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BACKGROUND: Scuba diving activities expose divers to serious accidents, which can require early hospitalization. Helicopters are used for early evacuation. On the French Mediterranean coast, rescue is made offshore mainly by a French Navy Dauphin or at a landing zone by an emergency unit EC 135 helicopter.METHODS: We retrospectively analyzed diving accidents evacuated by helicopter on the French Mediterranean coast from 1 September 2014 to 31 August 2016. We gathered data at the Center for Hyperbaric Medicine and Diving Expertise (SMHEP) of the Sainte-Anne Military Hospital (Toulon, France), the 35 F squadron at Hyres (France) Naval Air Station, and the SAMU 83 emergency unit (Toulon, France).RESULTS: A total of 23 diving accidents were evacuated offshore by Dauphin helicopter and 23 at a landing zone on the coast by EC 135 helicopter without hoist. Immersion pulmonary edema (IPE) accounted for one-third of the total diving accidents evacuated by helicopter with identified causes. It was responsible for at least half of the deaths at the dive place. A quarter of the rescued IPE victims died because of early cardiac arrest.DISCUSSION: Helicopter evacuation is indicated when vital prognosis (IPE and pulmonary overpressure in particular) or neurological functional prognosis (decompression sickness) is of concern. IPE is the primary etiology in patients with serious dive injuries that are life-threatening and who will benefit from helicopter evacuation. A non-invasive ventilation device with inspiratory support and positive expiratory pressure must be used, in particular for IPE.Corgie L, Huiban N, Pontier J-M, Brocq F-X, Boulard J-F, Monteil M. Diving accident evacuations by helicopter and immersion pulmonary edema. Aerosp Med Hum Perform. 2020; 91(10):806811.

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Introduction: Previous studies have suggested that the circulatory system was involved in the production of circulatory bubbles after diving. This study was designed to research the cardio-vascular function characteristics related to the production of high bubble grades after diving. Methods: Thirty trained divers were investigated both at baseline and after a 30-msw SCUBA dive. At baseline, the investigations included blood pressure measurement, echocardiography, and assessment of aerobic fitness using VO2 peak measurement. Blood samples were taken at rest, to measure the plasma concentration of NOx and endothelin-1. After diving, circulating bubbles were detected in the pulmonary artery by pulsed Doppler at 20-min intervals during the 90 min after surfacing. The global bubble quantity production was estimated by the KISS index. Results: Divers with a high bubble grade (KISS > 7.5) had systolic blood pressure, pulse pressure, weight, and height significantly higher than divers with a low bubble grade. By contrast, total arterial compliance, plasma NOx level, and percentage of predicted value of peak oxygen uptake were significantly lower in divers with a high bubble grade. Cardiac dimensions, left ventricular function, and plasma endothelin-1 concentration were not significantly different between groups. The multivariate analysis identified blood pressure as the main contributor of the quantity of bubble production. The model including pulse pressure, plasma NOx level, and percentage of predicted value of peak oxygen uptake has an explanatory power of 49.22%. Conclusion: The viscoelastic properties of the arterial tree appeared to be an important contributor to the circulating bubble production after a dive.

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PURPOSE: Previous studies have shown vascular dysfunction of main conductance arteries and microvessels after diving. We aim to evaluate the impact of bubble formation on vascular function and haemostasis. To achieve this, we used a vibration preconditioning to influence bubble levels without changing any other parameters linked to the dive. METHODS: Twentty-six divers were randomly assigned to one of three groups: (1) the "vibrations-dive" group (VD; n = 9) was exposed to a whole-body vibration session 30 min prior the dive; (2) the "diving" group (D; n = 9) served as a control for the effect of the diving protocol; (3) The "vibration" protocol (V; n = 8) allowed us to assess the effect of vibrations without diving. Macro- and microvascular function was assessed for each subject before and after the dive, subsequently. Bubble grades were monitored with Doppler according to the Spencer grading system. Blood was taken before and after the protocol to assess any change of platelets or endothelial function. RESULTS: Bubble formation was lower in the VD than the diving group. The other measured parameters remained unchanged after the "vibration" protocol alone. Diving alone induced macrovascular dysfunction, and increased PMP and thrombin generation. Those parameters were no longer changed in the VD group. Conversely, a microvascular dysfunction persists despite a significant decrease of circulating bubbles. CONCLUSIONS: Finally, the results of this study suggest that macro- but not microvascular impairment results at least partly from bubbles, possibly related to platelet activation and generation of pro-coagulant microparticles.

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INTRODUCTION: Many fisherman divers in Vietnam suffer from decompression sickness (DCS) causing joint pain, severe neurological deficit or even death. The objective of this pilot study was to evaluate the effectiveness of a training programme to prevent DCS and also treat DCS using the method of in-water recompression (IWR). METHODS: 63 divers were interviewed and trained over a period of 3 years from 2009. Fifty one per cent of all trained divers were reinterviewed in 2011-2012 to collect mortality and morbidity data as well as information on changes in diving practices. RESULTS: Since 2009, most fisherman divers have changed their practices by reducing bottom time or depth. Mortality was reduced and the incidence of severe neurological DCS decreased by 75%. Twenty four cases of DCS were treated by IWR. Ten cases of joint pain were treated with IWR using air, affording immediate relief in all cases. Out of 10 cases of neurological DCS, 4/4 recovered completely after IWR with oxygen whereas only 2/6 subjects recovered immediately after IWR with air. In addition, 3/4 further cases of DCS treated with IWR using oxygen immediately recovered. CONCLUSIONS: Our results suggest that IWR is effective for severe neurological DCS in remote fishing communities, especially with oxygen.

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Literature highlights the involvement of disseminated thrombosis in the pathophysiology of decompression sickness (DCS). We examined the effect of several antithrombotic treatments targeting various pathways on DCS outcome: acetyl salicylate, prasugrel, abciximab, and enoxaparin. Rats were randomly assigned to six groups. Groups 1 and 2 were a control nondiving group (C; n = 10) and a control diving group (CD; n = 30). Animals in Groups 3 to 6 were treated before hyperbaric exposure (HBE) with either prasugrel (n = 10), acetyl salicylate (n = 10), enoxaparin (n = 10), or abciximab (n = 10). Blood samples were taken for platelet factor 4 (PF4), thiobarbituric acid reactive substances (TBARS), and von Willebrand factor analysis. Onset of DCS symptoms and death were recorded during a 60-min observation period after HBE. Although we observed fewer outcomes of DCS in all treated groups compared with the CD, statistical significance was reached in abciximab only (20% vs. 73%, respectively, P = 0.007). We also observed significantly higher levels of plasmatic PF4 in abciximab (8.14 ± 1.40 ng/ml; P = 0.004) and enoxaparin groups (8.01 ± 0.80 ng/ml; P = 0.021) compared with the C group (6.45 ± 1.90 ng/ml) but not CD group (8.14 ± 1.40 ng/ml). Plasmatic levels of TBARS were significantly higher in the CD group than the C group (49.04 ± 11.20 µM vs. 34.44 ± 5.70 µM, P = 0.002). This effect was prevented by all treatments. Our results suggest that abciximab pretreatment, a powerful glycoprotein IIb/IIIa receptor antagonist, has a strong protective effect on decompression risk by significantly improving DCS outcome. Besides its powerful inhibitory action on platelet aggregation, we suggest that abciximab could also act through its effects on vascular function, oxidative stress, and/or inflammation.

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INTRODUCTION: Splenic platelets have been recognized to have a greater prothrombotic potential than others platelets. We studied whether platelets released by splenic contraction could influence the severity and outcome of decompression sickness (DCS) and bubble-induced platelet activation. METHODS: Sixteen, male Sprague-Dawley rats were randomly assigned to either a control or a splenectomized group. Both groups were compressed to 1,000 kPa (90 metres' sea water) for 45 min while breathing air before staged decompression (5 min at 200 kPa, 5 min at 160 kPa and 10 min at 130 kPa). The onset time of DCS symptoms and of death were recorded during a 60-min observation period post dive. Parameters measured were platelet factor 4 (PF4) for platelet activation, thiobarbituric acid reactive substances (TBARS) for oxidative stress status and Von Willebrand factor (VWf) for endothelial activation. RESULTS: There were no differences between the groups in DCS outcome or in PF4, TBARS and VWf concentrations. CONCLUSION: These results do not support that the spleen and its exchangeable platelet pool is involved in DCS pathogenesis in a rat model, invalidating the hypothesis that increased decompression-induced platelet aggregation could be influenced by splenic contraction and then play a role in DCS outcome.

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PURPOSE: Previous studies have shown that bubble formation induced endothelial damage on conduit arteries. We aim to evaluate the effect of diving on microvascular and macrovascular function. METHODS: Nine divers took part in a SCUBA dive at 30 msw (400 kPa), for 30 min of bottom time. Pre- and post-dive, they underwent an assessment of endothelial-dependent (acetylcholine) and endothelial-independent (sodium nitroprusside) microvascular function (laser Doppler flowmetry), as well as endothelial-dependent (flow-mediated dilation) and endothelial-independent (nitroglycerin-mediated dilation) function. Bubble grades were monitored with Doppler according to the Spencer grade. RESULTS: The mean KISS bubble score ranged from 21.10 ± 4.7 at rest to 55.03 ± 8.8 after knee flexion. The increase in cutaneous vascular conductance elicited by either acetylcholine (25.34 ± 6.71 to 7.63 ± 1.25 %, p = 0.021) or sodium nitroprusside (35.24 ± 8.75 to 7.61 ± 1.86 %, p = 0.017) was significantly reduced after diving. Similarly, both flow-mediated dilation (10.8 ± 0.9 to 5.4 ± 1.5 %, p = 0.002) and nitroglycerin-mediated dilation (15 ± 1.1 to 6.5 ± 1.6 %, p = 0.002) were also significantly decreased. There were no correlations between vascular parameters and bubble formation. CONCLUSIONS: There appears to be a reduction in endothelium-dependent and endothelium-independent, macro- and microvascular function associated with diving. Our results suggest that in the process of vascular dysfunction during diving, functional changes in the vessel wall may not be limited to the endothelium and may be mediated by alterations in vascular smooth muscle.

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We previously showed microvascular alteration of both endothelium-dependent and -independent reactivity after a single SCUBA dive. We aimed to study mechanisms involved in this postdive vascular dysfunction. Ten divers each completed three protocols: (1) a SCUBA dive at 400 kPa for 30 min; (2) a 41-min duration of seawater surface head immersed finning exercise to determine the effect of immersion and moderate physical activity; and (3) a simulated 41-min dive breathing 100% oxygen (hyperbaric oxygen [HBO]) at 170 kPa in order to analyze the effect of diving-induced hyperoxia. Bubble grades were monitored with Doppler. Cutaneous microvascular function was assessed by laser Doppler. Endothelium-dependent (acetylcholine, ACh) and -independent (sodium nitroprusside, SNP) reactivity was tested by iontophoresis. Endothelial cell activation was quantified by plasma Von Willebrand factor and nitric oxide (NO). Inactivation of NO by oxidative stress was assessed by plasma nitrotyrosine. Platelet factor 4 (PF4) was assessed in order to determine platelet aggregation. Blood was also analyzed for measurement of platelet count. Cutaneous vascular conductance (CVC) response to ACh delivery was not significantly decreased by the SCUBA protocol (23 ± 9% before vs. 17 ± 7% after; P = 0.122), whereas CVC response to SNP stimulation decreased significantly (23 ± 6% before vs. 10 ± 1% after; P = 0.039). The HBO and immersion protocols did not affect either endothelial-dependent or -independent function. The immersion protocol induced a significant increase in NO (0.07 ± 0.01 vs. 0.12 ± 0.02 µg/mL; P = 0.035). This study highlighted change in microvascular endothelial-independent but not -dependent function in highly trained divers after a single air dive. The results suggest that the effects of decompression on microvascular function may be modified by diving acclimatization.

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Bubble-induced platelet aggregation offers an index for evaluating decompression severity in humans and in a rat model of decompression sickness. Endothelial cells, blood platelets, or leukocytes shed microparticles (MP) upon activation and during cell apoptosis. The aim was to study blood platelet MP (PMP) release and bubble formation after a scuba-air dive in field conditions. Healthy, experienced divers were assigned to 1 experimental group (n = 10) with an open-sea air dive to 30 msw for 30 min and 1 control group (n = 5) during head-out water immersion for the same period. Bubble grades were monitored with a pulsed doppler according to Kissman Integrated Severity Score (KISS). Blood samples for platelet count (PC) and PMP (annexin V and CD41) were taken 1 h before and after exposure in both groups. The result showed a decrease in post-dive PC compared with pre-dive values in experimental group with no significant change in the control group. We observed a significant increase in PMP values after the dive while no change was revealed in the control group. There was a significant positive correlation between the PMP values after the dive and the KISS bubble score. The present study highlighted a relationship between the post-dive decrease in PC, platelet MP release, and bubble formation. Release of platelet MPs could reflect bubble-induced platelet aggregation and could play a key role in alteration of the coagulation. Further studies must investigate endothelial and leukocyte MP release in the same field conditions.

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Decompression sickness (DCS) with alterations in coagulation system and formation of platelet thrombi occurs when a subject is subjected to a reduction in environmental pressure. Blood platelet consumption after decompression is clearly linked to bubble formation in humans and offers an index for evaluating DCS severity in animal models. Previous studies highlighted a predominant involvement of platelet activation and thrombin generation in bubble-induced platelet aggregation (BIPA). To study the mechanism of the BIPA in DCS, we examined the effect of acetylsalicylic acid (ASA), heparin (Hep), and clopidogrel (Clo), with anti-thrombotic dose pretreatment in a rat model of DCS. Male Sprague-Dawley rats (n = 208) were randomly assigned to one experimental group treated before the hyperbaric exposure and decompression protocol either with ASA (3×100 mg·kg(-1)·day(-1), n = 30), Clo (50 mg·kg(-1)·day(-1), n = 60), Hep (500 IU/kg, n = 30), or to untreated group (n = 49). Rats were first compressed to 1,000 kPa (90 msw) for 45 min and then decompressed to surface in 38 min. In a control experiment, rats were treated with ASA (n = 13), Clo (n = 13), or Hep (n = 13) and maintained at atmospheric pressure for an equivalent period of time. Onset of DCS symptoms and death were recorded during a 60-min observation period after surfacing. DCS evaluation included pulmonary and neurological signs. Blood samples for platelet count (PC) were taken 30 min before hyperbaric exposure and 30 min after surfacing. Clo reduces the DCS mortality risk (mortality rate: 3/60 with Clo, 15/30 with ASA, 21/30 with Hep, and 35/49 in the untreated group) and DCS severity (neurological DCS incidence: 9/60 with Clo, 6/30 with ASA, 5/30 with Hep, and 12/49 in the untreated group). Clo reduced fall in platelet count and BIPA (-4,5% with Clo, -19.5% with ASA, -19,9% with Hep, and -29,6% in the untreated group). ASA, which inhibits the thromboxane A2 pathway, and Hep, which inhibits thrombin generation, have no protective effect on DCS incidence. Clo, a specific ADP-receptor antagonist, reduces post-decompression platelet consumption. These results point to the predominant involvement of the ADP release in BIPA but cannot differentiate definitively between bubble-induced vessel wall injury and bubble-blood component interactions in DCS.

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INTRODUCTION: The preconditioning of divers to reduce post-dive decompression sickness (DCS) has gained increased interest in diving medical research over the last few years. The beneficial effects of physical exercise, oxygen breathing, hyperbaric exposure, heat exposure, hyperhydration, or nitroglycerin administration before the dive are only a few examples of ongoing research. In this work, we investigated the effects of pre-dive whole-body vibration on post-dive bubble formation. METHODS: Following French Navy standard dive procedures, 14 healthy male military divers performed 2 identical dives 1 wk apart to 30 m of seawater (msw) for 30 min. One of the dives was randomly preceded by a 30-min whole-body vibration session (frequencies 35-40 Hz) 1 h before the dive. Post-dive bubbles were measured precordially 30, 60, and 90 min after the dive and were graded according to the Kissman Integrated Severity Score (KISS) protocol, with and without knee flexing. Arterial endothelial function was measured before and after vibration using flow mediated dilation (FMD) measurement. RESULTS: A significant reduction in bubble scores was observed after the "vibration" dive. CONCLUSION: As there was no observed change in FMD after vibration, we do not believe a nitric oxide mediated mechanism is involved; rather, a mechanical dislodgement or enhanced lymphatic elimination of gas nuclei is hypothesized.

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Previous studies have highlighted that bubble-induced platelet aggregation is a predictor index of decompression sickness (DCS) severity in animals and bubble formation after a single air dive in humans. The present study attempted to investigate plasmatic indexes of the coagulation system and platelet activation in our rat model of DCS. Male Sprague-Dawley rats were assigned to one experimental group with a hyperbaric exposure and one control group maintained at atmospheric pressure. Rats were compressed to 1,000 kPa (90 m saltwater) for 45 min while breathing air. The onset of death time and DCS symptoms were recorded during a 30-min observed period after rats had surfaced. Plasmatic indexes were platelet factor 4 (PF4) for platelet activation, soluble glycoprotein V (sGPV) for thrombin generation, and thrombin-antithrombin complexes for the coagulation system. Blood samples for a platelet count and markers were taken 3 wk before the experimental protocol and within the 30 min after rats had surfaced. We confirmed a correlation between the percent fall in platelet count and DCS severity. Plasmatic levels of sGPV and PF4 were significantly increased after the hyperbaric exposure, with no change in the control group. The present study confirms platelet consumption as a potential index for evaluating decompression stress and DCS severity. The results point to the participation of thrombin generation in the coagulation cascade and platelet activation in bubble-induced platelet aggregation. In our animal model of DCS, the results cannot prejudge the mechanisms of platelet activation between bubble-induced vessel wall injury and bubble-blood component interactions.

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It is generally accepted that the incidence of decompression sickness (DCS) from hyperbaric exposures is low when few or no bubbles are present in the circulation. To date, no data are available on the influence of in-water oxygen breathing on bubble formation following a provocative dive in man. The purpose of this study was to compare the effect of post-dive hyperbaric versus normobaric oxygen breathing (NOB) on venous circulating bubbles. Nineteen divers carried out open-sea field air dives at 30 msw depth for 30 min followed by a 9 min stop at 3 msw. Each diver performed three dives: one control dive, and two dives followed by 30 min of hyperbaric oxygen breathing (HOB) or NOB; both HOB and NOB started 10 min after surfacing. For HOB, divers were recompressed in-water to 6 msw at rest, whereas NOB was performed in a dry room in supine position. Decompression bubbles were examined by a precordial pulsed Doppler. Bubble count was significantly lower for post-dive NOB than for control dives. HOB dramatically suppressed circulating bubble formation with a bubble count significantly lower than for NOB or controls. In-water recompression with oxygen to 6 msw is more effective in removing gas bubbles than NOB. This treatment could be used in situations of "interrupted" or "omitted" decompression, where a diver returns to the water in order to complete decompression prior to the onset of symptoms. Further investigations are needed before to recommend this protocol as an emergency treatment for DCS.

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INTRODUCTION: It has been suggested that repeated compression-decompression cycles reduce diver susceptibility to decompression sickness (DCS). This study examined whether intensive scuba dive training would reduce bubble formation and modulate endothelial function as shown by skin circulation. METHODS: There were 22 military divers who were studied before and after a 90-d program of physical training and open-sea air diving (mean 67 dives total). Skin blood flow in the forearm was measured at rest (baseline), during post-occlusive hyperemia (endothelium-dependent vasodilatation), and with local heating to 42 degrees C (maximal vasodilatation). Subjects were also examined by pulsed Doppler for venous bubbles 30, 60, and 90 min after surfacing from a hyperbaric exposure to 400 kPa (30 msw) for 30 min in a dry chamber. RESULTS: None of the divers experienced DCS during the training period. There was no change in weight, body mass index, maximal oxygen uptake, or endothelial function. Bubble grades by the Kisman Integrated Severity Score were significantly decreased immediately after the diving training period (3.6 +/- 9.2 vs. 16.4 +/- 14.3) and increased 3 mo after this period (10.3 +/- 13.9 vs. 3.6 +/- 9.2). DISCUSSION: The results highlight that repeated scuba dives and regular physical exercise activity reduce bubble formation and probably have a protective effect against DCS risk. Although this phenomenon has been observed for decades, the mechanism remains complex and the results cannot elucidate the effects of physical exercise and NO production. Bubble formation could activate the stress response which could be the basis for diving acclimatization.

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INTRODUCTION: Previous human studies reported that platelet count (PC) is decreased following decompression. Platelet aggregation and adherence to the bubble surface has been demonstrated in severe decompression sickness (DCS). The present study was designed to clarify the relationship between post-dive changes in blood PC and the level of bubble formation in divers. METHODS: There were 40 healthy experienced divers who were assigned to 1 experimental group (N = 30) with an open-sea air dive to 30 msw for 30 min in field conditions and 1 control group (N = 10) without hyperbaric exposure. Bubble grades were monitored with a pulsed Doppler according to the Spencer scale and Kissman integrated severity score (KISS). Blood samples for red blood cell counts (RBC), hematocrit (Hct), and PC were taken 1 h before and after exposure in two groups. RESULTS: None of the divers developed any signs of DCS. In two groups, the results showed significant increase in RBC count and Hct related with hemoconcentration and no change in PC. Divers with a high KISS score (39 +/- 5.8; mean +/- SD) presented a significantly more pronounced percent fall in PC than divers with a lower KISS score. We found a significant correlation between the percent fall in PC after a dive and the bubble KISS score. DISCUSSION: The present study highlighted a relationship between the post-dive decrease in PC and the magnitude of bubble level after decompression. Our primary result is that the post-dive decrease in PC could be a predictor of decompression severity after diving.

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BACKGROUND: Decompression sickness (DCS) affecting the spinal cord is the most dangerous form of diving-related injury with potential sequelae. This study was conducted to evaluate the relationship between spinal cord lesions on MRI and clinical findings in divers with spinal DCS. METHODS: We studied 45 cases of DCS that were referred to our hyperbaric facility with clinical evidence of spinal involvement during the period 2002-2007. The study included only patients who underwent MRI within 10 d of injury. The severity of spinal DCS for each patient was rated numerically for both the acute event and 1 mo later. The presence or absence of back pain was also noted. RESULTS: Spinal cord lesions were significantly more frequent in divers with severe DCS, and did not occur in any diver who experienced a favorable outcome (sensitivity = 67%, specificity = 100%, negative predictive value = 77%, positive predictive value = 100%). The presence of vertebral degenerative changes that impinged on the spinal cord was strongly associated with MRI abnormalities, but not with a negative outcome. Acute back pain was associated with hyperintense lesions and persistence of neurological sequelae [OR = 14 (95% CI, 3.1 to 63.5)]. CONCLUSION: The results show that MRI could be helpful in predicting clinical outcome in divers with spinal cord DCS. The presence of medullary compressive factors and vertebral back pain after surfacing indicate increased likelihood of severe myelopathy with incomplete recovery.

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INTRODUCTION: Previous animal studies reported that platelet count (PC) is decreased following decompression. Adherence and aggregation of platelets to the bubble surface has been demonstrated in severe decompression sickness (DCS). The present study was designed to clarify the relationship between post-dive platelet levels and the severity of DCS in a rat model. METHODS: A total of 57 male Sprague-Dawley rats were assigned to either one experimental group with a hyperbaric exposure (N = 22) or one control group (N = 27). Rats were compressed to 1000 kPa (90 msw) for 45 min while breathing air and decompressed to surface in 38 min with stops at 200, 160, and 130 kPa. Onset of neurological DCS and death time were recorded during a 120-min observation period after surfacing. In the control group, rats were maintained at atmospheric pressure in the same chamber for an equivalent period of time. Blood samples for PC were taken 30 min before and immediately after exposure in two groups. RESULTS: Blood PC after hyperbaric exposure had significantly decreased, whereas PC had increased in the control group. We found a correlation between % fall in PC and latency to death time. The platelet loss tended to decrease when fatal DCS was delayed. Rats suffering from severe DCS with a short latency to death presented a pronounced decline in platelets. DISCUSSION: The present study highlighted a relationship between the post-dive decrease in PC and DCS severity in rats. Platelet consumption could offer a new index for evaluating decompression stress.

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OBJECTIVES: To evaluate the effects of a submaximal exercise performed 2 h before a simulated dive on bubble formation and to observe the haemodynamic changes and their influence on bubble formation. PARTICIPANTS AND METHODS: 16 trained divers were compressed in a hyperbaric chamber to 400 kPa for 30 min and decompressed at a rate of 100 kPa/min with a 9 min stop at 130 kPa (French Navy MN90 procedure). Each diver performed two dives 3 days apart, one without exercise and one with exercise before the dive. All participants performed a 40 min constant-load submaximal and calibrated exercise, which consisted of outdoor running 2 h before the dive. Circulating bubbles were detected with a precordial Doppler at 30, 60 and 90 min after surfacing. Haemodynamic changes were evaluated with Doppler echocardiography. RESULTS: A single bout of strenuous exercise 2 h before a simulated dive significantly reduced circulating bubbles. Post-exercise hypotension (PEH) was observed after exercise with reductions in diastolic and mean blood pressure (DBP and MBP), but total peripheral resistance was unchanged. Stroke volume was reduced, whereas cardiac output was unchanged. Simulated diving caused a similar reduction in cardiac output independent of pre-dive exercise, suggesting that pre-dive exercise only changed DBP and MBP caused by reduced stroke volume. CONCLUSION: A single bout of strenuous exercise 2 h before a dive significantly reduced the number of bubbles in the right heart of divers and protected them from decompression sickness. Declining stroke volume and moderate dehydration induced by a pre-dive exercise might influence inert gas load and bubble formation.

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BACKGROUND: A single bout of aerobic exercise 24 h before a dive significantly reduces the formation of circulating venous gas emboli (VGE) on decompression. The purpose of this investigation was to determine the effect of aerobic exercise 2 h before a dive. METHODS: There were 16 trained military divers who were compressed to 30 msw (400 kPa) for 30 min breathing air in a dry hyperbaric chamber at rest, then decompressed at a rate of 10 m x min(-1) with a 9-min stop at 3 msw. Each diver performed two dives 3 d apart, one with and one without exercise that consisted of running for 45 min at 60-80% of maximum heart rate (estimated as 220 - age). VGE were graded according to the Spencer scale using a pulsed Doppler detector on the precordium at 30 min (T30) and 60 min (T60) after surfacing. RESULTS: Mean bubble grades at T60 were 1.25 for control dives and 0.44 for dives preceded by exercise, the difference being highly significant. None of the divers showed an increase in venous bubble grade after exercise. CONCLUSION: Like exercise 24 h ahead, 45 min of running 2 h before a dive decreases bubble formation after diving, suggesting a protective effect of aerobic exercise against DCS. The threshold of exercise intensity and duration necessary to change venous circulating bubbles is unknown. Mechanisms underlying the protective effect of exercise remain unclear. Rather than altering the nitrogen elimination rate, exercise may affect the population of gaseous nuclei from which bubbles form.

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