Search

We studied the effects of age on different physiological parameters, including those derived from (i) maximal cardiopulmonary exercise testing (CPET), (ii) moderate-intensity step transitions, and (iii) tensiomyography (TMG)-derived variables in moderately active women. Twenty-eight women (age, 19 to 53 years), completed 3 laboratory visits, including baseline data collection, TMG assessment, maximal oxygen uptake test via CPET, and a step-transition test from 20 W to a moderate-intensity cycling power output (PO), corresponding to oxygen uptake at 90% gas exchange threshold. During the step transitions, breath-by-breath pulmonary oxygen uptake, near infrared spectroscopy derived muscle deoxygenation (ΔHHb), and beat-by-beat cardiovascular response were continuously monitored. There were no differences observed between the young and middle-aged women in their maximal oxygen uptake and peak PO, while the maximal heart rate (HR) was 12 bpm lower in middle-aged compared with young (p = 0.016) women. Also, no differences were observed between the age groups in τ pulmonary oxygen uptake, ΔHHb, and τHR during on-transients. The first regression model showed that age did not attenuate the maximal CPET capacity in the studied population (p = 0.638), while in the second model a faster τ pulmonary oxygen uptake, combined with shorter TMG-derived contraction time (Tc) of the vastus lateralis (VL), were associated with a higher maximal oxygen uptake (∼30% of explained variance, p = 0.039). In conclusion, long lasting exercise involvement protects against a maximal oxygen uptake and τpulmonary oxygen uptake deterioration in moderately active women. Novelty: Faster τ pulmonary oxygen uptake and shorter Tc of the VL explain 33% of the variance in superior maximal oxygen uptake attainment. No differences between age groups were found in τ pulmonary oxygen uptake, τΔHHb, and τHR during on-transients.

The present study examined whether differences in the heart rate recovery following flywheel exercise cessation were associated with differences in maximal oxygen uptake ($${\dot{\text{V}}}$$ V ˙ O2 max.), age and sex in trained adults. Eleven men (age range 22–49 years, $${\dot{\text{V}}}$$ V ˙ O2 max. = 43.6 ± 7.6 mL kg min−1) and ten women (age range 20—53 years, $${\dot{\text{V}}}$$ V ˙ O2 max. = 38.0 ± 5.7 mL kg min−1) were randomly assigned to complete a squat-exercise on the flywheel ergometer set at three different moments of inertia, while their cardiovascular responses were continuously monitored. During the flywheel exercise the mean arterial pressure rose by ~ 35 to 40% (p = .001), and the increment was more robust in men than women. The cardiac index was two-fold greater across both sexes compared to the baseline (p = .001), while the rise in heart rate (~ 144 bpm) was more pronounced in women to compensate for their load-dependent stroke index decline (p = .001). The load-independent time-course changes in heart rate recovery markers were comparable between the sexes. When these indicators were pooled, a stepwise regression revealed age as the only relevant predictor of both fast and slow components of the heart rate recovery (~ 30% of the shared variance explained, p = .014). The present data suggest that the heart rate recovery declines with age, irrespective of sex, or well-preserved cardiorespiratory fitness in moderately-trained adults.

BACKGROUND The cardiovascular response to variable load exercise on a flywheel ergometer is still unknown. OBJECTIVE This study examined the effects of flywheel exercise on cardiovascular response and brachial artery vasodilation capacity in healthy, active men. METHODS In this cross-sectional study, nineteen men (20-57 years old) completed three laboratory visits, including a ramp exercise test to determine their maximal oxygen uptake JOURNAL/blpmo/04.03/00126097-202106000-00008/inline-graphic1/v/2021-04-27T091817Z/r/image-tiff max, and exercise intervention on a flywheel ergometer set at 0.075 kg·m2 moment of inertia. After the ramp test cessation, all participants were allocated into aerobically untrained (n = 10) and trained (n = 9) groups. Throughout the flywheel exercise, cardiovascular demands were continuously monitored via Finapres, while a pre/postflow-mediated dilation (FMD) assessment was performed using ultrasound imaging. RESULTS There were no differences observed between the groups in their anthropometrics, age or resting brachial artery diameter, while the JOURNAL/blpmo/04.03/00126097-202106000-00008/inline-graphic2/v/2021-04-27T091817Z/r/image-tiff max was ~15% higher (P = 0.001) in trained compared to aerobically untrained group. The cardiovascular response to the flywheel exercise was similar between the groups, with peak mean arterial pressure and heart rate readings reaching ~160 mmHg and ~140 bpm, respectively. The flywheel exercise did not impair the FMD (%) response, which was comparable between the groups (P = 0.256). When these data were pooled, the regression analysis showed an inverse relationship among FMD (%), age (β = -0.936, P = 0.001) and JOURNAL/blpmo/04.03/00126097-202106000-00008/inline-graphic3/v/2021-04-27T091817Z/r/image-tiffmax. (β = -0.359, P = 0.045). CONCLUSION Although aerobic fitness alone does not directly explain the FMD response to flywheel exercise, aerobically untrained individuals, as they get older, tend to have lower brachial artery FMD.

This manuscript quantified spleen volume changes and examined the relationship between those changes and oxygen uptake kinetics during supine cycling. Ten volunteers (age = 22 ± 3), completed 3 step transitions from 20 W to their power output at 90% gas exchange threshold. Ultrasonic measurements of the spleen were performed each minute. The largest spleen volume reduction was 105 mL (p = 0.001). No associations existed between i) spleen volumes at rest; and ii) spleen volume changes (%) and tau pulmonary oxygen uptake (τV̇O2p). Larger resting spleen volume and greater emptying do not correlate with a faster τV̇O2p. Novelty: Greater splenic contractions do not augment τV̇O2p, irrespective of spleen emptying and subsequent erythrocyte release.

Purpose: The purpose of this study was to determine the reliability, validity, and usefulness of 30?15 Intermittent Fitness Test (30- 15(IFT)) in female basketball players. Methods: Nineteen female basketball players (17.82 ? 1.94 yr, 175.4 ? 7.3 cm, 67.9 ? 7.7 kg) competing in the National Croatian League performed one trial of a continuous treadmill running test and two trials of the 30-15(IFT). The 30-15(IFT) involves 30-s runs across a 40-m course interspersed with 15 s of walking, with running speed increasing every 45 s. The continuous treadmill running test was used as the criterion for validation. Results: High to very high reliability across test?retest trials were observed for maximal oxygen uptake (VO(2)max) (CV = 4.9%, ICC = 0.85), the 30-15(IFT) end-running velocity (V-IFT) (CV = 6.0%, ICC = 0.85), and maximal heart rate (HRmax) (CV = 4.8%, ICC = 0.96). Criterion validity was supported for the 30-15(IFT) with strong to very strong relationships with VO(2)max (r =0.69), V-IFT (r =0.74), and HRmax (r =0.73) attained during the continuous treadmill running test. The typical error (TE) of the 30-15(IFT) was greater than the smallest worthwhile change for VO(2)max (1.16 > 0.42 ml/kg/min), V-IFT (0.56 > 0.20 km/h), and HRmax (2.15 > 1.89 bpm) adjudging usefulness of the test as marginal. The TE of 0.56 km/h (90% CI = 0.44?0.77 km/h) demonstrates changes in the performance of one to two stages (0.5?1.0 km/h) are meaningful. Conclusions: The 30-15(IFT) possesses acceptable reliability and validity to assess maximal aerobic fitness capacity in female basketball players. While the usefulness of the 30-15(IFT) was marginal, meaningful changes in performance consisted of only one to two stages. The present findings support the 30-15(IFT) as a practical testing option for basketball practitioners to assess fitness capacities in female players.

PURPOSE: Athletes in Olympic combat sports experience body water fluctuations resulting from training and intentional dehydration when making weight. Despite the popularity of urine specific gravity (USG) and urine osmolality (UOSM) measurement in characterizing fluid fluctuations, their utility remains questioned. This systematic review/meta-analysis examined the utility of urinary hydration indices in laboratory and field settings in Olympic combat sport athletes. METHODS: 27 articles met the inclusion criteria for systematic review, 15 studies were included in the meta-analysis ; with USG and UOSM the main outcome variables. Meta-regression analyses evaluated the interrelationship among body mass (BM), fluid intake, and urine measures. RESULTS: Significant USG alterations were observed following different sampling time frames: dehydration (ES 0.59 ; 95% CI 0.46-0.72 ; p = 0.001), follow-up period (ES 0.31 ; 95% CI 0.11-0.50 ; p = 0.002) and rehydration (ES - 0.34 ; 95% CI - 0.56 to - 0.12 ; p = 0.003). Direct comparison of laboratory (ES 0.20 ; 95% CI - 0.19 to 0.59 ; p = 0.324) and field (ES 0.35 ; 95% CI 0.14-0.56 ; p = 0.001) sampling showed marginally trivial and small effects. Small effects on UOSM were observed following dehydration (ES 0.31 ; 95% CI 0.12-0.74, p = 0.15), follow-up period (ES 0.39 ; 95% CI 0.08-0.70, p = 0.015) and rehydration (ES - 0.45 ; 95% CI - 0.60 to 0.30, p = 0.001). Meta-regression analysis suggests only fluid intake predicts USG alterations (p = 0.044) during rehydration protocols. CONCLUSIONS: There were likely small changes in both USG and UOSM readings across all experimental conditions, with moderate-to-large heterogeneity in all studies, except for USG readings during dehydration protocols. The meta-regression failed to provide conclusive evidence concerning the interrelationship among urine measures, BM fluctuations, and fluid intake.

This study investigated (i) the prevalence of hypohydration and (ii) association between urinary indices of hydration status and confounding factors (e.g., urine protein content, water intake) in elite youth boxers during their weight-stable phase before competition. Sixteen national champion boxers (all male, 17 ± 1 y) were measured on 3 occasions (baseline, day 3, day 10), 30-day prior to competition. Body mass, total body water, urine specific gravity (USG), osmolality (UOSM) and total protein content (TPC) were evaluated to determine hydration status and fluid balance. Overall macronutrient and water intake were assessed using dietary records. Both UOSM and USG increased from day 3 to day 10 by 16% and 0.4% (P < 0.001), despite athletes being in their weight-stability period, and regardless of ad libitum fluid intake. Hypohydration was universally prevalent among all athletes on both test days with USG: 1.027 ± 0.003 g · mL-1 and UOSM: 1035 ± 108 mOsmol · kg-1. An inverse association between mean UOSM values and mean water intake was observed (R = -0.52, P = 0.04), while TPC was not associated with any urinary dehydration markers (USG, P = 0.51 ; UOSM, P = 0.61). The present outcomes find that the most prevalent urinary dehydration markers used to classify hydration status in competition exhibit large variability, even during weight-stable periods.

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. Copyright © 2009 Elsevier B.V. All rights reserved.

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.

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.

Repeated hypoxemia in obstructive sleep apnea patients increases sympathetic activity, thereby promoting arterial hypertension. Elite breath-holding divers are exposed to similar apneic episodes and hypoxemia. We hypothesized that trained divers would have increased resting sympathetic activity and blood pressure, as well as an excessive sympathetic nervous system response to hypercapnia. We recruited 11 experienced divers and 9 control subjects. During the diving season preceding the study, divers participated in 7.3 ± 1.2 diving fish-catching competitions and 76.4 ± 14.6 apnea training sessions with the last apnea 3–5 days before testing. We monitored beat-by-beat blood pressure, heart rate, femoral artery blood flow, respiration, end-tidal CO2, and muscle sympathetic nerve activity (MSNA). After a baseline period, subjects began to rebreathe a hyperoxic gas mixture to raise end-tidal CO2 to 60 Torr. Baseline MSNA frequency was 31 ± 11 bursts/min in divers and 33 ± 13 bursts/min in control subjects. Total MSNA activity was 1.8 ± 1.5 AU/min in divers and 1.8 ± 1.3 AU/min in control subjects. Arterial oxygen saturation did not change during rebreathing, whereas end-tidal CO2 increased continuously. The slope of the hypercapnic ventilatory and MSNA response was similar in both groups. We conclude that repeated bouts of hypoxemia in elite, healthy breath-holding divers do not lead to sustained sympathetic activation or arterial hypertension. Repeated episodes of hypoxemia may not be sufficient to drive an increase in resting sympathetic activity in the absence of additional comorbidities.

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(PET,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.

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 (approximately 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.

Purpose: A similar postexercise hypotension (PEH) has been reported in sedentary and mildly endurance-trained individuals of both sexes after a single dynamic submaximal exercise. In endurance-trained men, the hypotension was associated with a reduction of cardiac output, whereas the peripheral vasodilatation was the main mechanism of this fall in other groups. The present study investigated the occurrence and mechanisms of PEH after a short maximal exercise in professional soccer players with greater endurance capacity than previously reported in PEH studies. Methods: Arterial blood pressure, cardiac output (Q), heart rate (HR), and diffusing lung capacity for carbon monoxide (DLCO) before and 30 and 60 min after short maximal field exercise were studied in 20 professional soccer players. Results: Diastolic blood pressure (DBP) and systolic blood pressure (SBP), Q, stroke volume, and DLCO decreased, whereas HR increased at both times after exercise. Decreases in DBP were greater in subjects with lesser [latin capital V with dot above]O2max (r = -0.73, P = 0.0001), whereas SBP was more decreased the higher it was at baseline (r = 0.51, P = 0.023). Total peripheral resistance (TPR) did not change significantly after exercise. Conclusion: These findings indicate that, in moderately trained athletes, postexercise hypotension is associated primarily with reduced cardiac output because of reduced stroke volume, suggesting venous pooling. In addition, the occurrence of hypotension is more frequent in trained subjects with lower cardiopulmonary fitness level or higher resting SBP

We have previously shown in a rat model that a single bout of high-intensity aerobic exercise 20 h 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 280 kPa at a rate of 100 kPa min(-1) breathing air and remaining at pressure for 80 min. The ascent rate was 9 m min(-1) with a 7 min stop at 130 kPa. 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 3 min, followed by exercise at 50% of maximum heart rate for 2 min; this was repeated eight times for a total exercise period of 40 min. Venous gas bubbles were monitored with an ultrasonic scanner every 20 min for 80 min 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.

The growing urge to breathe that occurs during breath-holding results in development of involuntary breathing movements (IBMs). The present study determined whether IBMs are initiated at critical levels of hypercapnia and/or hypoxia during maximal apnoea. Arterial blood gasses at the onset of IBM were monitored during maximal voluntary breath-holds. Eleven healthy men performed breath holds after breathing air, hyperoxic–normocapnia, hypoxic–normocapnia, and normoxic–hypercapnia. Pre-breathing of the gas mixtures facilitated the IBM onset, reducing the time-to-onset for ∼46% (hyperoxic condition) and for ∼80% (hypoxic condition) compared to the normoxic air breathing time. A strong correlation (R = 0.83, P = 0.002) between arterial partial pressure of CO2 ( Pa CO 2 ) at IBM onset after pre-breathing hyperoxic and hypercapnic gas mixtures was observed, suggesting the existence of a possible IBM Pa CO 2 threshold level of ∼6.5 ± 0.5 kPa. No clear “threshold” was observed for partial pressure of arterial O2 ( Pa O 2 ). However, we observed that IBM onset was influenced, in part, by an interaction between Pa O 2 and Pa CO 2 levels during maximal apnoea. This study demonstrated the complex interaction between arterial blood-gases and the physiological response to maximal breath holding.

The growing urge to breathe that occurs during breath-holding results in development of involuntary breathing movements (IBMs). The present study determined whether IBMs are initiated at critical levels of hypercapnia and/or hypoxia during maximal apnoea. Arterial blood gasses at the onset of IBM were monitored during maximal voluntary breath-holds. Eleven healthy men performed breath holds after breathing air, hyperoxic-normocapnia, hypoxic-normocapnia, and normoxic-hypercapnia. Pre-breathing of the gas mixtures facilitated the IBM onset, reducing the time-to-onset for ∼46% (hyperoxic condition) and for ∼80% (hypoxic condition) compared to the normoxic air breathing time. A strong correlation (R=0.83, P=0.002) between arterial partial pressure of CO₂ (PaCO₂) at IBM onset after pre-breathing hyperoxic and hypercapnic gas mixtures was observed, suggesting the existence of a possible IBM PaCO₂ threshold level of ∼6.5 ± 0.5 kPa. No clear "threshold" was observed for partial pressure of arterial O₂(PaO₂). However, we observed that IBM onset was influenced, in part, by an interaction between PaO₂ and PaCO₂ levels during maximal apnoea. This study demonstrated the complex interaction between arterial blood-gases and the physiological response to maximal breath holding.

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.

Apnea divers increase intrathoracic pressure voluntarily by taking a deep breath followed by glossopharyngeal insufflation. Because apnea divers sometimes experience hypotension and syncope during the maneuver, they may serve as a model to study the mechanisms of syncope. We recorded changes in hemodynamics and sympathetic vasomotor tone with microneurography during breath holding with glossopharyngeal insufflation. Five men became hypotensive and fainted during breath holding with glossopharyngeal insufflation within the first minute. In four divers, heart rate dropped suddenly to a minimum of 38 ± 4 beats/min. Therefore, cardioinhibitory syncope was more common than low cardiac output syncope.

Involuntary apnea episodes in obstructive sleep apnea patients result in selective potentiation of peripheral chemoreceptor regulation of sympathetic vasomotor tone. Breath-hold diving is associated with repeated "voluntary" apnea episodes and massive arterial oxygen desaturation, which could also perturb chemoreflex function. We measured ventilation, heart rate, blood pressure, cardiac stroke volume, and muscle sympathetic nerve activity (MSNA) during isocapnic hypoxia in 11 breath-hold divers and eleven matched control subjects. The study was carried out at least 1 month after intense apnea training. Baseline MSNA frequency was 30 +/- 4 bursts/min in control subjects and 31 +/- 7 bursts/min in divers (ns). During hypoxia MSNA frequency and total activity increased similarly in both groups (30 and 66% in controls and 27 and 60% in divers, respectively). MSNA remained increased after termination of hypoxia and approached baseline measurements after 20 min. 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-induced tachycardia drove an increase in cardiac output whereas total peripheral resistance decreased. Blood pressure remained unchanged. We conclude that after the end of intensive training/competition periods, apnea divers show normal peripheral chemoreflex regulation of ventilation and sympathetic vasomotor tone. Although voluntary apnea may not lead to sustained changes in sympathetic nervous system regulation, we cannot exclude the possibility that repeated sympathetic activation elicited by voluntary apnea imposes a burden on the cardiovascular system.

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.

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.

Hypercapnic cerebrovascular reactivity is decreased in obstructive sleep apnea and congestive heart disease patients. Ventilatory response to hypercapnia and/or hypoxia is blunted in apnea divers, whereas cerebrovascular reactivity to hypercapnia is presently unknown. We hypothesized that cerebrovascular reactivity to hypercapnia is increased in elite apnea divers, compared to control subjects, as a part of the O2 conserving mechanism to maintain adequate brain O2 supply. In the present study we determined cerebrovascular reactivity by measuring change in middle cerebral artery velocity per mmHg change in PETCO2 in response to two hyperoxic hypercapnia rebreathing maneuvers in seven elite apnea divers and seven control subjects. Ventilatory response to hypercapnia was blunted in divers compared to controls. Hypercapnia-induced ventilation increase was significantly lower in divers due to lower respiratory frequency. Cerebrovascular reactivity was unchanged in both groups (3.7± 1.4 vs 3.4± 1.3 %/mmHg PETCO2 in divers and controls) and the same was found for cerebral vascular resistance and a time for middle cerebral artery velocity recovery to baseline value. Results indicate that the regulation of the cerebral circulation in response to hypercapnia shows no difference between divers and controls serving as protective mechanism against chronic intermittent cerebral hypoxia/hypercapnia.

We report a case of right-to-left intrapulmonary (IP) shunting of venous gas bubbles at a high level of exercise after diving. The diagnosis was made using a 4-chamber view of the heart via echocardiography during exercise. This case is the first in which we could find evidence of IP shunt recruitment during exercise after diving, and the bubble grade was the highest ever seen in our laboratory. Venous bubbles crossing over through IP shunts during exercise after diving is a very rare event.

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 (approximately 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 (P0.001), 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.

The effect of post-dive exercise on bubble formation remains controversial, although the current practice of divers and aviators is to avoid strenuous exercise after diving. Previously, we have shown that exercising 24 h before a dive, or during a decompression stop, significantly reduces bubble formation in man. The objective of this study was to determine whether a short period of strenuous post-dive exercise promotes venous bubble formation.Seven male military divers performed an open-sea field dive to a maximum depth of 30 m for 30 min. At maximum depth, subjects performed mild underwater fin swimming, followed by standard decompression. Diving was followed by a post-dive exercise session consisting of short, strenuous incremental upright cycle ergometry, up to 85% of maximal oxygen uptake, for about 10 min. Subjects were monitored for venous gas bubbles in the right heart with an echo-imaging system starting 20 min post-dive while in the supine position, during cycle ergometry in the seated upright position, and immediately after exercise in a supine position.The average number of bubbles was 1.5 +/- 1.4 bubbles x cm(-2) 20 min after diving. Changes in posture from supine to seated upright resulted in significant reduction of bubbles to 0.6 +/- 1.3 bubbles x cm(-2) (p = 0.043), with further reduction to 0.2 +/- 0.3 bubbles x cm(-2) at the end of exercise (p = 0.02). No cases of DCS or intra-pulmonary shunt were observed during or following post-dive exercise.These results suggest that post-dive strenuous exercise after a single field dive reduces post-dive gas bubble formation in well-trained military divers. Additional findings are needed for normal sports divers.

Venous gas emboli are frequently observed in divers even if proper decompression procedures are followed. This study was initiated to determine if pulmonary artery pressure increases in asymptomatic divers, which could increase the risk of arterial embolization due to passage of venous gas emboli from the right to the left side of the heart. Recordings of venous gas emboli and estimation of pulmonary artery pressure by non-invasive transthoracic echocardiography were applied in 10 recreational scuba diving volunteers before and 20,40,60, and 80 min after simulated dives to 18 m (80 min bottom time) in a hyperbaric chamber. The ratio between pulmonary artery acceleration time and right ventricular ejection time was used as an estimate of pulmonary artery pressure. None of investigated divers had signs of decompression sickness. Despite the post-dive presence of the venous gas emboli, measured in the region of the pulmonary valve annulus (mean = 1.71 bubbles . cm -2 , 40 min after dive), the ratio between pulmonary artery acceleration time and right ventricular ejection time did not decrease, but actually increased (from 0.43 ± 0.06 to 0.49 ± 0.06, 40 min after dive; p < 0.05), suggesting a decrease in pulmonary artery pressure after the dive. We conclude that diving-induced venous gas bubbles do not cause significant changes in the central circulation which could increase the risk of arterial embolization.

We have previously shown in a rat model that a single bout of high intensity aerobic exercise 20 hours before a simulated dive reduces bubble formation and after dive protects from lethal decompression sickness. The present study investigates the importance of these findings in man. Twelve healthy, male divers were compressed in a hyperbaric chamber to 280 kPa at a rate of 100 kPa · ; min-1 breathing air, remaining at pressure for 80 minutes. The ascent rate was 9 m · ; min-1 with a seven minutes stop at 130 kPa. Each diver underwent two randomly assigned simulated dives, with and without preceding exercise. A single interval exercise performed 24 hours before the dive consisted of treadmill running at 90% of maximum heart rate for three minutes followed by exercise at 50% of maximum heart rate for two minutes ; this was repeated eight times for a total exercise period of 40 minutes. Venous gas bubbles were monitored with an ultrasonic scanner every 20 minutes for 80 minutes after reaching surface pressure. The study demonstrated that a single bout of strenuous exercise 24 hours before a dive to 18 meters of seawater significantly reduced the average number of bubbles in the pulmonary artery from 0.98 to 0.22 bubbles/cm2 (p = 0.006) compared to dives without preceding exercise. The maximum bubble grade 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 novel approach to prevent serious decompression sickness.

We tested the hypothesis that peripheral chemoreceptor function in response to hypoxia is normal in breath-hold divers (BHD) after detraining period. We compared ventilatory, sympathetic (MSNA), heart rate and blood pressure responses to isocapnic hypoxia in 11 BHD and 11 control subjects. The study was carried out at least one month after all divers finished most intensive apnea training. After baseline period for instrumentation, subjects breathed isocapnic hypoxic mixture to reduce arterial saturation to 0.8. During hypoxia burst frequency (MSNAf) and total activity (MSNAt, au/min) increased similarly in both groups (27% and 60% in BHD and 30% and 66% in controls), respectively. Increased MSNAf and MSNAt returned to baseline after 20 min after termination of hypoxia. Hypoxia-induced stimulation of minute ventilation was similar in both groups. Cardiac output was increased during hypoxia and since mean blood pressure was unchanged, total peripheral resistance was similarly reduced in both groups. We conclude that elite divers at least 1 month after the end of intensive training/competition period have normal peripheral chemosensitivity without any ventilatory, hemodynamic and autonomic differences from those observed in control subjects.