European journal of applied physiology
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Eur. J. Appl. Physiol. · Feb 2012
ReviewVenous gas embolism as a predictive tool for improving CNS decompression safety.
A key process in the pathophysiological steps leading to decompression sickness (DCS) is the formation of inert gas bubbles. The adverse effects of decompression are still not fully understood, but it seems reasonable to suggest that the formation of venous gas emboli (VGE) and their effects on the endothelium may be the central mechanism leading to central nervous system (CNS) damage. Hence, VGE might also have impact on the long-term health effects of diving. ⋯ We observed that NO reduced VGE during decompression, and pharmacological blocking of NO production increased VGE formation following a dive. The importance of micro-nuclei for the formation of VGE and how it can be possible to manipulate the formation of VGE are discussed together with the effects of VGE on the organism. In the last part of the review we introduce our thoughts for the future, and how the enigma of DCS should be approached.
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Eur. J. Appl. Physiol. · Feb 2012
Acute and chronic loading of sodium bicarbonate in highly trained swimmers.
In the present study, 200-m swim time in highly trained male swimmers was measured on two consecutive days (Trial 1 and Trial 2) and under three conditions [(1) acute loading, AcL; (2) chronic loading, ChL; (3) Placebo, PLA]. No sodium bicarbonate (NaHCO(3)) was administered between Trial 1 and Trial 2 under each condition. ⋯ We did not observe any difference in blood [La(-)] between the three conditions at any stage post-exercise (P > 0.05). The results indicate that acute and chronic loading of NaHCO(3) does not improve 200-m swim time in highly trained male swimmers.
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Eur. J. Appl. Physiol. · Feb 2012
Artificial gravity training reduces bed rest-induced cardiovascular deconditioning.
We studied 15 men (8 treatment, 7 control) before and after 21 days of 6º head-down tilt to determine whether daily, 1-h exposures to 1.0 G(z) (at the heart) artificial gravity (AG) would prevent bed rest-induced cardiovascular deconditioning. Testing included echocardiographic analysis of cardiac function, plasma volume (PV), aerobic power (VO(2)pk) and cardiovascular and neuroendocrine responses to 80º head-up tilt (HUT). Data collected during HUT were ECG, stroke volume (SV), blood pressure (BP) and blood for catecholamines and vasoactive hormones. ⋯ AG prevented increases in pre-tilt levels of plasma renin activity [pre- to post-bed rest change; control: 1.53 ± 0.23, AG: -0.07 ± 0.34 ng/mL/h (p = 0.001)] and angiotensin II [pre- to post-bed rest change; control: 3.00 ± 1.04, AG: -0.63 ± 0.81 pg/mL (p = 0.009)] and increased HUT aldosterone [post-bed rest; control: 107 ± 30 pg/mL, AG: 229 ± 68 pg/mL (p = 0.045)] and norepinephrine [post-bed rest; control: 453 ± 107, AG: 732 ± 131 pg/mL (p = 0.003)]. We conclude that AG can mitigate some aspects of bed rest-induced cardiovascular deconditioning, including orthostatic intolerance and aerobic power. Mechanisms of improvement were not cardiac-mediated, but likely through improved sympathetic responsiveness to orthostatic stress.