Abstract
PURPOSE: Endurance exercise training in young adults seems to cause more incidence of orthostatic intolerance. This study was sought to test the hypothesis that aerobic exercise training prevented age-related cardiovascular deconditioning without compromising orthostatic tolerance (OT) in elderly humans. METHODS: Eight healthy sedentary volunteers (67.0±1.7 years old, 4 women) participated in 1-year training (stationary bicycle and/or treadmill) at 65%-70% of the individual’s peak heart rate (HRpeak). Peak O2 uptake (VO2peak) and HRpeak were determined by a maximal stress test using a cycle ergometer. Resting carotid baroreceptor (CBR) control of HR and mean arterial pressure (MAP) were assessed by a neck pressure-suction protocol and the maximal gains (Gmax) were derived from a logistical fitting. OT was tested using lower-body negative pressure (LBNP) graded to -50 mmHg; the sum of the product of LBNP intensity and time (mmHg•min) was calculated as cumulative OT index (COTI). RESULTS: Training significantly (P <0.05) increased VO2peak (before vs after: 22.40±1.10 vs 27.56±1.44 ml/min/kg) and HRpeak (154±4 vs 159±3 beats/min); decreased resting HR (65±5 vs 59±5 beats/min) and MAP (99±2 vs 87±2 mmHg). CBR stimulus-response curves showed a leftward shift with an increase in CBR-HR Gmax (from -0.129±0.023 to -0.269±0.035 bpm/mmHg, P=0.010). COTI was increased (P = 0.025) from 767±68 mmHg•min pre-training to 946±44 mmHg•min post-training. CONCLUSIONS: Aerobic exercise training improves exercise tolerance and OT in elderly individuals. An increased OT is likely associated with an improved CBR function that has been reset to help maintain cerebral tissue oxygenation, i.e., cerebral perfusion, during LBNP.
Published Version
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