Captopril does not Potentiate Post-Exercise Hypotension: A Randomized Crossover Study.

To evaluate whether captopril (3×50 mg/day) potentiates post-resistance exercise hypotension (PREH) in hypertensives (HT), 12 HT men received captopril and placebo for 4 weeks each in a double-blinded, randomized-crossover design. On each therapy, subjects underwent 2 sessions: Control (C - rest) and Resistance Exercise (RE - 7 exercises, 3 sets to moderate fatigue, 50% of 1 RM -repetition maximum). Measurements were taken before and after 30-60 min (Post1) and 7 h (Post2), and ambulatory blood pressure (BP) was monitored for 24 h. There were no differences in PREH characteristics and mechanisms between the placebo and captopril periods. At Post1, systolic/diastolic BP decreased significantly and similarly after RE with both therapies (Placebo=-13±2/-9±1 mmHg vs. Captopril=-12±2/-10±1 mmHg, P<0.05). RE reduced cardiac output in some subjects and systemic vascular resistance in others. Heart rate and cardiac sympathetic modulation increased, while stroke volume and baroreflex sensitivity decreased after RE (Placebo: +13±2 bpm, +21±5 nu, -11±5 ml, -4±2 ms/mmHg; Captopril: +13±2 bpm, +35±4 nu, 17±5 ml, -3±1 ms/mmHg, P<0.05). At Post2, all variables returned to pre-intervention values. Ambulatory BP was similar between the sessions. Thus, captopril did not potentiate the magnitude and duration of PREH in HT men, and it did not influence PREH mechanisms.

Physiological responses during active video games in spinal cord injury: a preliminary study.

OBJECTIVES: Investigate the physiological responses to active video games (AVG) in individuals with spinal cord injury by comparing oxygen consumption (VO2) and heart rate (HR) during an AVG session and at the ventilatory thresholds (i.e., anaerobic threshold and respiratory compensation point); and by calculating the session energy expenditure (EE). METHOD: Eight paraplegic individuals with spinal cord injury underwent cardiopulmonary exercise tests in an arm cycle ergometer to determine ventilatory thresholds. Then, they underwent three experimental sessions: two of AVG (4 sets of 3 min of Tennis and 4 min of Boxing) and one control (watching a movie). HR and VO2 were continuously measured, and the total energy expenditure was calculated from it. RESULTS: HR and VO2 were similar in both AVG sessions and higher than in the control session (p < .05). Mean HR and VO2 in Tennis and Boxing were, respectively, 100 ± 7 and 114 ± 9 bpm and 7.9 ± 1.2 and 10.3 ± 1.4 ml.kg-1.min-1.HR and VO2 during both games did not differ significantly from the anaerobic threshold (121 ± 2 bpm and 10.6 ± 1.0 ml.kg-1.min-1, p > .05). Mean energy expenditure during the AVG sessions was 2.4 METS, while the total was 136 kcal. CONCLUSION: The AVG generated an aerobic stimulus equivalent to the anaerobic threshold that increased basal metabolism 2.6 times, characterizing a low-intensity aerobic exercise.