No abstract

Hyperoxia causes hemodynamic alterations. We hypothesized that cardiovascular and autonomic control changes last beyond the end of hyperoxic period into normoxia. Ten healthy volunteers were randomized to breathe either medical air or 100% oxygen for 45 min in a double-blind study design. Measurements were performed before (baseline) and during gas exposure, and then 10, 30, 60, and 90 min after gas exposure. Hemodynamic changes were studied by Doppler echocardiography. Changes in cardiac and vasomotor autonomic control were evaluated through changes in spectral power of heart rate variability and blood pressure variability. Cardiac baroreflex sensitivity was assessed by the sequence method. Hyperoxia significantly decreased heart rate and increased the high frequency power of heart rate variability, suggesting a chemoreflex increase in vagal activity since the slope of cardiac baroreflex was significantly decreased during hyperoxia. Hyperoxia increased significantly the systemic vascular resistances and decreased the low frequency power of blood pressure variability, suggesting that hyperoxic vasoconstriction was not supported by an increase in vascular sympathetic stimulation. These changes lasted for 10 min after hyperoxia (p < 0.05). After the end of hyperoxic exposure, the shift of the power spectral distribution of heart rate variability toward a pattern of increased cardiac sympathetic activity lasted for 30 min (p < 0.05), reflecting a resuming of baseline autonomic balance. Cardiac output and stroke volume were significantly decreased during hyperoxia and returned to baseline values (10 min) later than heart rate. In conclusion, hyperoxia effects continue during return to normoxic breathing, but cardiac and vascular parameters followed different time courses of recovery.

Thermoneutral water immersion increases cardiac preload and changes the neuroendocrine settings of blood volume regulation. The resulting marked diuresis may lead to significant haemodynamic changes after the end of a prolonged water immersion. Ten volunteers underwent 6 h of complete thermoneutral water immersion. Changes in cardiovascular status were assessed 1 h and 16 h after water immersion. Haemodynamic changes were assessed by Doppler echocardiography. Arterial wall distensibility was estimated by pulse wave velocity analysis. One hour after water immersion, mean weight loss was 1.78 kg and urine volume amounted to 1.5 litres. Echocardiographic measurements evidenced a significant decrease in dimensions of the left cardiac chambers and inferior vena cava. The decreased cardiac preload was paralleled by a lower stroke volume and cardiac output. A peripheral vasoconstriction associated with a relative decrease in the lower limb blood flow was evidenced by an increase in carotid-pedal pulse wave velocity and by a decrease in ankle brachial index. Sixteen hours after water immersion, cardiac preload and cardiac output remained below baseline values and peripheral vascular tone was still higher than at baseline. Marked haemodynamic changes had not returned to baseline 16 h after water immersion. There is a need to design fluid-replacement protocols to improve this recovery.

Immersion, body cooling, hyperoxia, increased hydrostatic pressure and strenuous exercise likely combine to induce pulmonary oedema in patients without cardiac disease. This study underlines new physiopathological tracks related to the frequent occurrence of symptoms noticed in the last part of the ascent and a higher incidence in women.

In this pilot study, we wished to determine whether a 5-month multidisciplinary programme of a combined dietary-nutritional education-exercise intervention would have favourable effects on the health status of 18 obese adolescent girls. Before and after the clinical intervention, body composition and habitual physical activity were assessed by bioelectrical impedance and accelerometry, respectively. Aerobic fitness and substrate utilization were determined by gas exchange using an incremental field test that mimics habitual conditions. Despite a significantly (P < 0.001) greater loss of fat mass (-8.7 +/- 4.1 kg) compared with fat-free mass (-2.8 +/- 2.2 kg), energy expenditure at rest decreased by 9% following the intervention. Maximal oxygen consumption [Vdot]O2max related to fat-free mass increased by 7% (P < 0.05), whereas substrate utilization during exercise did not change following the intervention. Moderate and intense physical activity increased by 15% (+20 min . day(-1); P < 0.05) and 45% (+25 min . day(-1); P < 0.01), respectively. A significant relationship was observed between change in habitual physical activity and change in .[Vdot]O2max fat-free mass (r = 0.56, P = 0.01). The present multidisciplinary programme enhanced the loss of fat mass relative to fat-free mass but not sufficiently so to prevent a decline in metabolic rate during rest. Our results suggest a coupling in the improvement of aerobic fitness and habitual physical activity in obese adolescent girls, and hence an improvement in behaviour in relation to physical activity.

Data in the literature suggest that compared to dry-land exercise fin swimming might delay the activation of the anaerobic metabolism. To verify this hypothesis, we explored indirect indices such as the oxygen pulse (VO(2)/HR), carbon dioxide production (VCO(2)), and ventilatory threshold, comparing fin swimming exercise to dry-land cycling. Thirteen participants, experienced or inexperienced in fin swimming, completed an incremental fin swimming exercise and a maximal exercise on a cycloergometer with breath-by-breath measurements of heart rate (HR), ventilation (VE), tidal volume (VT), VO(2), VCO(2), and VO(2)/HR and determination of the ventilatory threshold and maximal oxygen uptake (VO(2)max). Compared to dry-land cycling exercise, fin swimming resulted in elevated or absent ventilatory threshold. Although VO(2)max did not differ in either condition, in fin swimming the maximal HR value was lower (-18%, p=0.0072), maximal VO(2)/HR higher (+20%, p=0.0325), and maximal VCO(2) lower (-17%, p=0.0071). We also measured significant reduction of VE, VT, and HR variations for the same VO(2) increase. This study suggests that the anaerobic muscle metabolism might be delayed in fin swimming. An attenuated chemoreflex drive to the heart and respiratory centres exerted by muscle metabolites might explain the depressed cardiopulmonary response to fin swimming.

No abstract

Cardiac changes induced by repeated breath-hold diving were investigated after a fish-catching diving competition. Eleven healthy subjects carried out repeated breath-hold dives at a mean maximal depth of 20 ± 2.7 msw (66 ± 9 fsw) during 5 h. One hour after the competition, the body mass loss was -1.7 ± 0.5 kg. Most of the breath-hold divers suffered from cold and although the core temperature remained normal, a decrease in cutaneous temperature was recorded in the extremities. Systolic blood pressure was reduced in both upper and lower limbs. Heart rate was unchanged, but left ventricular (LV) stroke volume was reduced leading to a decrease in cardiac output (-20%). Left atrial and LV diameters were significantly decreased. LV filling was assessed on a trans-mitral profile. An increase in the contribution of the atrial contraction to LV filling was observed. Right cavity diameters were increased. The cardiac autonomic alterations were in favor of sympathetic hyperactivity. After a fish-catching diving competition in cold water, alterations suggesting dehydration, contraction in plasma volume and sympathetic hyperactivity were observed. Furthermore, enlargements of right cavities were in favor of right ventricular strains. Repeated apnea and swimming in cold water may account for these alterations.