The effects of exercise duration on post-exercise hypotension

STUDY 1: Thirteen normotensive participants with average baseline blood pressure of 126/71 mm Hg participated in the study. Participants performed bouts of cycle ergometry for 15, 30 and 45 min at 70% VO2 Peak. Blood pressure was monitored by the Finapres method with 2 min windows recorded at rest, 5, 10, 15, 30, 45 and 60 min post-exercise. Following exercise, systolic blood pressure (SBP) was similar between the three trials and was reduced from pre-exercise values at 5 through 60 min of measurement. Diastolic blood pressure (DBP) was also unaffected by the duration of exercise and was lower than before exercise at 30 through 45 min post-exercise. STUDY 2: Eight borderline hypertensive participants with average baseline blood pressure of 133/79 mm Hg participated in the study. Subjects performed bouts of cycle ergometry for 10 and 30 min at 70% VO2 Peak. Following exercise, blood pressure was monitored as in study 1. SBP was similar between both trials and was reduced from baseline at 5 through 60 min post-exercise. The largest decrement of SBP was 14 mm Hg and occurred 15 min post-exercise. DBP was also unaffected by the duration of exercise and was lower than pre-exercise levels at 5 min and again at 15 through 45 min post-exercise. Mean arterial pressure (MAP) also showed significant decrements throughout the entire 1 h post-exercise period by a maximum of 9 mm Hg at 15 min post-exercise, irrespective of exercise duration. We conclude that moderately intense exercise may be as brief as 10 min in duration in order to elicit a decrease in resting blood pressure and may have potential benefits as a non-pharmacological aid to hypertension.     

Factors affecting post-exercise hypotension in normotensive and hypertensive humans

BACKGROUND: Post-exercise hypotension has been extensively described under laboratory conditions. However, studies investigating the persistence of this post-exercise decrease in blood pressure for longer periods have produced controversial results. The present investigation was conducted to verify the effect of a single bout of exercise on ambulatory blood pressure and to identify potential factors that might influence this post-exercise ambulatory blood pressure fall. DESIGN: The study was a randomized controlled clinical trial. METHODS: Thirty normotensive and 23 hypertensive subjects were submitted to two ambulatory blood pressure monitorings (using the SpaceLabs 90207, SpaceLabs, Redmond, Washington, USA), which were performed after 45min of seated rest (control session) or cycling exercise at 50% peak oxygen uptake (exercise session). RESULTS: Normotensive subjects demonstrated a lower 24h blood pressure level in the exercise session. Hypertensive patients showed no significant difference in ambulatory blood pressure level between the two experimental sessions. Further data analysis revealed that approximately 65% of the subjects in both groups experienced a fall in blood pressure after exercise. Moreover, in the normotensive subjects, this blood pressure fall was significantly and positively correlated with clinic and ambulatory blood pressure, and negatively correlated with weight and body mass index. The blood pressure response to exercise was also greater in women. In the hypertensive patients, the post-exercise blood pressure decrease was significantly and positively correlated with clinic and ambulatory blood pressure as well as with the peak oxygen uptake, and negatively correlated with age and body mass index. CONCLUSIONS: 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.     

NOS II inhibition attenuates post-suspension hypotension in Sprague-Dawley rats

The reduction in mean arterial pressure observed in astronauts may be related to the impairment of autonomic function and/or excessive production of endothelium-derived relaxing factors. Here, we examined the role of a nitric oxide synthase II (NOS II) inhibitor AMT (2-amino-dihydro-6-methyl-4H-1,3-thiazine) against the post-suspension reduction in mean arterial pressure (MAP) in conscious male Sprague-Dawley rats. Direct MAP and heart rate were determined prior to tail-suspension, daily during the 7-day suspension and every 2 hrs post-suspension. Prior to release from suspension and at 2 and 4 hrs post-suspension, AMT (0.1 mg/kg), or saline, were administered intravenously. During the 7-day suspension, MAP was not altered, nor were there significant changes in heart rate. The reduction in MAP post-suspension in saline-treated rats was associated with significant increases in plasma nitric oxide and prostacyclin. 2-Amino-dihydro-6-methyl4H-1,3-thiazine reduced plasma nitric oxide levels, but not those of prostacyclin, attenuated the observed post-suspension reduction in MAP and modified the baroreflex sensitivity for heart rate. Thus, the post suspension reduction in mean arterial pressure is due, in part, to overproduction of nitric oxide, via the NOS II pathway, and alteration in baroreflex activity.     

Effect of 12 weeks of resistance exercise on post-exercise hypotension in stage 1 hypertensive individuals

Post-exercise hypotension (PEH), the reduction of blood pressure (BP) after a single bout of exercise, is of great clinical relevance. As the magnitude of this phenomenon seems to be dependent on pre-exercise BP values and chronic exercise training in hypertensive individuals leads to BP reduction; PEH could be attenuated in this context. Therefore, the aim of the present study was to investigate whether PEH remains constant after resistance exercise training. Fifteen hypertensive individuals (46 ± 8 years; 88 ± 16 kg; 30 ± 6% body fat; 150 ± 13/93 ± 5 mm Hg systolic/diastolic BP, SBP/DBP) were withdrawn from medication and performed 12 weeks of moderate-intensity resistance training. Parameters of cardiovascular function were evaluated before and after the training period. Before the training program, hypertensive volunteers showed significant PEH. After an acute moderate-intensity resistance exercise session with three sets of 12 repetitions (60% of one repetition maximum) and a total of seven exercises, BP was reduced post-exercise (45-60 min) by an average of aproximately -22 mm Hg for SBP, -8 mm Hg for DBP and -13 mm Hg for mean arterial pressure (P<0.05). However, this acute hypotensive effect did not occur after the 12 weeks of training (P>0.05). In conclusion, our data demonstrate that PEH, following an acute exercise session, can indeed be attenuated after 12 weeks of training in hypertensive stage 1 patients not using antihypertensive medication.     

Haemodynamic contributions to post-exercise hypotension in young adults with hypertension and rapid resting heart rates.

The haemodynamic effects of 45 min of treadmill exercise (at 70% of resting heart rate reserve) were determined in 5 young adults with hypertension and rapid resting heart rates (greater than 90 beats/min in clinic) and were compared with those of 5 age-matched normotensive subjects. Blood pressure was lower after exercise in the hypertensive, but not the normotensive subjects. Mean cardiac output before exercise was similar in the two groups, and fell from 6.8 +/- 0.6 before to 5.4 +/- 0.6 l/min 60 min after exercise in the hypertensive group (P less than 0.01). Total peripheral resistance tended to be higher at this time. Neither variable was affected by prior exercise in the normotensive group. The depressor effects of prior exercise on mean arterial pressure (-8.6 +/- 1.0 vs. -1.4 +/- 2.5 mmHg; P less than 0.04) and cardiac output (-1.4 +/- 0.3 vs. -0.1 +/- 0.1 l/min; P less than 0.005) and the increase in total peripheral resistance (+3.0 +/- 1.2 vs. 0.0 +/- 1.0 Units; P less than 0.05) were greater in the hypertensive group. Thus, the post-exercise hypotension in this selected group of young hypertensive subjects with rapid resting heart rates was mediated by a decrease in cardiac output and stroke volume disproportionate to the fall in blood pressure, suggesting sustained compromise of their cardiac performance after acute exercise.     

Impaired glucose tolerance as a determinant of early deterioration of left ventricular diastolic function in middle-aged healthy subjects

To clarify the determinants of an abnormal relaxation diastolic pattern assessed by Doppler echocardiography, 131 middle-aged healthy subjects were analyzed. By multivariate logistic regression analysis, fasting insulin levels (p = 0.0016) and peak glucose levels (p = 0.046) were independent predictors of an abnormal relaxation diastolic pattern 2 hours after 75 g OGTT.     

Acarbose, an alpha-glucosidase inhibitor, attenuates postprandial hypotension in autonomic failure

Postprandial hypotension is an important clinical condition that predisposes to syncope, falls, angina, and cerebrovascular events. The magnitude of the fall in blood pressure after meals depends on enteric glucose availability. We hypothesized that acarbose, an alpha-glucosidase inhibitor that decreases glucose absorption in the small intestine, would attenuate postprandial hypotension. Acarbose or placebo was given 20 minutes before a standardized meal in 13 patients with postprandial hypotension in the setting of autonomic failure (age: 65+/-2.64 years; body mass index: 25+/-1.08 kg/m(2); supine plasma norepinephrine: 110+/-26.6 pg/mL). Four patients were studied in a single-blind protocol and 9 patients in a double-blind, randomized, crossover fashion. Patients were studied supine, and blood pressure, heart rate, and neuroendocrine parameters were obtained at baseline and for 90 minutes after meal intake. After adjusting for potential confounders, acarbose significantly attenuated the postprandial fall in systolic and diastolic blood pressures by 17 mm Hg (95% CI: 7 to 28; P=0.003) and 9 mm Hg (95% CI: 5 to 14; P=0.001), respectively. Furthermore, acarbose effectively reduced plasma levels of insulin, a known vasodilator, by 11 microU/mL (95% CI: 5 to 18; P=0.001) compared with placebo. After adjusting for insulin levels, the attenuation of postprandial hypotension by acarbose remained significant, indicating that additional mechanisms contribute to this effect. In conclusion, 100 mg of acarbose successfully improved postprandial hypotension in patients with severe autonomic failure. This effect is not explained solely by a reduction in insulin levels.     

Prevalence and significance of postexercise hypotension in apparently healthy subjects

Although a decrease in systolic blood pressure (BP) occurring during treadmill exercise is often a sign of severe left ventricular dysfunction, the prevalence and significance of postexertional hypotension is unclear. The postexercise systolic BP response to maximal treadmill exercise was analyzed in 781 asymptomatic volunteers, aged 21 to 96 years (mean 51 +/- 16) from the Baltimore Longitudinal Study on Aging. Fifteen subjects (1.9%) had a postexercise decrease in systolic BP of at least 20 mm Hg from preexercise sitting values, to a level of 90 mm Hg or less. The prevalence of postexercise hypotension was 3.1% (14 of 449) in subjects younger than 55 years, but only 0.3% (1 of 332) in those older than 55 (p less than 0.01). Before exercise these 15 subjects demonstrated a slight orthostatic decrease in systolic BP of -1.7 +/- 4.8 mm Hg compared with an increase of 5.3 +/- 5.1 mm Hg in age-matched control subjects (p less than 0.001). The lowest systolic BP averaged 78 +/- 9 mm Hg (range 62 to 90) and occurred between 4 and 9 minutes after exercise in 80% of cases. All but 3 episodes were symptomatic, with dizziness dominant. In only 2 subjects was the hypotension associated with vagal symptoms and bradycardia. Compared with control subjects, subjects with postexercise hypotension had higher maximal heart rates (184 +/- 15 vs 173 +/- 11 beats/min, p less than 0.05), but showed no difference in exercise tolerance or systolic BP at submaximal or maximal effort. Postexercise ST-segment abnormalities suggesting ischemia occurred in one-third of the hypotensive subjects but none of the control subjects (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Fish consumption and early atherosclerosis in middle-aged men

To investigate the association between fish consumption and early atherosclerosis, we analyzed the relationship between fish consumption and average intima-media thickness (AveIMT) by carotid ultrasound in middle-aged Japanese men. Participants were 250 randomly selected, community-based Japanese men aged 40 to 49 years without a prior history of cardiovascular disease. AveIMT was calculated from the mean of 1-cm lengths of both the right and the left carotid arteries at 8 locations. A lifestyle survey was carried out using a self-administered questionnaire including the frequency of fish intake. There were 147 men in the fewer than 4 times per week fish consumption group and 103 men in the 4 or more times per week group. The mean AveIMT was significantly higher in the low fish consumption group than in the high fish consumption group (0.623+/-0.068 vs 0.605+/-0.065 mm, P=.03). After adjustment for age, waist circumference, pack-years of smoking, alcohol consumption, diabetes, and lipid-lowering medications, the significant difference in the AveIMT between the 2 groups remained. However, after further adjustment for low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, and C-reactive protein in the model, the significant difference disappeared. Fish consumption may be protective against early atherosclerosis in middle-aged men, probably through its beneficial effects on inflammation.     

Caffeine slows heart rate autonomic recovery following strength exercise in healthy subjects

Introduction and objectivesStudies assessing the effects of caffeine (CAF) on the cardiovascular system have demonstrated that CAF can delay cardiac recovery following exercise. This study intended to assess the impact of CAF intake before physical exercise on heart rate variability (HRV) and cardiovascular parameters.MethodsThis is a prospective, crossover, controlled clinical trial conducted at the University of Pernambuco, Petrolina, PE, Brazil. The experimental protocol was split into three stages with a minimum of 48 hours between them. Exercises intensity was standardized based on the one repetition maximum test (1RM), obtaining the load of each volunteer for the intensity of 75% of 1RM. In the second and third phases, the control protocols were applied and 300 mg caffeine was given 45 minutes before training. HRV indices were determined at the subsequent times: 0 to 5 minutes of rest (before) and during 30 minutes of recovery (Rec) (after exercise), divided into six intervals, each of 5 minutes.ResultsThe final sample involved 30 volunteers. CAF delayed HRV recovery after resistance exercise. In general, CAF impaired recovery of HRV after resistance exercise. Significant changes were observed in the RMSSD, SDNN, TINN, SD1, low frequency and high frequency indices between the control and CAF group.ConclusionCAF protocol delayed parasympathetic regulation of heart rhythm following exercise, slowing recovery of HR, blood pressure and HRV indices after exercise.     

Autonomic responses to glucose ingestion in elderly subjects with orthostatic hypotension

The cardiovascular and plasma catecholamine responses to oral glucose (50 g) ingestion were investigated in five elderly subjects with orthostatic hypotension and five elderly control subjects. All the orthostatic hypotension subjects showed blood pressure falls after glucose ingestion, as compared to only one of the control subjects. Significantly greater falls in the orthostatic hypotension as compared to control patients were observed for systolic blood pressure (P less than 0.01) at 60 and 90 min following glucose and mean blood pressure (P less than 0.05) at 60 min following glucose. The orthostatic hypotension subjects did not have evidence of reduced heart-rate or plasma catecholamine responses to the glucose ingestion. It is concluded that, in elderly patients with orthostatic hypotension, disorder of blood pressure control may also cause hypotension associated with eating.     

Hyperthermic pretreatment decreases microvascular protein leakage and attenuates hypotension in anaphylactic shock in rats

Systemic anaphylaxis is a life-threatening allergic reaction and its pathologic conditions, such as edema, bronchospasm, and hypotension, have been attributed to release of vasoactive mediators. Heat shock protein (HSP) is known to play a protective role in living cells under various stresses. In these studies, we investigated the protective role of heat shock response in anaphylactic shock, focusing on changes of blood pressure (BP) and vascular permeability. Adult sensitized rats were injected intravenously with Evans blue (EB) and challenged with bovine serum albumin (BSA). The rats were treated with whole-body hyperthermia at 41.5 +/- 0.5 degrees for 15 min 24 h before BSA challenge. Vascular protein leakage in tissues was analyzed with the EB technique. The results showed that BSA challenge induced EB extravasation in all sensitized rats. EB values (EB/tissue; microg/g) in heart and lung (112.3 +/- 41 and 244.4 +/- 90.6; mean +/- SD; n = 6) in the nonheated rats were significantly higher than those (33.4 +/- 23.3 and 103.4 +/- 63.9; n = 9) in the heated rats (P < 0.05). The results showed that BSA challenge caused BP to fall drastically in the sensitized rats. BP in the heated rats was significantly higher than BP in the nonheated rats from 4 to 15 min during anaphylactic shock (P < 0.001). Inducible HSP72 appeared overexpressed in heart, lung, and liver tissue in the heated rats tested by Western immunoblotting. The results indicate that reduction of increased protein leakage and attenuation of hypotension may result from induction of HSP by whole-body hyperthermia.     

Effect of type 2 diabetes on plasma kallikrein activity after physical exercise and its relationship to post-exercise hypotension

AimThe present study was undertaken to determine the effects of type 2 diabetes (T2D) on plasma kallikrein activity (PKA) and postexercise hypotension (PEH).MethodsTen T2D patients (age: 53.6 ± 1.3 years; body mass index: 30.6 ± 1.0 kg/m²; resting blood glucose: 157.8 ± 40.2 mg dL⁻¹) and 10 non-diabetic (ND) volunteers (age: 47.5 ± 1.0 years; body mass index: 28.3 ± 0.9 kg/m²; resting blood glucose: 91.2 ± 10.5 mg dL⁻¹) underwent two experimental sessions, consisting of 20 min of rest plus 20 min of exercise (EXE) at an intensity corresponding to 90% of their lactate threshold (90LT) and a non-exercise control (CON) session. Blood pressure (BP; Microlife BP 3AC1-1 monitor) and PKA were measured during rest and every 15 min for 135 min of the postexercise recovery period (RP).ResultsDuring the RP, the ND individuals presented with PEH at 30, 45 and 120 min (P < 0.05) while, in the T2D patients, PEH was not observed at any time. PKA increased at 15 min postexercise in the ND (P < 0.05), but not in the T2D patients.ConclusionT2D individuals have a lower PKA response to exercise, which probably suppresses its hypotensive effect, thus reinforcing the possible role of PKA on PEH.     

Association between fasting glucose and C-reactive protein in middle-aged subjects.

AIMS: C-reactive protein (CRP), a marker of subclinical inflammation, predicts the occurrence of coronary heart disease in healthy subjects. Hyperglycaemia is known to stimulate the release of inflammatory cytokines from various cell types and can lead to the induction and secretion of acute-phase reactants by adipocytes. The aim of the present study was to determine the relation between glycaemic status and CRP in healthy subjects. METHODS: We studied the relation of high-sensitivity CRP to fasting glucose and other components of the metabolic syndrome in a population-based cross-sectional study (n = 1000; age 50 +/- 9 years). RESULTS: Plasma CRP levels increased continuously from the lowest quartile of normal fasting glucose level to impaired fasting glucose and to diabetes (ln CRP 0.47 +/- 0.09, 0.95 +/- 0.12, and 1.11 +/- 0.13, respectively; Ptrend < 0.0001). Increasing CRP with higher fasting glucose levels was apparent even among subjects with fasting glucose in the normal range (Ptrend = 0.039), and subjects with fasting glucose level in the upper quartile of normal fasting glucose had higher CRP levels compared with subjects in the lower quartile (P = 0.035). There was a positive crude correlation between CRP and smoking, post-menopausal hormone use, body mass index, fasting glucose, triglycerides, hypertension, and uric acid (r = 0.11-0.36, P = 0.002-0.0001). A negative correlation was found between CRP and HDL-cholesterol (r = 0.12, P < 0.0001) and physical activity (r = 0.11, P = 0.002). After adjustment for potential confounders in a stepwise multivariate linear regression model, fasting glucose remained significantly and independently related to CRP levels (correlation coefficient 0.06; 95% confidence interval 0.014-0.11, P = 0.011). CONCLUSIONS: Fasting glucose is significantly and positively associated with plasma CRP in middle-aged subjects. CRP levels increase continuously across the spectrum of fasting glucose, beginning in the lowest quartile of normal fasting glucose. This finding suggests that a proinflammatory effect may contribute to the adverse cardiovascular outcome associated with diabetes, impaired fasting glucose, and increasing glucose levels within the normal range.