Table of Contents

Pulmonary gas exchange in diving

Diving-related pulmonary effects are due mostly to increased gas density, immersion-related increase in pulmonary blood volume, and (usually) a higher inspired P o 2. Higher gas density produces an increase in airways resistance and work of breathing, and a reduced maximum breathing capacity. An additional mechanical load is due to immersion, which can impose a static transrespiratory pressure load as well as a decrease in pulmonary compliance. The combination of resistive and elastic loads is largely responsible for the reduction in ventilation during underwater exercise. Additionally, there is a density-related increase in dead space/tidal volume ratio (V d /V t ), possibly due to impairment of intrapulmonary gas phase diffusion and distribution of ventilation. The net result of relative hypoventilation and increased V d /V t is hypercapnia. The effect of high inspired P o 2 and inert gas narcosis on respiratory drive appear to be minimal. Exchange of oxygen by the lung is not impaired, at least up to a gas density of 25 g/l. There are few effects of pressure per se, other than a reduction in the P50 of hemoglobin, probably due to either a conformational change or an effect of inert gas binding.

despite having evolved in and adapted to an atmosphere with gas density close to 1 g/l, the performance of the human lung in the diving environment is remarkable. Adequate ventilation and gas exchange have been achieved at an ambient pressure up to 71 atmospheres absolute (ATA) [701 m of sea water (msw); 2,310 ft of sea water (fsw)] with an ambient P o 2 of 0.39 ATA (49), and with a P o 2 of 0.2 ATA up to a gas density of 25 g/l (50). Adequate exchange of oxygen and carbon dioxide while diving requires the ability to maintain ventilation in the face of significantly increased resistive and elastic loads. Resistance is increased primarily by the increase in breathing gas density. Elastic load is enhanced primarily by changes in transrespiratory pressure (PTR). Inertial mechanical load is also increased, although this has a minimal effect on the diver. Added challenges include blunted respiratory drive due to elevated partial pressures of inert gas and oxygen, and possibly impaired diffusion within the alveolus (7). While in most dives the breathing gas is hyperoxic, thus precluding hypoxemia, hypercapnia is common. Hyperoxia, particularly in the venous blood, can induce a small reduction in CO2 solubility, and hence an increase in venous P co 2 via the Haldane effect (27, 122). Arterial P co 2 (PaCO2) is not affected by the Haldane effect because of regulation of breathing via the chemoreceptors, although hypercapnia does occur for other reasons as discussed below.

Studies of pulmonary gas exchange under hyperbaric conditions designed to simulate diving have been performed since the 1950s. Measurements have included ventilation, oxygen consumption, carbon dioxide elimination, and both end-tidal and arterial gas tensions (51, 53). Ensuing experiments demonstrated hypercapnia at rest (91), but to a greater extent during exercise (11, 25, 40–42, 52, 74, 89–91, 107, 118). The increase in PaCO2 is due to two phenomena: 1) relative hypoventilation (6, 37, 40, 50, 55, 74, 91, 103, 104, 107, 126), and 2) elevated dead space, as discussed below.

A recently described phenomenon is a change in breathing pattern in endurance underwater swimming [oxygen uptake (V̇ o 2) of 1.5–2 l/min, depth of 4 ft]. Fifteen minutes after the start of constant exercise an abrupt 20–25% increase in ventilation has been observed (130). When the study was repeated at a depth of 55 ft (2.7 ATA) breathing air (P o 2 0.56 ATA), there was a similar increase, although it occurred more gradually (85). The investigators interpreted these data as consistent with respiratory compensation for metabolic acidosis, and possibly respiratory muscle fatigue. The effects of this on blood gases, pH, pulmonary hemodynamics, and gas exchange are unknown.


Traditional measures of respiratory load include resistive, elastic, and inertial components. Diving induces an increase in all three components. The primary effect of diving on resistance is mediated by the proportional increase in breathing gas density with the depth of immersion. This occurs because breathing underwater can only occur if breathing gas is delivered to the diver at a pressure within a few cmH2O of the ambient pressure at the diver’s depth. For turbulent gas flow, which is present throughout most of the conducting airways, flow resistance is proportional to density. During diving the external breathing apparatus adds an additional resistive load. Additionally, there is an increase of the total inertance of the respiratory system due to increased mass of the breathing gas.

Internal resistance.

Although gas viscosity is unchanged at increased pressure (at least within the pressure range to which humans have been exposed), gas density is increased in direct proportion to ambient pressure. Breathing gas density has a major effect on airways resistance. This can be readily measured by a reduction in forced expiratory volume in 1 s (FEV1), peak expiratory flow, and maximum voluntary ventilation (MVV) (50, 65, 99, 114). The increase in airways resistance purely due to turbulent flow can be augmented further by expiratory flow limitation due to airway collapse (126). Peak expiratory flow or MVV at any gas density (ρ) can be approximated by the following formula (125, 128):

where A is either MVV or peak expiratory flow at a gas density ρ; A is MVV (or peak expiratory flow) at 1 ATA; ρ is gas density at 1 ATA; ρ is the gas density; and k is a constant with the value 0.4–0.5. A similar equation has been verified for the relationship between airway conductance and gas density (4).

External resistance.

In addition to internal respiratory resistance, some amount of external resistance is present in all underwater breathing apparatus. Resistance varies with different apparatus, and resistance levels frequently differ between the inspired and expired breathing circuits. High breathing resistance increases subjective dyspnea scores (91, 117) and raises P co 2 levels in subjects performing various levels of exercise at the surface (102, 132) and at a range of depths (117–119).


During water immersion there is a redistribution of 500–800 ml of blood from the legs into the large veins and pulmonary vessels. There is also a negative transthoracic pressure when the diver is in the head-up position (e.g., during head-out immersion), due to the pressure difference between the mouth and the centroid of the lung (see Fig. 1). As a consequence of this pressure difference, there is a reduction in lung volume and its subsets, for example residual volume, vital capacity, and expiratory reserve volume (ERV) (2). This occurs to a greater extent in cold water than in warm, presumably due to active peripheral vasoconstriction and hence greater volume of blood redistributed from the periphery into the pulmonary vessels (46).

Fig. 1.

Fig. 1.Transrespiratory pressure (PTR) [static lung load (SLL)]. A: a person immersed to the neck (negative PTR). 1 ATA, 1 atm absolute. B and D: an open-circuit diver for whom the breathing regulator delivers gas at the hydrostatic pressure of the mouth. C: a closed-circuit rebreather diver, for whom the reservoir (counterlung) is at a lower hydrostatic pressure than the lung centroid (negative PTR). In the head-up position PTR is negative; in the head-down position PTR is positive, analogous to the clinical application, continuous positive airway pressure (CPAP). [Reproduced from Lundgren (60) with permission. Copyright Informa Healthcare Books.]

Although chest wall compliance does not change significantly, most investigators have reported a concomitant reduction in lung compliance, particularly at low lung volumes, possibly due to the vascular engorgement (16). Others have attributed the compliance change and attendant increase in elastic work solely to the difference in hydrostatic pressure between the lung and the mouth, which is neutralized by supplying breathing gas at a pressure close to lung centroid pressure (105, 106).

ERV during exercise in a dry hyperbaric chamber at depth tends to be increased as subjects breathe at higher lung volumes (37, 98, 117). Similarly, the reduction in ERV during immersion tends to be attenuated at increasing depth as subjects breathe at higher lung volumes, probably in an attempt to increase airway diameter, thus reducing the increase in airways resistance (37, 98, 106, 117). The increase in ERV has the effect of increasing internal respiratory load by raising the elastic lung load (14), which allows more passive expiration but results in a requirement for higher negative inspiratory pressures (76). The increased elastic load induced by immersion augments the gas density-related decrease in MVV (129).

Transrespiratory pressure (static lung load).

In an immersed diver, a static positive or negative pressure may be exerted across the respiratory system [PTR, or static lung load (SLL)] due to the difference between the pressure of the gas delivered to the mouth and the external hydrostatic pressure at the centroid of the lung (see Fig. 1). Positive or negative PTR alters the equilibrium volume, and measurements in humans have revealed increased or decreased ERV, respectively (107). During negative PTR, ERV is not determined simply by the relaxation volume of the thorax but is defended to some degree with active inspiratory muscle activity, thus causing additional inspiratory muscle work (106). PTR is a major determinant of exercise performance in divers. Positive PTR during immersed heavy exercise is associated with a reduction in dyspnea. Conversely, negative PTR is poorly tolerated by divers, as it seems to increase dyspnea (107). One possible mechanism for the ameliorative effect of positive PTR on dyspnea is the benefit of an increased lung volume (decreased airways resistance), which is offset by an increase in elastic work of breathing. PTR could exert its beneficial effect by reducing the inspiratory elastic work necessary to maintain lung volume at a level that would minimize airways resistance.


Inertance of the respiratory system and the breathing system is the property related to the mass of the chest wall and the gas flowing within the airways and breathing apparatus. There is also a small component due to the mass of the water surrounding the chest. Respiratory system inertance at 1 ATA, typically 0.01 cmH2O·l −1 ·s 2 , increases in direct proportion to gas density (67, 81). Inertial impedance tends to offset elastic impedance. In a cyclic breathing pattern inertial impedance is less than elastic impedance at frequencies less than resonant frequency of the system, which at 1 ATA is typically 6 Hz; inertial impedance exceeds elastic impedance at frequencies greater than the resonant frequency. If breathing gas density increases 10-fold, the resonant frequency decreases to ∼2 Hz. Thus, given the normally slower breathing frequency exhibited by exercising divers (36, 74, 91), inertial impedance has only a limited role in determining respiratory effort. In an exercising diver breathing a gas with density 10 g/l, assuming a peak acceleration of 30 l/s 2 , the transrespiratory pressure due to inertance would be ∼3 cmH2O. On the other hand, if the inertance of a breathing circuit is deliberately increased such that the resonant frequency is reduced to within the normal breathing range, elastic work and inertial work can offset each other and reduce peak-to-peak (inspiratory-to-expiratory) pressure. Using a tunable closed-circuit breathing apparatus, Fothergill et al. (28) demonstrated that divers took advantage of this by adjusting their respiratory rate to equal the resonant frequency of the system.

On the other hand, during experimental measurements of ventilation using traditional open-circuit techniques in dense gas environments, gas inertance can produce artifacts. At high flow rate the gas can continue to flow from the inspired source through the valve system to the expired collection bag following end expiration and end inspiration (39). Such “blowby” will result in an artifactual increase in measured ventilation. This can be a problem particularly at high ventilation rates.


The process by which inspired gas mixes with gas resident in the alveoli at end expiration is determined by several processes (23). Convective mixing occurs in large conducting airways in which there is turbulent flow. Taylor dispersion occurs during laminar flow in small tubes where there is a parabolic distribution of flow, with the flow rate at the center of the tube being greater than at the periphery. This velocity gradient generates a radial concentration gradient; radial diffusion along such a gradient facilitates mixing between inspired and resident gases. Diffusion occurs in distal gas exchange units. Mixing is further augmented by cardiogenic oscillations (97).

An increase in density of the breathing gas could affect all of the factors listed above. An increase in density should expand the distribution of turbulent flow to more distal airways, thus enhancing convective mixing and improving the efficiency of gas exchange. High gas density has been predicted to enhance cardiogenic mixing (97). On the other hand a high gas density would diminish the effect of Taylor dispersion (and worsen gas exchange) by concomitantly reducing the number of airways with laminar flow. Increased density reduces gas phase diffusivity (113).

Diffusion depends not only on diffusivity, but also on concentration gradients, time for diffusion, and the shape of the space in which the gas is contained (112). A relevant principle is acinar diffusional screening. This refers to oxygen diffusion along the acinar airway, where it is absorbed preferentially by the more proximal alveolar surfaces along the path. Oxygen molecules may not reach the more distal alveoli, which are therefore functionally “screened” (92). In effect this process reduces the available gas exchange area for diffusion of oxygen and carbon dioxide. The screening effect would be more evident at high gas density (120) and would furthermore affect carbon dioxide to a greater degree than oxygen (92).

An observation that appeared to demonstrate gas phase diffusion impairment was the behavior of goats inside a hyperbaric chamber in a helium-oxygen atmosphere at 39.7 ATA. After increasing the pressure to 49.8 ATA by adding helium (density increase from 7.44 to 10.74 g/l), the animals displayed behavioral disturbances and progressive paralysis (9). This quickly resolved when the ambient P o 2 was raised from 154 to 191 mmHg. This observation, which was attributed to diffusion-related hypoxia, provided a major rationale for maintaining a high P o 2 in operational and experimental deep-dive exposures. Since then, studies in humans have refuted this hypothesis by demonstrating adequate blood oxygenation at even higher densities (50, 91).

Ventilation with the highest conceivable fluid density was achieved in experiments performed by Kylstra and colleagues, who examined oxygen and carbon dioxide diffusion by ventilating the lungs with saline. Studies in anesthetized dogs ventilated with hyperoxygenated saline (inspired P o 2 3,300–3,640 mmHg) revealed that despite evidence for diffusion limitation of both oxygen and carbon dioxide exchange, adequate arterial P o 2 and P co 2 could be achieved (47). These animal experiments were followed up by a study in patients undergoing therapeutic lung lavage for alveolar proteinosis and a human volunteer, using a double-lumen endotracheal tube. Saline was cycled in and out of one lung while the contralateral lung was ventilated with oxygen (48). In these humans there was no evidence for incomplete diffusive equilibrium between alveoli and capillary blood. However, unlike the dog experiments the respiratory cycle time exceeded 30 s. The prolonged cycle time presumably permitted equilibrium to occur even in the face of extremely low diffusivity.

In summary, the effects of an increase in gas density are predicted to impair gas phase diffusion but augment convective mixing. Despite at least a theoretical understanding of these processes during static or quasi-static flow within conduits of simple geometry or in simple experimental models, with currently available technology it has been challenging to elucidate their respective contributions to pulmonary gas exchange (22, 77).


The distribution of ventilation is dependent on cyclic changes in externally applied pressure and regional mechanical properties. Despite the wide range in path length from large airways to gas exchange units within the lung, time constants of different lung units are close enough to one another such that under normal circumstances ventilation of different lung regions is acceptably uniform. Differences in time constants among lung regions would increase heterogeneity of ventilation. This could result from higher breathing gas density and increased turbulence in conducting airways, to a differing degree depending on diameter. In airways in which turbulent flow predominates, increased gas density would cause an increase in flow resistance to a degree dependent on the flow characteristics and airway geometry. Time constants would become more disperse and ventilation of different lung units more asynchronous. Breathing a gas of higher density must therefore result in an increased heterogeneity of ventilation. This is supported by the model of Pedley et al. (79) and the observation by Forkert et al. (26) that, compared with air, dynamic compliance is reduced by an increase in breathing gas density using SF6-O2.

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Gas distribution may also depend on other factors. It is usually assumed that pleural pressure swings are uniform over the entire lung; however, there is evidence to the contrary (23). During resting breathing, regional pressure changes are less in the upper than in the lower chest (17). Regional pressure variations may occur due to gravitational effects, the position of the heart relative to the lung, interactions between the lung and the abdominal contents or between the shapes of the lung and the chest wall, or selective contraction of muscles of ventilation (23, 131). An additional mechanism that may produce asynchrony of ventilation is therefore topical variability of distribution of pleural pressure swings within the thorax, which under increased respiratory load in a dense gas environment could become more exaggerated.

Although evidence against regional differences in ventilation is provided by a study using 133 Xe to image topographic ventilation during SF6-O2 breathing, that technique is limited to visualization of differences between large regions; it cannot detect ventilation changes in small compartments within a region.

Unless inequalities of ventilation are matched by regional changes in perfusion then gas exchange would become less efficient. Intriguingly, although little is known about the effects of dense gas breathing on blood flow distribution per se, several investigators have reported that breathing dense gas is associated with a decrease in the alveolar-arterial P o 2 difference (P a O2−PaO2) (10, 25, 33, 89, 127) (see Fig. 2). This suggests more efficient matching of ventilation and perfusion. However, under similar conditions dead space/tidal volume ratio (V d /V t ) is increased (66, 74, 89, 91, 127), an effect that appears independent of P o 2 over a range from 0.2 to 3 ATA.

Fig. 2.

Fig. 2.Top: effect of gas density (ρ) on dead space. V d /V t , dead space/tidal volume ratio. Data from Saltzman et al. (89), Wood et al. (127), Salzano et al. (91), McMahon et al. (66), and Mummery et al. (74). •, Human data; ○ is from a liquid-breathing experiment in dogs (47). Bottom: alveolar-arterial P o 2 difference (P a O2−PaO2) as a function of breathing gas density. Data from Saltzman et al. (▴; 89), Flynn et al. (⧫; 25), Wood et al. (•; 127), Gledhill et al. (▪; 33), and Christopherson and Hlastala (○; 10).

Reduced diffusivity adversely affects gas exchange of both molecules, while enhanced cardiogenic mixing would effect an improvement. Wood et al. (127) have speculated that increased breathing gas density reduces P a O2−PaO2 because it promotes intraregional convective mixing and hence reduced ventilation/perfusion (V̇ a /Q̇) dispersion, which affects V d /V t to a lesser degree than P a O2−PaO2. Wood et al. have proposed that the increase in V d /V t is predominantly due to impaired molecular diffusion of carbon dioxide. Although oxygen diffusion should be similarly affected, they speculated that this is insufficient to offset the convective mixing effect. While there is no straightforward explanation for these two contradictory observations, preliminary observations using the multiple inert gas technique lend support for impaired distribution of ventilation as the cause of the increased dead space (see Fig. 3).

Fig. 3.

Fig. 3.Ventilation/perfusion distribution using the multiple inert gas (MIG) elimination technique in a human volunteer during upright dry exercise at 1 ATA (top) and a pressure equivalent to 130 feet of sea water (fsw) (4.94 ATA, bottom), breathing 4.25% O2/balance (bal) N2 measured in a dry hyperbaric chamber. Minute ventilations were, respectively, 94 and 62 l/min. Bohr dead space was higher at depth (0.29 vs. 0.21 liter); dead space measured using the MIG technique (116) was 0.15 and 0.03 liter, respectively. The data are consistent with the higher Bohr dead space at pressure being due to increased dispersion of ventilation (log SD of the ventilation distribution 0.55 and 1.12 at 1 and 4.94 ATA, respectively).

Effects of immersion on ventilation and perfusion.

The engorgement of the pulmonary vessels and reduction in lung volume tend to be associated with several effects that could affect gas exchange. Several investigators have observed an increase in closing volume (CV) (5, 19, 83), consistent with some gas trapping. Also in support of gas trapping is the observation that during immersion residual volume by body plethysmography exceeds that measured by inert gas dilution (87). When CV exceeds ERV in upright immersion, there is an inversion of the normal cephalo-caudad distribution of blood flow, such that blood flow per gas exchange unit is higher at the apex than at the base of the lung (83). However, varied effects have been observed on pulmonary gas exchange. During immersion, one study indicated an increase in P a O2−PaO2 (13), while one other observed a transient decrease, and after a few minutes of immersion, a return to baseline (20). In the presence of mild pulmonary pathology, immersion may have an additional effect: loss of an observable phase IV of the single-breath inert gas washout curve, which is traditionally interpreted as signaling the onset of airway closure (54), which, in a group of mild asthmatic subjects, was interpreted by the investigators as evidence of airway closure throughout the entire vital capacity maneuver.

It has been hypothesized that if CV impinges on tidal volume (i.e., CV exceeds ERV), PaO2 should decrease. This was confirmed by Cohen et al. (13) and Prefaut et al. (84), but not by Derion et al. (20). In the latter study, shunt measured by multiple inert gas elimination was slightly increased in older subjects (ages 40–54 yr) but not in younger subjects (ages 20–29 yr). PaO2 did not decrease in the older subjects, possibly because of a large increase in V t , which could have reduced the fraction of V t within CV. However, when the observations from two studies were combined, there was a clear increase in P a O2−PaO2 as CV approached ERV + V t (see Fig. 4).

Fig. 4.

Fig. 4.Effect of closing volume (CV) on oxygen exchange as assessed by alveolar-arterial gradient. ERV, expiratory reserve volume. Data are from Derion et al. (20) and Prefaut et al. (84). [Redrawn from Derion and Guy (19), copyright 1994, with permission from Elsevier.]

Pulmonary-blood transfer of oxygen.

Altered affinity of hemoglobin for oxygen has been observed at high pressures. Increased hemoglobin-oxygen affinity has been observed in studies in vitro (32, 43, 44, 86) and in a human in vivo study during a saturation dive to 69 ATA (101) (Fig. 5). During the latter study, erythrocyte 2,3-DPG levels were slightly decreased from control (mean ± SD, control: 15.9 ± 3.5; hyperbaric exposure: 13.7 ± 2.6 μmol/g Hb); however, the change was insufficient to explain the decrease in the P o 2 at 50% hemoglobin saturation (P50) (100). These small changes in P50 appear to be due to conformational changes in hemoglobin induced by high pressure and, to a small extent with gases actually breathed by divers, binding by inert gas. It is unlikely that these small changes in hemoglobin P50 have any significant effect on pulmonary gas exchange or exercise capacity (115).

Fig. 5.

Fig. 5.Hemoglobin-oxygen (Hb-O2) dissociation curve measured at pressure during a saturation dive (mean ± SD of all measurements in 3 divers over the pressure range indicated). Control curve was obtained at 1 ATA; P < 0.05. [Redrawn from Stolp et al. (101), copyright 1984, with permission from Undersea and Hyperbaric Medical Society.]


Hypercapnic ventilatory response (HVR) varies among individuals and has been proposed as a predictor of P co 2 during underwater exercise. In one case study (71), a diver with an extremely low HVR was studied during exercise at 4 atmospheres absolute (ATA) and demonstrated hypoventilation and hypercapnia to an extent far greater than that seen in most normal volunteers. Other studies have indeed shown a correlation between low HVR and hypercapnia in exercise studies at the surface and at depth (52, 70). Overall, however, HVR is a poor predictor of P co 2 at depth (8, 62). In a study of military divers, only 60% of subjects with hypercapnia at depth also had a low HVR (52).

This poor predictive value may be due to intrasubject HVR variability on different days (88) and in different conditions. It can also be affected by respiratory muscle training, which tends to decrease the HVR of both low and high responders toward the mean (80): muscle training attenuates the HVR of individuals with high values and increases it in low responders. HVR tends to be decreased in scuba divers (24, 71, 93) although not all studies have confirmed this (29). Kerem et al. (42) observed higher end-tidal P co 2 (P et CO2) in divers compared with nondivers during exercise at 1 ATA, but there was no difference between the diver and control groups when breathing 40% O2 and 60% N2 at 4 ATA (42). Unfortunately, it is difficult to compare surface vs. depth P co 2 during exercise using end-tidal measurements, since P et CO2 overestimates PaCO2 at the surface (56, 74) but more accurately reflects PaCO2 under hyperbaric conditions (74).

Effect of hyperoxia.

Respiratory drive could be affected by a high partial pressure of oxygen, which for a fixed O2 fraction increases linearly with depth. Hyperoxia therefore occurs in divers even when diving with a breathing gas that is normoxic at the surface. Still higher P o 2 is produced by enriched oxygen breathing gas mixtures that are intentionally used in an effort to reduce inert gas load. Hyperoxia attenuates the ventilatory response to hypercapnia (15, 30, 69, 78) and has been noted to decrease ventilation during exercise (1, 21, 38, 51, 68, 82, 124). Mild hypercapnia (PaCO2 = 44 mmHg) has been observed during heavy exercise while breathing 100% O2 at 2 ATA (11). Few hyperbaric studies exist in which exercise was tested as a function of P o 2 at constant breathing gas density. One such study demonstrated attenuation of the ventilatory response to heavy bicycle exercise in the dry at 2 ATA (103). Arterial blood samples were obtained 7–9 min following completion of 5 min of exercise up to 1,800 Kp·m·min −1 , and demonstrated slightly higher pH and lower base deficits in hyperoxia. Therefore it was not possible to confirm a direct effect of hyperoxia on respiratory drive. Another study failed to find an effect of P o 2 on arterial P co 2 between 0.7 and 1.3 ATA during immersed prone exercise at 4.7 ATA (8). Factors besides respiratory drive attenuation that may contribute to the reduction in exercise ventilation include peripheral chemoreceptor inhibition and attenuation of the acidemia that occurs during heavy exercise (51).

Paradoxically, in some studies, after a few minutes of hyperoxia at 1 ATA, hyperventilation has been observed (18). A possible explanation has been proposed, based on observations of increased firing rates of solitary complex neurons in brain slices exposed to hyperbaric hyperoxia (73). However, despite increased ventilation and reduced P et CO2, PaCO2 in human hyperoxia studies is generally normal (27, 35). The observations in brain slices (73), in which tissue P o 2 is higher than could occur in human divers, may reflect toxic effects of oxygen.

Effect of narcosis.

It has been suggested that when breathing nitrogen-oxygen mixtures, nitrogen narcosis could also contribute to hypercapnia during diving. While HVR is attenuated at increased ambient pressure, studies using nonnarcotic gases support increased gas density vs. nitrogen narcosis as the mechanism (8, 31, 61).

Effect of mechanical load and ventilation.

A major contributor to hypoventilation and increased PaCO2 seen in diving is increased work of breathing as discussed above. Investigators have traditionally argued that in the setting of increased respiratory load, ventilatory effort (and hence the alveolar ventilation) represents a compromise between the drive to maintain normocapnia and the greater work of breathing that would be required to achieve it (63). Several studies have supported a major effect of increased gas density on exercise ventilation. A human study by Linnarsson et al. (55) in a dry hyperbaric chamber measured exercise ventilation while breathing four different gases (air and SF6-O2 at 1–1.3 ATA; He-O2, and N2-O2 at 5.5 ATA). These combinations created two different gas densities (1.1 and 6.0 g/l) at each ambient pressure. P o 2 was 0.2 ATA under all conditions. There was a significant density-related decrease in exercise ventilation (Fig. 6). In explaining the hypoventilation during exercise in divers, this experiment excluded ambient pressure and supported the major role of increased gas density, although a narcosis effect could not be excluded. A recent study demonstrated that external resistive load increased PaCO2 during prone immersed exercise at 4.7 ATA (8).

Fig. 6.

Fig. 6.Differences in exercise ventilation (ΔV̇ i ) between 1-bar air (control) and 3 gas + pressure conditions with normal (5.5-bar He-O2) or 5.5 times increased gas density (1.3-bar SF6-O2, 5.5-bar N2-O2). Values are means ± SE. Effect of gas density on ventilatory response to exercise. Air at 1 ATA and heliox at 5.5 have density 1.1 g/l; SF6-O2 at 1.3 ATA and N2-O2 at 5.5 ATA have density 6 g/l. All gas mixtures were normoxic (P o 2 = 0.2 ATA). [Reproduced from Linnarsson et al. (55).]

During the transition from rest to exercise at the surface, carbon dioxide levels can increase by a small but significant amount in normal subjects (12). It is thought that this effect is due to a low ventilatory response to low levels of exercise. With submersion, this effect is slightly more pronounced (107) and is generally explained by the increased work of breathing during immersion, as discussed above. Submersion causes reduced lung compliance due to a redistribution of blood into the thorax and engorgement of the pulmonary capillaries (16, 72), which can be augmented by a negative PTR.

Work of breathing is also elevated with the addition of negative (72) or positive (14) PTR. The increased work of breathing with negative PTR can be attributed to an increase in internal respiratory resistance due to compression of the extrathoracic airways (2). Positive PTR causes subjects to have a higher expiratory reserve volume and increased elastic recoil of the lungs (14). However, several studies have shown that the increased work of breathing caused by changes in PTR between +10 and −20 cmH2O during exercise can cause dyspnea but does not translate into higher P et CO2 (40, 75, 107), although in these studies it is possible that PaCO2 was underestimated by P et CO2. It is also possible that positive PTR could increase dead space by increasing the caliber of the large airways, and thus increase PaCO2, although there is not yet any evidence to support this hypothesis.

All but a few studies examining contributors to hypercapnia at depth (8, 51, 74, 89–91) have used P et CO2 as an estimate of PaCO2, which under resting conditions is a good approximation. During exercise the approximation is not as good: P et CO2 is higher than PaCO2 during exercise at 1 ATA (56) and lower in conditions under which there is increased dead space, as may be the case with diving. Only one study has directly correlated the two in diving, in the dry at 2.8 ATA (74), demonstrating a reasonable correlation.


Theoretically, there could also be some effect of extremely high pressure on the control of breathing. A study in subjects at rest (89) found that while increased pressure caused PaCO2 to rise, gas density had only a small effect. However, that study investigated only resting conditions. Studies of hyperbaric exercise have tended to exclude pressure having any significant influence on ventilation (55).


Impaired gas exchange after saturation dives.

During saturation dives, divers remain in a hyperbaric environment for many days or weeks. Physical activity is limited, thus engendering loss of cardiorespiratory fitness, and the ambient P o 2 is higher than normal (typically 0.4–0.5 ATA), thus exposing the divers to oxygen tensions that could be mildly toxic to the lung. Additionally, venous gas embolism may occur during decompression, which can last several days. Observations by Thorsen et al. suggest that saturation dives may have persistent cardiorespiratory effects on divers. After deep saturation dives to 37 ATA, maximal V̇ o 2 (V̇ o 2max) and carbon monoxide transfer factor are reduced and respiratory dead space is increased (108). While the reduction in V̇ o 2max may in part reflect deconditioning due to many days of reduced aerobic exercise in the confined environment of a diving chamber, other explanations were proposed for the gas exchange impairment. The first was a cumulative effect of venous gas embolism on the lung. In support of this hypothesis was the observation that the fractional reduction in V̇ o 2max after the dive correlated with the cumulative venous bubble score as detected by ultrasound (108). The second proposed explanation was mild pulmonary oxygen toxicity, due to an inspired P o 2 of 0.4–0.5 ATA during the 18–28 days in which the divers were continuously under pressure. This second hypothesis is supported by a study in which volunteers were exposed in a hyperbaric chamber to a lower pressure (2.5 ATA) but with duration and inspired P o 2 similar to the deep dives, but with no detectable venous gas emboli. After this exposure there was a similar reduction in V̇ o 2max and carbon monoxide transfer factor. A control dive of similar duration but at a lower pressure (1.5 ATA) and P o 2 (0.2 ATA) produced no effect on carbon monoxide transfer factor (110). Logistic regression analysis of possible risk factors after a series of saturation dives implicated both hyperoxia and venous gas embolism as factors contributing to impairment in pulmonary gas exchange (109). These data suggest that hyperoxia, albeit at levels traditionally considered nontoxic, is a major contributor to pulmonary gas impairment after long saturation dives.

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Immersion pulmonary edema.

Immersion pulmonary edema (IPE) is a condition in which cough, hemoptysis, dyspnea, and hypoxemia develop after surface swimming or diving, often in young, healthy individuals (34, 45, 57, 64, 96, 123), including exceptionally fit military divers (59, 64, 95, 121). It occurs predominantly in males. The condition usually resolves spontaneously or with β2-adrenergic agonist or diuretic therapy, but it can be fatal (96). Risk factors may include cold water (45, 123), exertion (34, 94, 95, 121), fluid loading (121), negative PTR (111) or low vital capacity (95). The cause is unknown, although hydrostatic pulmonary edema is a strong possibility. Pulmonary artery wedge pressure in IPE at the time of evaluation has been reported as normal (34), although thus far there have been no measurements in IPE during the acute event. Post-event echocardiography is usually normal (34, 45, 57, 96). Bronchoalveolar lavage studies have revealed no evidence of inflammation. Capillary stress failure due to high pulmonary capillary flow/pressure has been implicated (45, 58). Proposed mechanisms involve the additive effects of immersion-induced increase in pulmonary blood volume and pulmonary artery hypertension due to exertion, and cold water (46).


Despite the diving-related increase in resistance to bulk flow and impairment of gas phase diffusion, it is surprising that the human lung is at all capable of supporting oxygenation and carbon dioxide elimination at gas densities severalfold higher than normal. Nevertheless, there remain several open questions. Ventilation/perfusion relationships during dense gas breathing have not yet been elucidated. Recent studies at 1 ATA suggest that the normal exercise-induced rise in cardiac output can be attenuated by external breathing resistance (3). However, studies to examine the effect on cardiac output of increased pulmonary resistive load are lacking. Although both physiological and safety-related measurements rely mostly on the analysis of end-tidal gas, only one study has been published comparing P et CO2 and arterial P co 2 during exercise, breathing air at 2.8 ATA (density 3.2 g/l) (74). There have been no reported studies at higher densities or P o 2. The effect of P o 2 on regulation of ventilation and arterial P co 2 has been incompletely studied during exercise, with the controls in most studies consisting of exercise runs at a different density (1 ATA), thus precluding the elimination of gas density as a confounder. Finally, indirect evidence of metabolic acidosis and respiratory muscle fatigue during endurance exercise pose questions related to the effects on cardiovascular performance and gas exchange. Intriguing recent evidence that respiratory muscle training may affect ventilatory control and endurance in divers needs further study.


This study was supported by US Navy NAVSEA contract no. N61331-03-C-0015.

The Effects Of Diving On The Circulatory System

Diving, especially deep sea diving, can have a number of effects on the circulatory system. The most obvious is the increased pressure on the body, which can lead to a condition called decompression sickness. This condition is caused by a sudden decrease in pressure, which can cause bubbles to form in the blood and tissues. These bubbles can block blood vessels and cause pain, paralysis, and even death. Another effect of diving on the circulatory system is the cold. Water conducts heat away from the body 25 times faster than air, so even in a warm ocean, divers can get cold very quickly. This can cause the blood vessels to constrict, which can lead to an increased heart rate and blood pressure. In extreme cases, this can lead to a heart attack. Divers also need to be careful of their breathing. When diving, the body is constantly using oxygen, but at the same time, it is getting rid of carbon dioxide. If a diver breathes too fast, they can get rid of too much carbon dioxide and become dizzy or lightheaded. This is because the blood vessels in the body are constantly expanding and contracting, and if there is not enough carbon dioxide in the blood, they will not be able to contract properly. Overall, diving can have a number of effects on the circulatory system, both good and bad. It is important for divers to be aware of these potential dangers and take precautions to avoid them.

PADI Pros Explain How Diving Can Affect Your Health and Circulatory System. The Divers Alert Network Medical Team’s website can be found at In scuba diving, you can experience many different types of effects, including immersion, cold, and Hyperbaric gases, as well as elevated breathing pressure and exercise. Recreational divers have the option of choosing a diving environment that is relatively easy to maintain without requiring much physical activity. When you breathe more oxygen, your body vasoconstricts, your blood pressure rises, and your heart rate and output fall. Furthermore, when you exercise while scuba diving, your body may produce more carbon dioxide. Diving, like swimming, has an effect on the autonomic nervous system, which regulates internal functions like heart rate and respiratory rate. A healthy person’s parasympathetic reactions improve, preserving their heart rate. However, as a result of diving under stressful conditions, the ANS moves in the opposite direction, resulting in sympathetic responses.

How Does Deep Diving Affect The Body?

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In descending, you experience an increase in water pressure as you descend, and a decrease in air volume as you go down. A ruptured eardrum, as well as sinus pain, can result from this. Your lungs’ air pressure rises as you ascend, and your water pressure falls. It can cause the air sacs in your lungs to rupture, making breathing difficult.

A recreational dive is not physically difficult as long as you stay within the depth and time limits set by dive schools. Commercial and deep sea diving, according to research, may be hazardous to the lungs and small airways for a long time. If we don’t do it right, we could be killed. We now have three ATMs on our bodies because seawater exerts the same pressure as one ATM every ten meters, implying that we have fewer ATMs on our bodies. Because of the extra pressure, our bodies are pushed to the tissues, where the gas Nitrogen (N2) is produced. For several decades, the safety record for scuba diving around the world has been excellent. When it comes to scuba diving, the instructor sets the diving limits, and if you adhere to those limits, you are extremely safe.

A reckless dive can be fatal, but we usually experience a variety of health issues, one of which is Decompression Sickness (DCS). It has been found that commercial divers are more likely to develop pulmonary problems. You have no long-term concerns when it comes to scuba diving. Over time, your ears may become infected with bacteria; however, this usually goes hand in hand with ear issues. As much as you might believe, diving almost never hurts or makes you feel physically ill.

Divers who specialize in commercial diving are exposed to a wide range of gas pressures ranging from the atmosphere at the surface to the pressure inside a pressure vessel. Divers may also be submerged for extended periods of time in cold water, putting them at risk of hypothermia. Divers who ascend quickly from a deep dive and descend slowly to the surface face the greatest risk of decompression sickness (the bends). In the case of bends, nitrogen bubbles form in the body as a result of the change in pressure from the surface to the bottom. Today’s scuba diving equipment is more reliable than it was in the past. The devices were not sturdy enough to withstand the rigors of daily use and could be easily damaged. As a result, modern scuba diving equipment has been much more reliable and has improved over time. This has been accomplished through the knowledge that manufacturers have acquired over time.

The Risks Of Deep Diving

Divers can have a lot of fun while staying within their dive school’s time and depth limits as long as they stay within those parameters. However, there is evidence that commercial and very deep diving, while safe for short periods of time, can have long-term negative effects on the lungs and small airways. Barotrauma is a condition that can occur when the gas inside the lungs expands and causes pain in surrounding tissue during deep diving. These long-term effects can have an impact on the lungs over time. Furthermore, during deep diving, the muscle cramps can be fatal if not treated immediately. As a result, while diving is not harmful to your health in and of itself, you should be aware of potential long-term health risks and strictly adhere to safe diving practices.

How Does Being Underwater Affect The Cardiovascular System?


Water immersion causes immediate blood transfer to the heart, as well as slower fluid autotransfusion from the cells to the vascular compartment, which affects the cardio-endocrine-renal axis. As a result of these changes, stroke volume and cardiac output increase.

Heart rate variability (HRV) is the study of longitudinal variations in heart rate, and it is a non-invasive method for studying the effect of neural mechanisms elicited by the autonomic nervous system on intrinsic heart rate. The sympathetic and parasympathetic nervous systems respond to immersion in pool conditions in very similar ways. If the physiological HRV of a person is intended to aid in adaptation and flexibility, diving should be avoided in healthy humans. HRVs are the results of neural control systems activated by the autonomic nervous system via a series of changes in heart rate. Chronic diseases such as heart and non-cardiac disorders are characterized by a loss of complex variability and an increase in periodic behavior. The HRV would be increased by simultaneously activate activating both sympathetic and parasympathetic processes during scuba diving. A total of 25 scuba divers (20 men, five women) were measured during the study.

Members of the German Underwater Club were present at all of these events. Electrodes were implanted in order to prevent bone motion artefacts. ECGs can be recorded with a two channel Holter monitor (Tracker; Reynolds Medical) and a waterproof pocket (TMT; ewa-marine). To record your heart rate, you’ll need an ECG analyser (Reynolds Medical) and the appropriate software (RR Tools). QRS signals were typically stored during the ECG analysis and were later used to separate regular beats from abnormal beats during subsequent analyses. The correlation between two consecutive RR intervals was calculated to eliminate supraventricular extra beats and pauses. As an index of the sympathetic-parasympathetic balance, the ratio (R) between LF and HF can be used.

Because it is regarded as a dubious measurement in short-term recordings, we did not consider the very low frequency component in our study. The amount of oxygen available in a diving pool was significantly lower than it was during immersion or submersion. As a result of immersion and submerging in low frequency (LF), the spectral density increased slightly; however, diving increased the density significantly. In response to low respiration rates, the respiratory sinus arrhythmia (RSA) shifted one portion from the HF to the LF range. The last three values were not significantly different under control conditions in the high frequency (HF) range. Diver experience has had the greatest impact on parasympathetic activity in diving. Diving can help to keep the water temperature (27 degrees Celsius) within the limits.

The sympathetic system is likely to be stimulated more during scuba diving at temperatures lower than in the pool. For short-term analyses, some HRV measures have been found to be unreliable. It is equivalent to performing a blood transfusion on the systemic and pulmonary circuits if water is immersed in them. The use of bath salts appears to have no negative effects on patients suffering from heart disease, but bathing may cause pulmonary oedema and acute heart failure in those suffering from cardiac insufficiency. When water’s HRV level rises, it acts as a protective factor against sudden cardiac death following myocardial infarction due to parasympathetic activation. As a result of our findings, we believe that the diving reflex does not directly induce face immersion in humans. Hypothalic pressure on the submerged chest may explain the slight increase in heart rate.

Slow deep breathing, regardless of temperature at the surface (28C during rest), has no effect on heart rate. The heart rate, as opposed to HRV, is more sensitive to the tone of the nervous system. The RSA fell predominantly in the LF range (0.12 Hz) during scuba diving, imitating increased sympathetic activity. Furthermore, because the heart rate did not decrease in response to the decrease in sympathetic system, there is little chance of dominance. It describes the variability of the heart rate during a period of continuous change and is used to investigate the modulation of the intrinsic heart rate via noninvasive measurement. Underwater swimming is thought to promote sympathetic and parasympathetic nervous system development, as well as induce a sense of well-being in both groups of people. The HRV is not an accurate way to determine whether or not a person is suited for scuba diving. This article is available for free download in the British Journal of Sports Medicine, 35 180-180 (first accessed on Jun.01) or for subscribers to read the entire article.

Scuba Diving Safety: How To Avoid Ear And Mask Injuries

Diver’s bodies’ air spaces are compressed as a result of an increase in pressure caused by descending, which causes the air to compress. The pressure inside the diver’s ear, mask, and lungs can be so great that they become like vacuums, which can cause pain and injury to the diver.

What Happens To Blood When Diving?

The blood in our bodies is constantly in motion, circulated by the heart. When we dive, the water pressure around us increases. This increase in pressure forces the blood in our bodies to move more slowly and the blood vessels to constrict. This is why we often feel cold when diving, as the blood is not moving as quickly to circulate warmth.

Sinus barotrauma, a condition that causes severe health problems, should be taken into consideration by divers. When the lining of the nose is ruptured during sinusitis, blood vessels in the lining burst, causing significant damage to the mucous membranes and even death. A fever, facial pain, intense pressure in the head or neck, difficulty breathing, or redness or swelling in the nose are all symptoms that should be investigated by a doctor. Avoid diving in areas with a high level of nitrogen if you are wearing a face mask and avoiding high-pressure dives.

Sinus Barotrauma: The Nose Knows

Sinus barotrauma is caused by small drips of blood from the nose (technically not from a nosebleed), as well as from the nose to the throat.

How Does Deep Sea Diving Affect The Respiratory System?

According to the law of gravitational attraction, as the depth or ambient pressure increases, the amount of air in the lungs decreases. As a result, the pressure and density of the gases within the lungs will rise.

Dangers Of Decompression Sickness

Decompression sickness, also known as “the bends,” can be serious if left untreated. The body’s tissues are subjected to a sudden, uncontrolled pressure decrease that causes them to contract involuntarily. The three most common symptoms are headache, nausea, and vomiting. Degenerative diseases, such as pulmonary edema (fluid in the lungs), can result from the failure to treat them properly.

Scuba Diving Effects On Body

When scuba diving, a person is exposed to changes in water pressure and temperature, which can have an effect on the body. The most common effects are barotrauma (injury from changes in pressure), hypothermia (decreased body temperature), and dehydration.

Diver safety is jeopardized when scuba diving. Diver training and instructions can help to reduce the risks that new divers face. Increased underwater physical activity can cause exhaustion, lack of hydration, and muscle cramps in the stomach and skeletal system. If you want to avoid hypothermia, you should wear warm clothing such as a warm coat, wet suit, or dry suit. Divers must return to the surface on numerous occasions to be thoroughly checked. Diver panic can occur as a result of an emergency situation, such as an out-of-flight situation or other unforeseen circumstance. The harm that is done by pressing the air pocket in the center of the ear results in a bruotrauma.

DCS is likely to be the most well-known diving-related injury. A blood vessel embolism is defined as a blockage in a conduit. It may occur to a scuba diver if air pockets in his lungs collapse. Nitrogen narcosis occurs when divers experience inebriation or energy at a deeper level. It is not uncommon for deep-sea divers to experience oxygen toxicity when they reach 135 feet below sea level. Corals, such as those found in the undersea, should never be touched or spoken to by divers. A faulty regulator can result in drowning or decompression sickness, whereas a faulty depth check can result in a gentle experience of decompression sickness.

Most dive activities teach beginners how to dive using an educational program created by an agency that is certified by the diving industry’s governing body. Four or five dives, plus swimming, are required to complete the PADI course. If you live in a mild climate, you may need to consider training with a diving instructor who will refer you to certified dives.

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Recreational diving at depths of less than 130 meters (420 feet) has been shown to be safe in good scientific research. Deep diving above the recreational limit, on the other hand, has been shown to have long-term effects on lungs. As a result, the development of small airways disease and the loss of lung function can occur. These effects, in particular, can be extremely damaging for commercial deep divers, who may lose their jobs and career opportunities. If you intend to dive to a depth beyond the recreational limit, it is critical to be aware of the risks. Before diving, you should consult with a dive school to ensure you are making the right decision. If you do have any issues, you should contact the company as soon as possible.

Deep Sea Pressure Effects On Humans

At depths of around 1,000 feet below the surface of the ocean, the pressure is about 2,000 pounds per square inch. This is about 200 times the atmospheric pressure at sea level. The human body is not designed to withstand such high pressures. At these depths, the body starts to experience the effects of pressure. The blood vessels and air spaces in the body start to collapse. This can cause serious problems, including paralysis and death.

One of only a few places on the planet where ocean floor spreading centers have deep sea vents, and the Juan de Fuca Ridge is one of them. The ALVIN has not visited the vents in some time, but it will do so for the first time this year. To be collected, it will take samples from living and non-living things, including bacteria, fish, and rocks that have been specially adapted for this purpose. Each square centimeter of space contains 1.033 kilograms of pressure inside your lungs, which is the same pressure as in the air around you. In this case, the pressure rises by one atmosphere every 10 meters below the surface. ALVIN has been specially designed to maintain the same pressure as we are at the surface. Humans have been able to go down 4,000 meters in the depths with the ALVIN sub. During testing, the sub’s spherical, titanium-doped steel body was subjected to extreme pressure at the sea’s bottom. Over the years, scientists have discovered a lost hydrogen bomb, found the Titanic, and explored hydrothermal vents.

The Dangers Of Diving To The Bottom Of The Ocean

There isn’t much air at the bottom of the ocean, and there isn’t even an air supply. If a person cannot breathe, they will die as soon as possible. Furthermore, the pressure at the bottom of the ocean is extremely high, making it extremely dangerous to swim in.

How Does Being Underwater Affect The Muscular System

The muscular system is responsible for the movement of the human body. Underwater, the body is more buoyant and requires less effort to move. The extra resistance of the water also provides a good workout for the muscles.

Underwater undulatory swimming, also known as dolphin kick or submerged propulsion, is a technique used in competitive swimming that focuses on underwater undulatory swimming. Swimming techniques (butterfly, backstroke, breaststroke, and front crawl) that improve UUS performance are likely to increase the time spent swimming during races. UUS research sought to determine how muscular coordination is maintained in the trunk and lower limb during elite swimming practice. We hypothesised that the upward and downward kicks would be derived from two synergy sources. Experiments were carried out in a 50-metre indoor pool at our university. The muscles measured on each swimmer’s right side were rectus abdominis (RA), internal abdominal muscle (IO), rectus femoris (RF), erector spinae (ES), multifidus (MF), tibialis anterior (TA), thigh biceps (TB), and bicep Surface electrodes attached to the muscles were parallel to the fibers. The maximum voluntary contraction (MVC) test was performed on each muscle prior to the measurement in water.

Yamakawa et al. ( 2016) have published an experimental protocol in the journal. To swim at maximum effort, the swimmers performed a 15-meter prone UUS. The electrodes were waterproofed with water-resistant tape. During MVC tests, the normalized Electrocardiogram data was normalized as a percentage of the highest RMS amplitude obtained. During this study, a kick cycle began at the highest toe vertical coordinate and ended at the next highest peak. Each kick cycle had its own kick phase, consisting of a downward kick and an upward kick.

The kick frequency and amplitude were determined by using the toe coordinates. The inclination of the pelvic region is defined as the angle between the line connecting ASIS and PSIS and the horizontal line. Modules were extracted from the linear envelope using a Hibert filter with a length of 10, as well as NMF. The first matrix consisted of normalized EMG data for each of the eight muscles and a three-cycle interval for each of them. We were able to iterate the analysis by varying the number of synergy in each subject from 1 to 8. Formulas 3 and 4 were used to calculate global and local VAFs. Table 1 contains kinematic variables in the United States.

The maximum tilt on pelvic backwards was 94.4 4.5 on the UUS cycle, which is 22%. Synergy 1’s activation coefficient peaked at 0–10%, 88–100%, and 99%, depending on the model. During this stage, the upward kick is replaced by the downward kick. When two synergies were applied, the swimmers did not reach the established thresholds (global VAF, 90 and local VAF, 75). Electromyographic data of each muscle in the United States is depicted in figures 3 and 4 as well as those of all subjects. Synergy 1 played a role in tilting the pelvis from an upward kick to a downward kick, with the assistance of the RA, IO, and RF. Figure 3 depicts the active phases of the BF, GS, and gastrocnemius as well as the ES,MF, and TA in the organism.

The Universal Strike (UUS) is a combination of upward and downward kicks that occurs on a regular basis. We discovered three common US swimming synergies among all swimmers. The IO and RA, in addition to tilt the pelvic region, played a role in this process. RF causes knee extension and hip flexion during trunk flexion, whereas RA and IO cause knee extension and hip flexion during hip extension. As the knee joint is extended in the downward direction, the hip joint is flexed. During this study, the pelvis tilts from forward to backward. The ES and MMF were thought to be activated in order to correct the pelvic position.

Synergy 2’s activation coefficient peaked 29% of the cycle during the UUS cycle. There are numerous limitations to this study. Because the angle of the pelvic surface is calculated based on global coordinates, the neutral pelvic surface cannot be distinguished. Because the UUS employs little rotational motion, an analysis of the sagittal plane is probably sufficient. A follow-up study comparing the current study with a group of swimmers who are new to swimming may provide a deeper understanding of this coordination strategy. During elite swimming in the United States, the upward kick and downward kick followed trunk muscles involved in the pelvic forward–backward tilt movement as well as the lower limb muscles. It was determined that no commercial or financial relationships existed during the research, which should alleviate any potential conflicts of interest.

According to a study published in the journal J. Sports Exerc, the key kinematic determinants of undulatory underwater swimming at maximal velocity are identified. Sci. A total of 42 papers were published, with a total of 77 papers being published. Electromagnetism. The 31st and the 14th of November, 2014, will be held. ( available from: Martens, J., Figueiredo, P., Staes, F., Fernandes, R., and Daly, D. (2016b) In front crawl swimming, surfaces electromyography are recorded in accordance with the pattern recognition of individual variability. Okubo et al. (

2010b) describe how to obtain and use a novel enzyme (Shiina, I., Tatsumura, M., and Izumi). Electromyographic analysis of the deep trunk muscles of the patient is performed after an exercise for the stabilization of the lower back. There are three hypotheses: 1) that the study is influenced by the context, 2) that it is influenced by the participants, or 3) that it is influenced by the researchers. Muscle fibre orientation of abdominal muscles and suggested surface electrode locations for eGMB. A systematic review of the evidence base for muscle synergy outcomes in clinics, robotics, and sports. Taborri, J., Agostini, V., Artemiadis, K., Ghislieri, M., Jacobs, D. A., and Roh, J. Biomech. It was published on 2018.49.

The Respiratory System And Deep Sea Diving

How does deep sea diving affect the respiratory system of a person who is not a diver?
It is impossible to breathe while submerged. To keep the tank in good working order, you must also perform the gas exchange. During the gas exchange process, air is taken in, carbon dioxide is exhaled, and water is exhaled. Swimming at deep sea can also be hazardous to your respiratory system because it requires a great deal of effort and muscle work.

Individual Diving Exposure

Divers are exposed to many risks while diving, but the most common and significant risks are those associated with the individual diver. These include drowning, entrapment, decompression sickness, and nitrogen narcosis.

Divers At Risk For Narcosis

Divers must wear an exposure suit at depths ranging from 100 meters to 330 meters (330 feet). This type of suit is made of heavy, watertight materials and completely covers the body. This is made of neoprene and is very similar to a typical wetsuit. Because of the risk of narcosis, the exposure suit must be worn at depths of 100 m or less. Breathing air at an ambient pressure of around 10 bar (1,000 kPa) is hazardous to divers at depths of 90 meters (300 feet).

Diving Conditions

Diving conditions can vary depending on the location. Some locations may have clear waters with little to no waves, while others may have murky waters with strong currents. It is important to check the conditions of the area before diving, so that you can be prepared for what you may encounter.

Divers from all over the world enjoy diving in this unique and fascinating environment. The kelp forests that dot the coastline of San Diego provide a variety of marine life with habitat. A shipwreck or artificial reef can be found offshore. These are some of the issues that scuba divers face when diving. Every year, over a hundred scuba divers drown in San Diego County.

Decompression Sickness

Compression sickness occurs when nitrogen dissolved in the blood and tissues under high pressure bubbles when the pressure falls. Muscles and joints can become fatigued and hurt as a result of the disease.

When nitrogen is dissolved in the blood and tissues at high pressure, it forms bubbles during compression sickness. A variety of symptoms can occur, including fatigue and pain in the joints and muscles. In the more severe cases, symptoms such as numbness, tingling, arm or leg weakness, unsteadiness, dizziness (spinning), difficulty breathing, and chest pain may resemble strokes. If you get decompression sickness, you can develop itching, skin mottling, rash, swelling of the arm, chest, or abdomen, and extreme fatigue. A sharp pain may appear, or it may be described as a deep or boring pain. The presence of brain involvement is similar to the presence of air embolism. There are neurological symptoms, such as numbness, paralysis, and death, in addition to numbness.

osteoarthritis is one of the most common causes of chronic pain and disability as a result of osteonecrosis. Divers who dive deeper than those who do not face this risk may be at a greater risk of death. Divers attempt to avoid forming gas bubbles in order to avoid decompression sickness. abnormalities in the brain or spinal cord can be detected with computed tomography or magnetic resonance imaging. Several divers use a few minutes to make a safety stop at a depth of 15 feet (4.5 meters). There are a small number of cases of decompression sickness that occur after no-stop dives. The most important thing you can do is to breathe 100% oxygen into a close-fitting face mask. After diving, compression therapy has the potential to improve your recovery time by up to 48 hours.

Divers: Be On The Lookout For Dcs

It is a medical emergency that necessitates immediate medical attention in order to avoid further injury. If you experience any of the following symptoms after diving, you should seek medical attention immediately: extreme fatigue, dizziness, nausea, vomiting, shortness of breath, or lightheadedness.

How is Scuba diving beneficial to your physical and psychological health?

What’s more enjoyable and more sensational than a small underwater trip in one of the best diving spots in the world in order to get away from the stress and the day to day problems? Equipped with your snorkel and diving mask, you are ready to explore a world rich in breathtaking and varied natural scenery on one of the most fascinating dive sites. Between large fishes and small nudibranchs, great corals and large caves, you are now in the heart of the underwater world. It is an exceptional adventure that everyone should experience at least once in your life.

At first, just think of going for a dive deeper underwater, on the seabed, in order to swim alongside large marine mammals such as whales, dolphins and maybe, even sharks, and you have chills. It’s normal! But with a little courage and determination, you will succeed and you will not regret to embark on this adventure, full of benefits for physical and psychological health.

Physical activity against cardiovascular and pulmonary diseases

Like any endurance sport, scuba diving helps develop and strengthen the cardio-respiratory system. It reduces blood pressure and heart rate. The regular practice of this exciting activity will benefit the optimization of the power and efficiency of the heart. While you dive on a great diving site, blood circulation in the heart is enhanced by a specific breathing technique and an endurance activity of medium intensity.

Water itself stimulates blood circulation and pumping. This practice therefore reduces the risk of cardiovascular disease. The benefits of scuba diving on respiratory function and system are also proven by the experts. This activity improves your ability to manage breathing but also increase your lung capacity. The more you control breathing, the more oxygenated your muscles will be.

Scuba diving to stay in good shape and fight overweight

Summer is approaching, it is the ideal occasion to enjoy a nice diving spot in order to burn the calories accumulated during the winter and to tone your body. The best dive sites might be the closest to your place. There is no need to go for a diving trip at the other side of the world. Professionals all agree on this point: scuba diving is ideal to sculpt and tone your body. This physical activity solicits all the upper and lower limbs of the body simultaneously. In addition, the micro-massages carried out by the pressure of the water act on the curves and shape the silhouette. They also have a very effective draining effect. Physical activity also promotes calorie loss. Studies show, moreover, that diving on a nice diving spot reduces the risk of osteoarthritis. It solicits, indeed, all the muscles. This practice improves the tone of the muscles and bones without traumatizing the joints.

Scuba diving: an effective anti-stress

Who would not be amazed to see a wide variety of aquatic fauna, beautiful wrecks and surprising seascapes in the best diving spots in the world? Scuba diving in a great dive spot will entertain and relax all the adventurers, even the most demanding. Far from the daily stress, you will be overjoyed to admire this unique, calm and quiet universe where your breathing is the best rhythm of your exploration.

During the activity, you will need to learn how to breathe and let go. The breathing exercise allows you to relax, to control your heartbeat and to evacuate all tensions and stress. Let yourself be seduced by this exceptional activity and discover a magnificent calm world where you only think of magnificent images of nature and cheerfulness of these species that surround you. Once out of the water, you will have a very empty head, positive thinking, a light heart and a calm mind. Scuba Diving is the best remedy against stress.

Scuba diving to boost self-confidence

Lack of self-confidence is a problem that affects many people in our modern world. You will surely be surprised to hear that scuba diving can help you have more self-esteem. But as everything, the first step is frightening but going over it will give your pride and confidence in order to trust your capacity to go over the first impression and doubt. But no worry, the instructor of a diving center will be there to make things easier for you.




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