Low- and high-intensity resistance exercises cause systolic post-exercise hypotension; however, only low-intensity exercise decreases diastolic BP. BP fall is due to CO decrease that is not compensated by SVR increase. BP fall is accompanied by HR increase due to an increase in sympathetic modulation to the heart.

In hypertensive women receiving captopril, a single bout of low-intensity resistance exercise reduces blood pressure. This reduction persists for 10 h, during the awake period, while patients were engaged in their daily living activities. It was greater in patients with higher ambulatory blood pressure.

Hypertension is a ubiquitous and serious disease. Regular exercise has been recommended as a strategy for the prevention and treatment of hypertension because of its effects in reducing clinical blood pressure; however, ambulatory blood pressure is a better predictor of target-organ damage than clinical blood pressure, and therefore studying the effects of exercise on ambulatory blood pressure is important as well. Moreover, different kinds of exercise might produce distinct effects that might differ between normotensive and hypertensive subjects.The aim of this study was to review the current literature on the acute and chronic effects of aerobic and resistance exercise on ambulatory blood pressure in normotensive and hypertensive subjects. It has been conclusively shown that a single episode of aerobic exercise reduces ambulatory blood pressure in hypertensive patients. Similarly, regular aerobic training also decreases ambulatory blood pressure in hypertensive individuals. In contrast, data on the effects of resistance exercise is both scarce and controversial. Nevertheless, studies suggest that resistance exercise might acutely decrease ambulatory blood pressure after exercise, and that this effect seems to be greater after low-intensity exercise and in patients receiving anti-hypertensive drugs. On the other hand, only two studies investigating resistance training in hypertensive patients have been conducted, and neither has demonstrated any hypotensive effect. Thus, based on current knowledge, aerobic training should be recommended to decrease ambulatory blood pressure in hypertensive individuals, while resistance exercise could be prescribed as a complementary strategy.

The post-exercise ambulatory blood pressure fall observed in normotensive and hypertensive humans depends on individual characteristics. Moreover, in both normotensive and hypertensive humans, post-exercise ambulatory hypotension is greater in subjects with a higher initial blood pressure level.

OBJECTIVE:The aim of this study was to describe blood pressure responses during resistance exercise in hypertensive subjects and to determine whether an exercise protocol alters these responses.INTRODUCTION:Resistance exercise has been recommended as a complement for aerobic exercise for hypertensive patients. However, blood pressure changes during this kind of exercise have been poorly investigated in hypertensives, despite multiple studies of normotensives demonstrating significant increases in blood pressure.METHODS:Ten hypertensive and ten normotensive subjects performed, in random order, two different exercise protocols, composed by three sets of the knee extension exercise conducted to exhaustion: 40% of the 1-repetition maximum (1RM) with a 45-s rest between sets, and 80% of 1RM with a 90-s rest between sets. Radial intra-arterial blood pressure was measured before and throughout each protocol.RESULTS:Compared with normotensives, hypertensives displayed greater increases in systolic BP during exercise at 80% (+80±3 vs. +62±2 mmHg, P<0.05) and at 40% of 1RM (+75±3 vs. +67±3 mmHg, P<0.05). In both exercise protocols, systolic blood pressure returned to baseline during the rest periods between sets in the normotensives; however, in the hypertensives, BP remained slightly elevated at 40% of 1RM. During rest periods, diastolic blood pressure returned to baseline in hypertensives and dropped below baseline in normotensives.CONCLUSION:Resistance exercise increased systolic blood pressure considerably more in hypertensives than in normotensives, and this increase was greater when lower-intensity exercise was performed to the point of exhaustion.

Alcohol intake has been shown to worsen obstructive sleep apnea and increase nocturnal hypoxemia. The mechanisms of this action are unclear. Animal studies suggest that a reduction in chemoreflex sensitivity may be implicated. Using a double-blind, randomized, vehicle-controlled design, we tested the hypothesis that oral alcohol intake depresses chemoreflex sensitivity in humans. We examined the effects of oral alcohol intake (1.0 g/kg body wt) on blood pressure, heart rate, heart rate variability, muscle sympathetic nerve activity, forearm vascular resistance, and minute ventilation in 16 normal male subjects. Peripheral and central chemoreflex sensitivity were measured in response to hypoxia (n = 10) and hypercapnia (n = 6), respectively. Plasma alcohol increased from 0 to 23.2 +/- 1.5 mmol/L (107 +/- 7 mg/dL) at 60 minutes and 20.2 +/- 1 mmol/L (93 +/- 4 mg/dL) at 85 minutes after alcohol intake (P < .0001). Alcohol induced an increase in heart rate from 59 +/- 2 to 66 +/- 2 beats per minute (P < .01) and increased the ratio of low- to high-frequency variability of heart rate (P < .05). Although alcohol increased sympathetic nerve activity by up to 239 +/- 22% of baseline values (P < .01), forearm vascular resistance after alcohol was lower than that after vehicle (P < .05). Blood pressure did not increase compared with the vehicle session. Oxygen saturation during hypoxia after alcohol was 4 +/- 1% lower than it was during hypoxia after vehicle (P < .05) although arterial blood PO2 was unchanged. Alcohol did not affect the cardiovascular, sympathetic, or ventilatory responses to either hypoxia or hypercapnia. Acute increases in plasma alcohol increase heart rate and sympathetic nerve activity; blood pressure is not increased, probably because of vasodilator effects of alcohol. Alcohol does not alter chemoreflex responses to hypoxia or hypercapnia; thus, alterations in chemoreflex sensitivity are unlikely to explain the effects of alcohol on sleep apnea. Alcohol may reduce the affinity of hemoglobin for oxygen.

To compare post-resistance exercise hypotension (PREH) and its mechanisms in normotensive and hypertensive individuals, 14 normotensives and 12 hypertensives underwent two experimental sessions: control (rest) and exercise (seven exercises, three sets, 50% of one repetition maximum). Hemodynamic and autonomic clinic measurements were taken before (Pre) and at two moments post-interventions (Post 1: between 30 and 60 min; Post 2: after 7 h). Ambulatory blood pressure (BP) was monitored for 24 h. At Post 1, exercise decreased systolic BP similarly in normotensives and hypertensives (-8 ± 2 vs -13 ± 2 mmHg, P > 0.05), whereas diastolic BP decreased more in hypertensives (-4 ± 1 vs -9 ± 1 mmHg, P < 0.05). Cardiac output and systemic vascular resistance did not change in normotensives and hypertensives (0.0 ± 0.3 vs 0.0 ± 0.3 L/min; -1 ± 1 vs -2 ± 2 U, P > 0.05). After exercise, heart rate (+13 ± 3 vs +13 ± 2 bpm) and its variability (low- to high-frequency components ratio, 1.9 ± 0.4 vs +1.4 ± 0.3) increased whereas stroke volume (-14 ± 5 vs -11 ± 5 mL) decreased similarly in normotensives and hypertensives (all, P > 0.05). At Post 2, all variables returned to pre-intervention, and ambulatory data were similar between sessions. Thus, a session of resistance exercise promoted PREH in normotensives and hypertensives. Although this PREH was greater in hypertensives, it did not last during the ambulatory period, which limits its clinical relevance. In addition, the mechanisms of PREH were similar in hypertensives and normotensives.

Indapamide-SR-based therapy is equivalent to enalapril-based therapy in reducing microalbuminuria with effective blood pressure reduction in patients with hypertension and type 2 diabetes.