and guinea pig. In contrast to ascorbate, GSH levels in anoxia-tolerant turtles, 2-3 mumol g-1 of tissue wet weight, were similar to those in mammalian or amphibian brain, with no consistent pattern associated with anoxia tolerance. GSH levels in pond turtle CNS were significantly higher (by 10-20%) than in rat for several regions but were generally lower than in guinea pig or frog. GSH in box turtle and snake CNS were the same or lower than in rat or guinea pig. The distribution GSH in the CNS also had a decreasing anterior-to-posterior gradient but with less variability than ascorbate: levels were similar in optic nerve, brainstem, and spinal cord. The paradoxically high levels of ascorbate in turtle brain, which has a lower rate of oxidative metabolism than mammalian, suggest that ascorbate is an essential cerebral antioxidant. High levels may have evolved to protect cells from oxidative damage when aerobic metabolism resumes after a hypoxic dive.
Freshwater turtles Trachemys scripta elegans endure prolonged severe hypoxia, and even complete anoxia, while diving or hibernating underwater. Metabolic adaptations supporting survival include the activation of glycogenolysis and glucose output from liver, as well as strong metabolic rate depression. The present study analyzes the enzymes of both the phosphorolytic (glycogen phosphorylase, phosphorylase b kinase, cAMP-dependent protein kinase) and glucosidic (alpha-glucosidase) pathways of glycogenolysis in turtle organs. Turtles were subjected to 5 hr of submergence in N2-bubbled water at 7 degrees C and then activities of phosphorolytic and glucosidic enzymes were assayed in liver, heart, brain, and red and white skeletal muscle, and compared with aerobic controls. In vitro incubations also assessed protein kinase A control of phosphorolytic enzymes. A functional enzyme cascade system for the activation of glycogen phosphorylase was found in all organs, and both phosphorylase and phosphorylase kinase were stimulated by in vitro incubation with the catalytic subunit of cAMP-dependent protein kinase. Anoxic submergence led to significant increases in phosphorylase activities in liver and heart (phosphorylase a rose 2- and 2.5-fold, respectively) but phosphorylase kinase and protein kinase A activities in liver were reduced after 5 hr exposure. Both acidic (pH 4) and neutral (pH 7) forms of alpha-glucosidase were detected in all five organs with highest activities in liver. Activity of acid alpha-glucosidase, which degrades lysosomal glycogen, increased by 2-fold in liver during anoxic submergence. The data show that glycogen breakdown in turtle liver during anoxic submergence may result from coordinated activations of both the cytoplasmic phosphorolytic and the lysosomal glucosidic pathways of glycogenolysis.
INTRODUCTION: Elevated arterial PCO2 (hypercapnia) increases the risk of CNS oxygen toxicity when diving with enriched oxygen gas mixtures. A CO2 detection and retention test is conducted as a matter of routine at the Israel Naval Medical Institute for physiological training, and as a screening tool for divers who may be prone to suffer from CNS oxygen toxicity. This test does not include an "attention distracter", which would provide a better simulation of the true situation during actual diving. The purpose of the present study was to examine the hypothesis that the addition of cognitive tasks to the CO2 detection and retention test might alter divers' detection ability. METHODS: We assessed ventilatory and perceptual responses to variations in inspired CO2 (range 0-5.6 kPa, 0-42 mmHg) during moderate exercise, with and without the addition of cognitive tasks, in 15 Israel Navy combat divers on active duty. The first stage was the CO2 detection training session, followed by the CO2 detection test session (TEST) and the CO2 detection test session while doing cognitive tasks (COGN). The latter two sessions were performed by some of the subjects in reverse order. RESULTS: We found that the mean (+/- SD) PICO2 at the detection threshold was significantly lower in the COGN (1.7 +/- 0.8 kPa, 12.7 +/- 6.0 mmHg) than in the TEST (2.4 +/- 0.6 kPa, 18.1 +/- 4.5 mmHg). The mean PETCO2 while inspiring 5.6 kPa (42 mmHg) CO2 was not significantly different in the two tests. CONCLUSION: We suggest that the ability to detect CO2 during a dive is not impaired, but rather improves when the diver's attention is focused on other tasks.
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Closed circuit rebreathers used by divers recirculate the respiratory gases through a scrubber to remove exhaled carbon dioxide. For systems used in deep diving applications, oxygen is mixed with a diluent gas to maintain a preset partial pressure of oxygen (PO2) that is within the physiologically acceptable limits for the diver. These systems accurately maintain the oxygen set point while the diver swims at constant depth. However, as a diver increases depth, the gas volume in his lungs and his underwater breathing apparatus (UBA) will be compressed. To avoid damage, a diluent gas, a breathable mixture of oxygen and some inert component such as nitrogen or helium, must be supplied to the breathing circuit to maintain constant volume. Because the composition of this diluent will normally be different from the desired circuit breathing mixture, it is important that the addition of this diluent will not have harmful physiological effects on the diver. The effects of UBA circuit volume, diver descent rate, oxygen consumption rate, and diluent composition on the oxygen partial pressures within the breathing circuit during descent are investigated in this article. Exposures to oxygen partial pressures in excess of 2.0 atmospheres absolute (ata) are shown to be possible during dives when using closed circuit UBAs with present PO2 levels of 0.7 ata. These elevated oxygen exposures are shown to diminish when a diver reaches depth, but could last in excess of 18 min during a dive to 200 ft of seawater.