Effect of 4 weeks of aerobic or resistance exercise training on arterial stiffness, blood flow and blood pressure in pre- and stage-1 hypertensives.

The benefits of aerobic exercise (AE) training on blood pressure (BP) and arterial stiffness are well established, but the effects of resistance training are less well delineated. The purpose of this study was to determine the impact of resistance vs aerobic training on haemodynamics and arterial stiffness. Thirty pre- or stage-1 essential hypertensives (20 men and 10 women), not on any medications, were recruited (age: 48.2 +/- 1.3 years) and randomly assigned to 4 weeks of either resistance (RE) or AE training. Before and after training, BP, arterial stiffness (pulse wave velocity (PWV)) and vasodilatory capacity (VC) were measured. Resting systolic BP (SBP) decreased following both training modes (SBP: RE, pre 136 +/- 2.9 vs. post 132 +/- 3.4; AE, pre 141 +/- 3.8 vs. post 136 +/- 3.4 mm Hg, P = 0.005; diastolic BP: RE, pre 78 +/- 1.3 vs post 74 +/- 1.6; AE, pre 80 +/- 1.6 vs. post 77 +/- 1.7 mm Hg, P = 0.001). Central PWV increased (P = 0.0001) following RE (11 +/- 0.9-12.7 +/- 0.9 ms(-1)) but decreased after AE (12.1 +/- 0.8-11.1 +/- 0.8 m s(-1). Peripheral PWV also increased (P = 0.013) following RE (RE, pre 11.5 +/- 0.8 vs. post 12.5 +/- 0.7 ms(-1)) and decreased after AE (AE, pre 12.6 +/- 0.8 vs post 11.6 +/- 0.7 m s(-1)). The VC area under the curve (VC(AUC)) increased more with RE than that with AE (RE, pre 76 +/- 8.0 vs. post 131.1 +/- 11.6; AE, pre 82.7 +/- 8.0 vs. post 110.1 +/- 11.6 ml per min per s per 100 ml, P = 0.001). Further, peak VC (VCpeak) increased more following resistance training compared to aerobic training (RE, pre 17 +/- 1.9 vs. post 25.8 +/- 2.1; AE, pre 19.2 +/- 8.4 vs post 22.9 +/- 8.4 ml per min per s per 100 ml, P = 0.005). Although both RE and AE training decreased BP, the change in pressure may be due to different mechanisms.

Oral arginine attenuates the growth hormone response to resistance exercise.

This study investigated the combined effect of resistance exercise and arginine ingestion on spontaneous growth hormone (GH) release. Eight healthy male subjects were studied randomly on four separate occasions [placebo, arginine (Arg), placebo + exercise (Ex), arginine + exercise (Arg+Ex)]. Subjects had blood sampled every 10 min for 3.5 h. After baseline sampling (30 min), subjects ingested a 7-g dose of arginine or placebo (blinded, randomly assigned). On the exercise days, the subject performed 3 sets of 9 exercises, 10 repetitions at 80% one repetition maximum. Resting GH concentrations were similar on each study day. Integrated GH area under the curve was significantly higher on the Ex day (508.7 +/- 169.6 min.ng/ml; P < 0.05) than on any of the other study days. Arg+Ex (260.5 +/- 76.8 min.ng/ml) resulted in a greater response than the placebo day but not significantly greater than the Arg day. The GH half-life and half duration were not influenced by the stimulus administered. The GH secretory burst mass was larger, but not significantly, on the Arg, Ex, and Arg+Ex day than the placebo day. Endogenous GH production rate (Ex > Arg+Ex > Arg > placebo) was greater on the Ex and Arg+Ex day than on the placebo day (P < 0.05) but there were no differences between the Ex and Arg+Ex day. Oral arginine alone (7 g) stimulated GH release, but a greater GH response was seen with exercise alone. The combined effect of arginine before exercise attenuates the GH response. Autonegative feedback possibly causes a refractory period such that when the two stimuli are presented there will be suppression of the somatotrope.

Reduction of plasma aldosterone and arterial stiffness in obese pre- and stage1 hypertensive subjects after aerobic exercise.

Obesity-related hypertension is associated with increased activity of the renin-angiotensin-aldosterone system (RAAS), increasing arterial stiffness. Aerobic exercise decreases pulse wave velocity (PWV), therefore a treatment option for hypertension and obesity. Assess RAAS activity and PWV before and after 4 weeks of aerobic training in unmedicated, pre-to-stage-1 hypertensives. Ten obese subjects (52±3.2 years, body mass index=33.5±1.4) performed 30 min of aerobic exercise on a treadmill 3 days per week at 65% of peak oxygen consumption (VO2peak). Descriptive characteristics, systolic and diastolic blood pressure (SBP and DBP), PWV, and a blood draw was performed at baseline, following the 4-week control and training interventions. No differences in descriptive characteristics during the control period were observed, however, a significant decrease in plasma aldosterone (ALDO) (255.4±75 to 215.8±66 pg ml(-1), P=0.001), SBP (140±12 to 136±10.4 mm Hg; P=0.02), DBP (89±4.2 to 85±6.3 mm Hg; P=0.03) and central PWV (11.2±0.6 to 9.8±0.8 m s(-1); P=0.04) was shown pre-to-post exercise training. Four weeks of moderate-intensity aerobic training in obese, hypertensives decreases plasma ALDO independently of body weight and is significantly correlated to decreases in PWV reductions.

Cardiac autonomic function and baroreflex changes following 4 weeks of resistance versus aerobic training in individuals with pre-hypertension.

AIM: Cardiac autonomic modulation and baroreflex sensitivity (BRS) are altered in individuals with hypertension. Aerobic exercise (AE) training has been shown to improve both measures, yet little is known about the effects of resistance exercise (RE). The purpose of this study was to examine the heart rate variability (HRV) and BRS following 4 weeks of resistance or aerobic training in a population with borderline high blood pressure (BP). METHODS: Twenty-nine mild hypertensives were recruited and randomly assigned to 4 weeks of RE or AE training. Before and after training, resting measures of HRV frequencies and BRS were obtained. RESULTS: There was a significant decrease in resting systolic BP for both exercise training modes (RE 136 +/- 3.0 pre- to 132 +/- 3.4 post-training vs. AE 142 +/- 4.0 pre- to 137 +/- 3.6 mmHg post-training, P = 0.019). Diastolic BP decreased significantly following both exercise training modes (RE 78 +/- 1.31 pre to 74 +/- 1.1 post vs. AE 80 +/- 1.7 pre to 77 +/- 1.6 mmHg post, P = 0.002). A significant time by training mode interaction for low frequency : high frequency (HF) ratio (P = 0.017) with AE decreasing the ratio (275.21 +/- 67.28 to 161.26 +/- 61.49) and RE increasing this ratio (143.73 +/- 65.00 to 227.83 +/- 59.41). Natural log-transformed (ln) HRV values showed a time-by-training mode interaction for ln HF (P = 0.05) as ln HF increased (4.7 +/- 0.38 to 5.4 +/- 0.35 ms(2)) following AE and decreased (5.98 +/- 0.37 to 5.76 +/- 0.42 ms(2)) following RE. BRS increased following aerobic training and decreased after resistance training (6.74 +/- 1.2 to 7.94 +/- 1.3 and 10.44 +/- 1.2 to 9.1 +/- 1.2 ms mmHg(-1) respectively, P = 0.021). CONCLUSIONS: Aerobic exercise improved the autonomic nervous system (increasing vagal tone, reducing sympathovagal balance while increasing BRS) while RE showed no improvements in cardiac autonomic tone and decreased BRS.

Arterial stiffness and baroreflex sensitivity following bouts of aerobic and resistance exercise.

We examined arterial stiffness, baroreflex sensitivity (BRS), and systolic arterial pressure (SAP) variability after an acute bout of aerobic exercise compared to resistance exercise. We hypothesized that arterial stiffness would be reduced after aerobic exercise, while it would be increased after resistance exercise, and these alterations would be associated with differential changes in BRS and SAP variability. Arterial stiffness, BRS, and SAP variability were assessed before and 20 min after a bout of aerobic exercise and resistance exercise in 13 male participants. Pulse wave velocity (PWV) was used to measure central (carotid-femoral) and peripheral (femoral-dorsalis pedis) arterial stiffness. BRS was derived via the sequence technique. Spectral decomposition of beat-to-beat SAP variability was used as an estimate of sympathetic vasomotor tone. A mode-by-time interaction (p < 0.001) was detected for central PWV, due to an increase in PWV (p < 0.05) following resistance exercise and a decrease in PWV following aerobic exercise (p < 0.05). A mode-by-time interaction was also detected for peripheral PWV (p < 0.05), due to a decrease in peripheral PWV following aerobic exercise (p < 0.05) with no change following resistance exercise. BRS was significantly lower following resistance compared with aerobic exercise (p < 0.004). SAP variability increased following resistance exercise (p < 0.05) but there was no interaction. In conclusion, aerobic exercise decreased both central and peripheral arterial stiffness, while resistance exercise significantly increased central arterial stiffness only. BRS was reduced after both bouts of exercise, but significantly greater reductions were seen following resistance exercise.