106 research outputs found

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

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    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

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    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

    Effects of ACEi and ARB on post-exercise hypotension induced by exercises conducted at different times of day in hypertensive men

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    Background: Post-exercise hypotension (PEH) is greater after evening than morning exercise, but antihypertensive drugs may affect the evening potentiation of PEH. Objective: To compare morning and evening PEH in hypertensives receiving angiotensin-converting enzyme inhibitors (ACEi) or angiotensin II receptor blockers (ARB). Methods: Hypertensive men receiving ACEi (n = 14) or ARB (n = 15) underwent, in a random order, two maximal exercise tests (cycle ergometer, 15 watts/min until exhaustion) with one conducted in the morning (7 and 9 a.m.) and the other in the evening (8 and 10 p.m.). Auscultatory blood pressure (BP) was assessed in triplicate before and 30 min after the exercises. Changes in BP (post-exercise–pre-exercise) were compared between the groups and the sessions using a two-way mixed ANOVA and considering P < .05 as significant. Results: In the ARB group, systolic BP decrease was greater after the evening than the morning exercise, while in the ACEi group, it was not different after the exercises conducted at the different times of the day. Additionally, after the evening exercise, systolic BP decrease was lower in the ACEi than the ARB group (ARB = −11 ± 8 vs −6 ± 6 and ACEi = −6 ± 7 vs. −8 ± 5 mmHg, evening vs. morning, respectively, P for interaction = 0.014). Conclusions: ACEi, but not ARB use, blunts the greater PEH that occurs after exercise conducted in the evening than in the morning
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