Water covers over 70% of the earth, has varying depths and temperatures and contains much of the earth's resources. Head-out water immersion (HOWI) or submersion at various depths (diving) in water of thermoneutral (TN) temperature elicits profound cardiorespiratory, endocrine, and renal responses. The translocation of blood into the thorax and elevation of plasma volume by autotransfusion of fluid from cells to the vascular compartment lead to increased cardiac stroke volume and output and there is a hyperperfusion of some tissues. Pulmonary artery and capillary hydrostatic pressures increase causing a decline in vital capacity with the potential for pulmonary edema. Atrial stretch and increased arterial pressure cause reflex autonomic responses which result in endocrine changes that return plasma volume and arterial pressure to preimmersion levels. Plasma volume is regulated via a reflex diuresis and natriuresis. Hydrostatic pressure also leads to elastic loading of the chest, increasing work of breathing, energy cost, and thus blood flow to respiratory muscles. Decreases in water temperature in HOWI do not affect the cardiac output compared to TN; however, they influence heart rate and the distribution of muscle and fat blood flow. The reduced muscle blood flow results in a reduced maximal oxygen consumption. The properties of water determine the mechanical load and the physiological responses during exercise in water (e.g. swimming and water based activities). Increased hydrostatic pressure caused by submersion does not affect stroke volume; however, progressive bradycardia decreases cardiac output. During submersion, compressed gas must be breathed which introduces the potential for oxygen toxicity, narcosis due to nitrogen, and tissue and vascular gas bubbles during decompression and after may cause pain in joints and the nervous system.

Human Physiology in an Aquatic Environment.

The partial pressure of end tidal carbon dioxide (PETCO 2), ventilatory sensitivity to CO 2, and cerebral perfusion are augmented during thermoneutral head out water immersion (HOWI). We tested the hypotheses that HOWI and acute hypercapnia augments minute ventilation, ventilatory sensitivity to CO 2, cerebral perfusion, and cerebrovascular reactivity to CO 2. Twelve subjects (age: 24 ± 3 years, BMI: 25.3 ± 2.9 kg/m2, 6 women) participated in two experimental visits: a HOWI visit (HOWI) and a matched hypercapnia visit (Dry + CO 2). A rebreathing test was conducted at baseline, 10, 30, 60 min, and post HOWI and Dry + CO 2. PETCO 2, minute ventilation, expired gases, blood pressure, heart rate, and middle cerebral artery blood velocity were recorded continuously. PETCO 2 increased throughout HOWI (baseline: 42 ± 2 mmHg; maximum at 10 min: 44 ± 2 mmHg, P ≤ 0.013) and Dry + CO 2 (baseline: 42 ± 2 mmHg; maximum at 10 min: 44 ± 2 mmHg, P ≤ 0.013) and was matched between conditions (condition main effect: P = 0.494). Minute ventilation was lower during HOWI versus Dry + CO 2 (maximum difference at 60 min: 13.2 ± 1.9 vs. 16.2 ± 2.7 L/min, P < 0.001). Ventilatory sensitivity to CO 2 and middle cerebral artery blood velocity were greater during HOWI versus Dry + CO 2 (maximum difference at 10 min: 2.60 ± 1.09 vs. 2.20 ± 1.05 L/min/mmHg, P < 0.001, and 63 ± 18 vs. 53 ± 14 cm/sec, P < 0.001 respectively). Cerebrovascular reactivity to CO 2 decreased throughout HOWI and Dry + CO 2 and was not different between conditions (condition main effect: P = 0.777). These data indicate that acute hypercapnia, matched to what occurs during HOWI, augments minute ventilation but not ventilatory sensitivity to CO 2 or middle cerebral artery blood velocity despite an attenuated cerebrovascular reactivity to CO 2.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.14814/phy2.13901

The effect of water immersion and acute hypercapnia on ventilatory sensitivity and cerebrovascular reactivity.

Deep diving refers to saturation diving to a depth of more than 180 m (1.9 MPa ambient pressure). In the 1990s diving to 400 m may be necessary on the Norwegian continental shelf. The safety margins are narrow and at such depths the respiratory system is subject to great strain. Respiratory resistance increases and the dynamic lung volumes are reduced as the pressure increases due to enhanced gas density. Helium is used together with oxygen as breathing gas and the lower density partly normalises the dynamic lung volumes. The respiratory system imposes clear limitations on the intensity and duration of physical work during deep diving. We lack systematic studies of lung mechanics, gas exchange and respiratory regulation in the different phases of deep dives. Demonstration of possible chronic occupational respiratory diseases connected to diving is dependent on follow-up over a long time.

Respiratory changes in deep diving

We previously demonstrated that the exposure to hyperbaric hyperoxia increased respiratory system elastance and both the “ohmic” and viscoelastic components of inspiratory resistances, probably because of increased oxygen tension toxic effects. We presently investigated the possible consequences of a single exposure to 2.5-atmospheres absolute air (hyperbarism) lasting 90 min. We used the end-inflation occlusion method on anesthetized rats after about 15 min from previous exposure to hyperbarism. The method allows the measurements of respiratory system elastance and of the ohmic and viscoelastic components of airway resistance, which respectively depend on the Newtonian pressure dissipation due to the ohmic airway resistance to airflow and on the viscoelastic pressure dissipation caused by respiratory system tissue stress relaxation. The expressions of inducible NO synthase (iNOS) and endothelial NO synthase (eNOS) in the lung’s tissues were also investigated, together with the histological characteristics of lung tissue. Data were compared with those obtained in control animals and in previously studied animals exposed to hyperoxic hyperbarism. Unlike with hyperoxic hyperbarism, hyperbarism per se did not change significantly the parameters of respiratory mechanics in the control animals (respiratory system elastance and ohmic and viscoelastic resistances were 2.01 ± 0.17 vs. 1.74 ± 0.08 cm H2O/ml, and 0.13 ± 0.02 vs. 0.13 ± 0.03 and 0.425 ± 0.04 vs. 0.33 ± 0.03 cm H2O/ml s−1 in control vs. experimental animals, respectively, none significantly different), nor did it induce evident effects on lung histology. An increment of both iNOS and eNOS expressions was documented instead (0.50 ± 0.05 vs. 0.75 ± 0.07 and 1.04 ± 0.1 and 1.4 ± 0.15, respectively). Our results indicate that, at variance with hyperoxic hyperbarism, the acute exposure to only hyperbarism does not affect either the elastic or the resistive respiratory system properties, or lung histology.

Hyperbaric air exposure at 2.5 ATA does not affect respiratory mechanics and lung histology in the rat.

The respiratory system is challenged by exposure to high or low ambient pressures and gravitational forces. These have effects on a range of respiratory functions, such as the mechanics of breathing, the exchange of respiratory gases at the lungs, and the control of pulmonary ventilation.

Gravitational and Hyper- and Hypobaric Stress

Human tolerance to He, Ne, and N2 at respiratory gas densities equivalent to He-O2 breathing at depths to 1200, 2000, 3000, 4000, and 5000 feet of sea water (predictive studies III).

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Human tolerance to He, Ne, and N2 at respiratory gas densities equivalent to He-O2 breathing at depths to 1200, 2000, 3000, 4000, and 5000 feet of sea water (predictive studies III).