Both intensive training and bed confinement impair orthostatic tolerance, however, moderate training may exert beneficial effect on cardiovascular adjustment to gravitational stimuli. It was hypothesized that moderate training attenuates effects of bed rest. To test this assumption 24 healthy male volunteers aged 20.8±0.9 yrs were subjected to 6° head down bed rest (HDBR) for 3 days before and after 6 weeks of moderate endurance training. Before and after HDBR graded LBNP tests (-15, -30, -50 mmHg) were performed. During these tests heart rate (HR), stroke volume (SV), blood pressure (BP), plasma catecholamines, ACTH, adrenomedullin, atrial natriuretic peptide, plasma renin activity (PRA) and hematocrit were determined. HDBR did not systematically influence LBNP tolerance up to -50 mmHg, but it enhanced rates of reduction of SV, cardiac output and systolic BP and increased elevations of HR and PRA. Training did not alter significantly effects of HDBR on LBNP-induced changes in HR, SV, CO and TPR but it attenuated decrease in systolic BP and diminished increases in plasma noradrenaline and PRA. In conclusion, training has negligible effect on the HDBR-induced changes in central hemodynamics during LBNP but may increase vascular sensitivity to some vasoconstricting factors.
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Bed rest (BR) deconditioning causes excessive increase of exercise core body tempera-ture, while aerobic training improves exercise thermoregulation. The study was designed to determine whether 3 days of 6° head-down bed rest (HDBR) affects body temperature and sweating dynamics during exercise and, if so, whether endurance training before HDBR modifies these responses. Twelve healthy men (20.7±0.9 yrs, VO2max: 46±4 ml·kg-1·min-1) underwent HDBR twice: before and after 6 weeks of endurance training. Before and after HDBR, the subjects performed 45 min sitting cycle exercise at the same workload equal to 60% of VO2max determined before training. During exercise the VO2, HR, tympanic (Ttymp) and skin (Tsk) temperatures were recorded; sweating dynamics was assayed from a ventilated capsule on chest. Training increased VO2max by 12.1% (p<0.001). Resting Ttymp increased only after first HDBR (by 0.22 ± 0.08 °C, p<0.05), while exercise equilibrium levels of Ttymp were increased (p<0.05) by 0.21 ± 0.07 and 0.26 ± 0.08 °C after first and second HDBR, respectively. Exercise mean Tsk tended to be lower after both HDBR periods. Total sweat loss and time-course of sweating responses were similar in all exercise tests. The sweating threshold related to Ttymp was elevated (p<0.05) only after first HDBR. In conclusion: six-week training regimen prevents HDBR-induced elevation of core temperature (Ttymp) at rest but not during ex-ercise. The post-HDBR increases of Ttymp without changes in sweating rate and the tendency for lower Tsk suggest an early (<3d) influence of BR on skin blood flow.
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