Vladimir Ivancev

Aerobic exercise before diving reduces venous gas bubble formation in humans

We have previously shown in a rat model that a single bout of high‐intensity aerobic exercise 20h before a simulated dive reduces bubble formation and after the dive protects from lethal decompression sickness. The present study investigated the importance of these findings in man. Twelve healthy male divers were compressed in a hyperbaric chamber to 280kPa at a rate of 100kPamin−1 breathing air and remaining at pressure for 80min. The ascent rate was 9mmin−1 with a 7min stop at 130kPa. Each diver underwent two randomly assigned simulated dives, with or without preceding exercise. A single interval exercise performed 24h before the dive consisted of treadmill running at 90% of maximum heart rate for 3min, followed by exercise at 50% of maximum heart rate for 2min; this was repeated eight times for a total exercise period of 40min. Venous gas bubbles were monitored with an ultrasonic scanner every 20min for 80min after reaching surface pressure. The study demonstrated that a single bout of strenuous exercise 24h before a dive to 18 m of seawater significantly reduced the average number of bubbles in the pulmonary artery from 0.98 to 0.22 bubbles cm−2(P= 0.006) compared to dives without preceding exercise. The maximum bubble grade was decreased from 3 to 1.5 (P= 0.002) by pre‐dive exercise, thereby increasing safety. This is the first report to indicate that pre‐dive exercise may form the basis for a new way of preventing serious decompression sickness.

Cardiovascular Regulation During Apnea in Elite Divers

Involuntary apnea during sleep elicits sustained arterial hypertension through sympathetic activation; however, little is known about voluntary apnea, particularly in elite athletes. Their physiological adjustments are largely unknown. We measured blood pressure, heart rate, hemoglobin oxygen saturation, muscle sympathetic nerve activity, and vascular resistance before and during maximal end-inspiratory breath holds in 20 elite divers and in 15 matched control subjects. At baseline, arterial pressure and heart rate were similar in both groups. Maximal apnea time was longer in divers (1.7±0.4 versus 3.9±1.1 minutes; P<0.0001), and it was accompanied by marked oxygen desaturation (97.6±0.7% versus 77.6±13.9%; P<0.0001). At the end of apnea, divers showed a >5-fold greater muscle sympathetic nerve activity increase (P<0.01) with a massively increased pressor response compared with control subjects (9±5 versus 32±15 mm Hg; P<0.001). Vascular resistance increased in both groups, but more so in divers (79±46% versus 140±82%; P<0.01). Heart rate did not change in either group. The rise in muscle sympathetic nerve activity correlated with oxygen desaturation (r2=0.26; P<0.01) and with the increase in mean arterial pressure (r2=0.40; P<0.0001). In elite divers, breath holds for several minutes result in an excessive chemoreflex activation of sympathetic vasoconstrictor activity. Extensive sympathetically mediated peripheral vasoconstriction may help to maintain adequate oxygen supply to vital organs under asphyxic conditions that untrained subjects are not able to tolerate voluntarily. Our results are relevant to conditions featuring periodic apnea.

The effects of acute oral antioxidants on diving-induced alterations in human cardiovascular function

Diving‐induced acute alterations in cardiovascular function such as arterial endothelial dysfunction, increased pulmonary artery pressure (PAP) and reduced heart function have been recently reported. We tested the effects of acute antioxidants on arterial endothelial function, PAP and heart function before and after a field dive. Vitamins C (2 g) and E (400 IU) were given to subjects 2 h before a second dive (protocol 1) and in a placebo‐controlled crossover study design (protocol 2). Seven experienced divers performed open sea dives to 30 msw with standard decompression in a non‐randomized protocol, and six of them participated in a randomized trial. Before and after the dives ventricular volumes and function and pulmonary and brachial artery function were assessed by ultrasound. The control dive resulted in a significant reduction in flow‐mediated dilatation (FMD) and heart function with increased mean PAP. Twenty‐four hours after the control dive FMD was still reduced 37% below baseline (8.1 versus 5.1%, P= 0.005), while right ventricle ejection fraction (RV‐EF), left ventricle EF and endocardial fractional shortening were reduced much less (∼2–3%). At the same time RV end‐systolic volume was increased by 9% and mean PAP by 5%. Acute antioxidants significantly attenuated only the reduction in FMD post‐dive (P < 0.001), while changes in pulmonary artery and heart function were unaffected by antioxidant ingestion. These findings were confirmed by repeating the experiments in a randomized study design. FMD returned to baseline values 72 h after the dive with pre‐dive placebo, whereas for most cardiovascular parameters this occurred earlier (24–48 h). Right ventricular dysfunction and increased PAP lasted longer. Acute antioxidants attenuated arterial endothelial dysfunction after diving, while reduction in heart and pulmonary artery function were unchanged. Cardiovascular changes after diving are not fully reversed up to 3 days after a dive, suggesting longer lasting negative effects.

Cerebral and peripheral hemodynamics and oxygenation during maximal dry breath-holds

The effects of maximal apneas on cerebral and brachial blood flow and oxygenation are unknown in humans. Middle cerebral artery blood velocity (MCAV), cerebral and muscle oxygenation (Sc(O2) and Sm(O2)) and brachial blood flow (BBF) were measured during apneas in breath-hold divers (BHD) and non-divers (ND). Brain oxyhemoglobin (O(2)Hb) was maintained in both groups until the end of apnea, whereas deoxyhemoglobin increased more in BHD. Therefore, Sc(O2) decreased more in BHD due to longer apnea duration and smaller initial MCAV increase. MCAV increased significantly more in BHD versus ND at the end of apnea. Cerebral desaturation for approximately 13% occurred at the end of apnea in BHD despite increased cerebral oxygen delivery for approximately 50%. Larger reduction in muscle O(2)Hb was found in BHD, with similar peripheral vasoconstriction. These data indicate that BHD have decreased Sc(O2) at the end of breath-hold despite large increases in MCAV. This is partly due delayed initial cerebral vasodilation. This study provides further evidence for the oxygen-conserving effect in elite divers.

Restoration of hemodynamics in apnea struggle phase in association with involuntary breathing movements

Involuntary breathing movements (IBM) that occur in the struggle phase of maximal apneas produce waves of negative intrathoracic pressure. This could augment the venous return, increasing thereby the cardiac output and gas exchange, and release the fresh blood from venous pools of spleen and liver. To test these hypotheses we used photoplethysmography and ultrasound for assessment of hemodynamics and spleen size before, during and after maximal dry apneas at large lung volume in 7 trained divers. During the easy-going phase cardiac output was reduced about 40%, due to reduction in stroke volume and in presence of reduced inferior vena cava venous return, while the spleen contracted for about 60 ml. Towards the end of the struggle phase, in presence of intense IBM, the spleen volume further decreased for about 70 ml, while cardiac output and caval flow almost renormalized. In conclusion, IBM coincide with splenic volume reduction and restoration of hemodynamics, likely facilitating the use of the last oxygen reserves before apnea cessation.

Cerebrovascular reactivity to hypercapnia is unimpaired in breath-hold divers

Hypercapnic cerebrovascular reactivity is decreased in obstructive sleep apnoea and congestive heart disease perhaps as a result of repeated apnoeas. To test the hypothesis that repeated apnoeas blunt cerebrovascular reactivity to hypercapnia, we studied breath hold divers and determined cerebrovascular reactivity by measuring changes in middle cerebral artery velocity (MCAV, cm s−1) per mmHg change in end‐tidal partial pressure of CO2 () in response to two hyperoxic hypercapnia rebreathing manoeuvres (modified Read protocol) in elite breath‐hold divers (BHD, n= 7) and non‐divers (ND, n= 7). In addition, ventilation and central (beat‐to‐beat stroke volume measurement with Modelflow technique) haemodynamics were determined. Ventilatory responses to hypercapnia were blunted in BHD versus ND largely due to lower breathing frequency. Cerebrovascular reactivity did not differ between groups (3.7 ± 1.4 versus 3.4 ± 1.3% mmHg−1 in BHD and ND, respectively; P= 0.90) and the same was found for cerebral vascular resistance and MCAV recovery to baseline after termination of the CO2 challenge. Cardiovascular parameters were not changed significantly during rebreathing in either group, except for a small increase in mean arterial pressure for both groups. Our findings indicate that the regulation of the cerebral circulation in response to hypercapnia is intact in elite breath‐hold divers, potentially as a protective mechanism against the chronic intermittent cerebral hypoxia and/or hypercapnia that occurs during breath‐hold diving. These data also suggest that factors other than repeated apnoeas contribute to the blunting of cerebrovascular reactivity in conditions like sleep apnoea.

Effects of indomethacin on cerebrovascular response to hypercapnea and hypocapnea in breath-hold diving and obstructive sleep apnea.

We tested whether breath hold divers (BHD) and obstructive sleep apnea (OSA) subjects had similar middle cerebral artery velocity (MCAV) responses to hypercapnea and hypocapnea. We analyzed changes in MCAV (cm/s) in response to hypocapnea and hyperoxic hypercapnea during placebo or after 90 min of oral indomethacin (100 mg) in BHD (N=7) and OSA (N=7). During control hypercapnea MCAV increased for 54.4% in BHD and 48.4% in OSA. Indomethacin blunted the MCAV increase in response to hypercapnea in BHD (P=0.02), but not in OSA. Indomethacin attenuated the mean arterial pressure response in BHD, but not in OSA. The blunted MCAV responses to hypercapnea with indomethacin in BHD, but not in OSA patients suggests that (a) the normal contribution of local vasodilating mechanisms to the cerebrovascular responses to hypercapnea is absent in OSA patients and (b) exposure to chronic/repeated apneas is not causal per se in limiting the contribution of vasodilating mechanisms to the cerebrovascular responses to hypercapnea in OSA.

Peripheral chemoreflex sensitivity and sympathetic nerve activity are normal in apnea divers during training season

Apnea divers are exposed to repeated massive arterial oxygen desaturation, which could perturb chemoreflexes. An earlier study suggested that peripheral chemoreflex regulation of sympathetic vasomotor tone and ventilation may have recovered 4 or more weeks into the off season. Therefore, we tested the hypothesis that peripheral chemoreflex regulation of ventilation and sympathetic vasomotor tone is present during the training season. We determined ventilation, heart rate, blood pressure, cardiac stroke volume, and muscle sympathetic nerve activity (MSNA) during isocapnic hypoxia in 10 breath hold divers and 11 matched control subjects. The study was carried out at the end of the season of intense apnea trainings. Baseline MSNA frequency was 30+/-4bursts/min in control subjects and 25+/-4bursts/min in breath hold divers (P=0.053). During hypoxia burst frequency and total sympathetic activity increased similarly in both groups. Sympathetic activity normalized during the 30-minute recovery. Hypoxia-induced stimulation of minute ventilation was similar in both groups, although in divers it was maintained by higher tidal volumes and lower breathing frequency compared with control subjects. In both groups, hypoxia increased heart rate and cardiac output whereas total peripheral resistance decreased. Blood pressure remained unchanged. We conclude that peripheral chemoreflex regulation of ventilation and sympathetic vasomotor tone is paradoxically preserved in apnea divers, both, during the off and during the training season. The observation suggests that repeated arterial oxygen desaturation may not be sufficient explaining sympathetic reflex abnormalities similar to those in obstructive sleep apnea patients.

Ultrasonic evidence of acute interstitial lung edema after SCUBA diving is resolved within 2-3h.

Recently, an increase in extravascular lung water (EVLW) accumulation with diminished left ventricular contractility within 60 min after SCUBA diving was reported. We have observed previously that diving was associated with reduced diffusing lung capacity for carbon monoxide (DLCO) and arterial oxygen pressure for up to 60-80 min postdive. Here we investigated whether increased EVLW persists 2-3h after successive deep dives in a group of seven male divers. The echocardiographic indices of pulmonary water accumulation (ultrasound lung comets (ULC)) and left ventricular function, respiratory functional measurements and arterial oxygen saturation (SaO(2)) were assessed 2-3h post diving, while venous gas bubbles (VGB) and the blood levels of NT-proBNP and proANP were analyzed 40 min after surfacing. Spirometry values, flow-volume, DLCO, SaO(2) and ULC were unchanged after each dive, except for significant increase in ULC after the second dive. Left ventricular function was reduced, while NT-proBNP and proANP levels were significantly elevated after majority of dives, suggesting a cardiac strain.

A no-decompression air dive and ultrasound lung comets

INTRODUCTION Increased accumulation of extravascular lung water after repetitive deep trimix dives was recently reported. This effect was evident 40 min post-dive, but in subsequent studies most signs of this lung congestion were not evident 2-3 h post-dive, indicating no major negative effects on respiratory gas exchange following deep dives. Whether this response is unique for trimix dives or also occurs in more frequent air dives is presently unknown. METHODS A single no-decompression field dive to 33 m with 20 min bottom time was performed by 12 male divers. Multiple ultrasound lung comets (ULC), bubble grade (BG), and single-breath lung diffusing capacity (DLCO) measurements were made before and up to 120 min after the dive. RESULTS Median BG was rather high with maximal values observed at 40 min post-dive [median 4 (4-4)]. Arterialization of bubbles from the venous side was observed only in one diver lasting up to 60 min post-dive. Despite high BG, no DCS symptoms were noted. DLCO and ULC were unchanged after the dive at any time point (DLCO(corr) was 33.6 +/- 1.9 ml x min(-1) mmHg(-1) pre-dive, 32.7 +/- 3.8 ml x min(-1) x mmHg(-1) at 60 min post-dive, and 33.2 +/- 5.3 ml x min(-1) x mmHg(-1) at 120 min post-dive; ULC count was 4.1 +/- 1.9 pre-dive, 4.9 +/- 3.3 at 20 min post-dive, and 3.3 +/- 1.9 at 60 min post-dive. DISCUSSION These preliminary findings show no evidence of increased accumulation of extravascular lung water in male divers after a single no-decompression air dive at the limits of accepted Norwegian diving tables.