24-h cardiac autonomic profile after exercise in sedentary subjects.

Most studies regarding the impact of exercise intensity on cardiac autonomic regulation were conducted with athletes and used exercise intensities exceeding those recommended by position stands. We evaluated the influence of exercise intensity in a typical ACSM-aerobic session on 24-h cardiac autonomic modulation in sedentary subjects. Ten healthy sedentary subjects participated in the 3-day study. On 2 days, subjects performed a moderate- or high-intensity aerobic exercise session (MI, HI). The post-exercise protocol consisted of a continuous electrocardiographic recording for 1 h at the laboratory plus 23 h under ambulatory conditions. On the third day 24-h electrocardiographic recording was done without prior exercise (NPE). Heart rate (HR) and frequency-domain parameters (LF, HF) of heart rate variability were evaluated during the entire recovery period. Higher values of HR and lower values of HF and LF were observed throughout the first hour after the HI compared with the MI session. This difference was not observed after in ambulatory awake condition, but reappeared during sleep, when HF values after HI were lower compared with the NPE and MI (p<0.05). Even within the submaximal intensity-range of a typical exercise session, the intensity of exercise influences the post-exercise cardiac autonomic modulation in sedentary subjects.

Impaired post exercise heart rate recovery in anabolic steroid users.

Previous study showed that muscle sympathetic nerve activity (MSNA) was augmented in anabolic steroids users (AASU). In the present study, we tested the hypothesis that the heart rate (HR) responses after maximal exercise testing would be reduced in AASU. 10 male AASU and 10 AAS nonusers (AASNU) were studied. Cardiopulmonary exercise was performed to assess the functional capacity and heart rate recovery. MSNA was recorded directly from the peroneal nerve by microneurography technique. Peak oxygen consumption (VO2) was lower in AASU compared to AASNU (43.66±2.24 vs. 52.70±1.68 ml/kg/min, P=0.005). HR recovery (HRR) at first and second minute was lower in AASU than AASNU (21±2 vs. 27±2 bpm, P=0.02 and 37±4 vs. 45±2 bpm, P=0.05, respectively). MSNA was higher in AASU than AASNU (29±3 vs. 20±1 bursts/min, P=0.01). Further analysis showed a correlation between HRR and MSNA (r=- 0.64, P=0.02), HRR at first minute and peak VO2 (r=0.70, P=0.01) and HRR at second minute and peak VO2 (r=0.62, P=0.02). The exacerbated sympathetic outflow associated with a lower parasympathetic activation after maximal exercise, which impairs heart rate recovery, strengthens the idea of autonomic imbalance in AASU.

Effects of diet and exercise training on neurovascular control during mental stress in obese women.

Since neurovascular control is altered in obese subjects, we hypothesized that weight loss by diet (D) or diet plus exercise training (D + ET) would improve neurovascular control during mental stress in obese women. In a study with a dietary reduction of 600 kcal/day with or without exercise training for 4 months, 53 obese women were subdivided in D (N = 22, 33 +/- 1 years, BMI 34 +/- 1 kg/m2), D + ET (N = 22, 33 +/- 1 years, BMI 33 +/- 1 kg/m2), and nonadherent (NA, N = 9, 35 +/- 2 years, BMI 33 +/- 1 kg/m2) groups. Muscle sympathetic nerve activity (MSNA) was measured by microneurography and forearm blood flow by venous occlusion plethysmography. Mental stress was elicited by a 3-min Stroop color word test. Weight loss was similar between D and D + ET groups (87 +/- 2 vs 79 +/- 2 and 85 +/- 2 vs 76 +/- 2 kg, respectively, P < 0.05) with a significant reduction in MSNA during mental stress (58 +/- 2 vs 50 +/- 2, P = 0.0001, and 59 +/- 3 vs 50 +/- 2 bursts/100 beats, P = 0.0001, respectively), although the magnitude of the response was unchanged. Forearm vascular conductance during mental stress was significantly increased only in D + ET (2.74 +/- 0.22 vs 3.52 +/- 0.19 units, P = 0.02). Weight loss reduces MSNA during mental stress in obese women. The increase in forearm vascular conductance after weight loss provides convincing evidence for D + ET interventions as a nonpharmacologic therapy of human obesity.

Effects of diet and exercise training on neurovascular control during mental stress in obese women

Since neurovascular control is altered in obese subjects, we hypothesized that weight loss by diet (D) or diet plus exercise training (D + ET) would improve neurovascular control during mental stress in obese women. In a study with a dietary reduction of 600 kcal/day with or without exercise training for 4 months, 53 obese women were subdivided in D (N = 22, 33 ± 1 years, BMI 34 ± 1 kg/m²), D + ET (N = 22, 33 ± 1 years, BMI 33 ± 1 kg/m²), and nonadherent (NA, N = 9, 35 ± 2 years, BMI 33 ± 1 kg/m²) groups. Muscle sympathetic nerve activity (MSNA) was measured by microneurography and forearm blood flow by venous occlusion plethysmography. Mental stress was elicited by a 3-min Stroop color word test. Weight loss was similar between D and D + ET groups (87 ± 2 vs 79 ± 2 and 85 ± 2 vs 76 ± 2 kg, respectively, P < 0.05) with a significant reduction in MSNA during mental stress (58 ± 2 vs 50 ± 2, P = 0.0001, and 59 ± 3 vs 50 ± 2 bursts/100 beats, P = 0.0001, respectively), although the magnitude of the response was unchanged. Forearm vascular conductance during mental stress was significantly increased only in D + ET (2.74 ± 0.22 vs 3.52 ± 0.19 units, P = 0.02). Weight loss reduces MSNA during mental stress in obese women. The increase in forearm vascular conductance after weight loss provides convincing evidence for D + ET interventions as a nonpharmacologic therapy of human obesity.