Poor sleep quality is associated with cardiac autonomic dysfunction in treated hypertensive men.

Hypertensives present cardiac autonomic dysfunction. Reduction in sleep quality increases blood pressure (BP) and favors hypertension development. Previous studies suggested a relationship between cardiovascular autonomic dysfunction and sleep quality, but it is unclear whether this association is present in hypertensives. Thus, this study evaluated the relationship between sleep quality and cardiac autonomic modulation in hypertensives. Forty-seven middle-aged hypertensive men under consistent anti-hypertensive treatment were assessed for sleep quality by the Pittsburgh Sleep Quality Index (PSQI-higher score means worse sleep quality). Additionally, their beat-by-beat BP and heart rate (HR) were recorded, and cardiac autonomic modulation was assessed by their variabilities. Mann-Whitney and t tests were used to compare different sleep quality groups: poor (PSQI > 5, n = 24) vs good (PSQI ≤ 5, n = 23), and Spearman's correlations to investigate associations between sleep quality and autonomic markers. Patients with poor sleep quality presented lower cardiac parasympathetic modulation (HR high-frequency band = 26 ± 13 vs 36 ± 15 nu, P = .03; HR total variance = 951 ± 1373 vs 1608 ± 2272 ms2 , P = .05) and cardiac baroreflex sensitivity (4.5 ± 2.3 vs 7.1 ± 3.7 ms/mm Hg, P = .01). Additionally, sleep quality score presented significant positive correlation with HR (r = +0.34, P = .02) and negative correlations with HR high-frequency band (r = -0.34, P = .03), HR total variance (r = -0.35, P = .02), and cardiac baroreflex sensitivity (r = -0.42, P = .01), showing that poor sleep quality is associated with higher HR and lower cardiac parasympathetic modulation and baroreflex sensitivity. In conclusion, in treated hypertensive men, poor sleep quality is associated with cardiac autonomic dysfunction.

Morning versus Evening Aerobic Training Effects on Blood Pressure in Treated Hypertension.

INTRODUCTION: The acute blood pressure (BP) decrease is greater after evening than morning exercise, suggesting that evening training (ET) may have a greater hypotensive effect. OBJECTIVE: This study aimed to compare the hypotensive effect of aerobic training performed in the morning versus evening in treated hypertensives. METHODS: Fifty treated hypertensive men were randomly allocated to three groups: morning training (MT), ET, and control (C). Training groups cycled for 45 min at moderate intensity (progressing from the heart rate of the anaerobic threshold to 10% below the heart rate of the respiratory compensation point), while C stretched for 30 min. Interventions were conducted 3 times per week for 10 wk. Clinic and ambulatory BP and hemodynamic and autonomic mechanisms were evaluated before and after the interventions. Clinic assessments were performed in the morning (7:00-9:00 AM) and evening (6:00-8:00 PM). Between-within ANOVA was used (P ≤ 0.05). RESULTS: Only ET decreased clinic systolic BP differently from C and MT (morning assessment -5 ± 6 mm Hg and evening assessment -8 ± 7 mm Hg, P < 0.05). Only ET reduced 24 h and asleep diastolic BP differently from C and MT (-3 ± 5 and -3 ± 4 mm Hg, respectively, P < 0.05). Systemic vascular resistance decreased from C only in ET (P = 0.03). Vasomotor sympathetic modulation decreased (P = 0.001) and baroreflex sensitivity (P < 0.02) increased from C in both training groups with greater changes in ET than MT. CONCLUSIONS: In treated hypertensive men, aerobic training performed in the evening decreased clinic and ambulatory BP due to reductions in systemic vascular resistance and vasomotor sympathetic modulation. Aerobic training conducted at both times of day increases baroreflex sensitivity, but with greater after ET.

Separate aftereffects of morning and evening exercise on ambulatory blood pressure in prehypertensive men.

BACKGROUND: Clinic postexercise hypotension (PEH) is different after aerobic exercise performed in the morning and in the evening. Thus, ambulatory PEH should also differ after exercises conducted at different times of day. However, because of the circadian pattern of blood pressure (BP), ambulatory PEH should be assessed considering a control condition. Thus, this study was designed to verify the effects of morning and evening exercises on postexercise ambulatory BP averages and circadian parameters by comparing responses obtained at each time of day after an exercise and a control session. METHODS: Thirteen prehypertensive men underwent four sessions (randomized order): two in the morning (9 am) and two in the evening (6:30 pm). At each time of day, a control (C) and an exercise (E: cycle ergometer 45 min, 50% VO2peak) sessions were performed. After the sessions, an ambulatory BP and heart rate (HR) monitoring was started for 24 h. Paired t-test or Wilcoxon Signed Rank Test were used to compare the E and the C sessions at each time of day. RESULTS: In the morning, 24 h, daytime and nighttime HR were higher after the E than the C session. In the evening, nighttime systolic BP (116±11 vs. 120±10 mmHg, P=0.04) and rate pressure product (7981±1294 vs. 8583±1523 mmHg.bpm, P=0.04), as well as MESOR (128±11 vs. 130±10 mmHg, P=0.03) were lower in the E than the C session. CONCLUSIONS: In prehypertensive men, morning exercise increased ambulatory HR, while evening exercise decreased nighttime BP and cardiac work, reducing the MESOR of systolic BP.

Post-Exercise Hypotension and Its Mechanisms Differ after Morning and Evening Exercise: A Randomized Crossover Study.

Post-exercise hypotension (PEH), calculated by the difference between post and pre-exercise values, it is greater after exercise performed in the evening than the morning. However, the hypotensive effect of morning exercise may be masked by the morning circadian increase in blood pressure. This study investigated PEH and its hemodynamic and autonomic mechanisms after sessions of aerobic exercise performed in the morning and evening, controlling for responses observed after control sessions performed at the same times of day. Sixteen pre-hypertensive men underwent four sessions (random order): two conducted in the morning (7:30 am) and two in the evening (5 pm). At each time of day, subjects underwent an exercise (cycling, 45 min, 50%VO2peak) and a control (sitting rest) session. Measurements were taken pre- and post-interventions in all the sessions. The net effects of exercise were calculated for each time of day by [(post-pre exercise)-(post-pre control)] and were compared by paired t-test (P<0.05). Exercise hypotensive net effects (e.g., decreasing systolic, diastolic and mean blood pressure) occurred at both times of day, but systolic blood pressure reductions were greater after morning exercise (-7±3 vs. -3±4 mmHg, P<0.05). Exercise decreased cardiac output only in the morning (-460±771 ml/min, P<0.05), while it decreased stroke volume similarly at both times of day and increased heart rate less in the morning than in the evening (+7±5 vs. +10±5 bpm, P<0.05). Only evening exercise increased sympathovagal balance (+1.5±1.6, P<0.05) and calf blood flow responses to reactive hyperemia (+120±179 vs. -70±188 U, P<0.05). In conclusion, PEH occurs after exercise conducted at both times of day, but the systolic hypotensive effect is greater after morning exercise when circadian variations are considered. This greater effect is accompanied by a reduction of cardiac output due to a smaller increase in heart rate and cardiac sympathovagal balance.