Post-exercise Systolic Blood Pressure Research Articles

Plasma catecholamine responses to dynamic exercise in patients with coronary artery disease--the relationship between sympathetic activity and systolic blood pressure and exercise-induced ventricular arrhythmias.

In order to investigate the relationship between sympathetic activity and postexercise systolic blood pressure (SBP) and exercise-induced ventricular arrhythmias in patients with coronary artery disease (CAD), we studied 38 patients and 9 normal subjects who underwent treadmill testing. Peak pressure-rate product was similar in the 2 groups. The plasma concentrations of norepinephrine and epinephrine at rest and immediately after exercise were significantly higher in patients with CAD compared with normal subjects (norepinephrine at rest, p < 0.01; norepinephrine immediately after exercise, p < 0.05; epinephrine at rest, p < 0.05; epinephrine immediately after exercise, p < 0.05). The level of norepinephrine immediately after exercise was significantly higher in 15 patients with a postexercise SBP increase than in 23 patients without that SBP change (p < 0.05), whereas the level of epinephrine was similar in the 2 groups. The level of epinephrine immediately after exercise was significantly higher in 10 patients with exercise-induced premature ventricular contractions than in 28 patients without those arrhythmias (p < 0.05), whereas the level of norepinephrine was similar in the 2 groups. We conclude that a postexercise SBP increase is related to the augmentation of sympathoneural activity and that exercise-induced ventricular arrhythmias are related to the augmentation of sympathoadrenal activity.

Mechanism of abnormal postexercise systolic blood pressure response and its diagnostic value in patients with coronary artery disease

To define the factors that affect an abnormal postexercise systolic blood pressure (SBP) response and to verify the diagnostic value of that response in patients with coronary artery disease (CAD), we studied 33 normal subjects, eight patients with hypertension who had no CAD, and 42 patients with documented CAD who underwent supine leg exercise testing. SBP recovery ratios were derived by dividing the values obtained 1 and 3 minutes after exercise by the peak value. The upper normal limit of the SBP ratio was defined by two standard deviations from the mean for 33 normal subjects. The specificity of this criterion for identifying patients with CAD was 97% and the sensitivity was 60%. None of the eight patients with hypertension showed an abnormal postexercise SBP response. At peak exercise the pulmonary artery wedge pressure was significantly greater in the patients with CAD having an abnormal response. In multiple regression analysis the exercise pulmonary artery wedge pressure, the exercise SBP, and the systemic vascular resistance after exercise were determining factors for an abnormal SBP response. Three-vessel disease was more common in patients with an abnormal response. Results of this study indicate that an abnormal postexercise SBP response appears to be determined by (1) the extent of exercise-induced impairment of left ventricular function and (2) peripheral vascular tone during recovery. This study also suggests that this criterion can increase the specificity of supine exercise testing in patients with CAD including those with hypertension and might provide a marker for the severity of impaired left ventricular function by exercise in CAD.

Prognostic value of abnormal postexercisesystolic blood peessure response: Prehospital discharge test after myocardial infarction in Japan

To assess the prognostic value of an abnormal postexercise response in systolic blood pressure (SBP), treadmill exercise testing was performed in 217 survivors of acute myocardial infarction at an average of 9.3 weeks after infarction. During the mean follow-up period of 4 years, cardiac events were noted in 34 patients (16%), including cardiac death in 13 (6%), nonfatal reinfarction in 12 (6%), and coronary artery bypass graft surgery in nine (4%). An abnormal postexercise SBP response was defined as the ratio of SBP at 3 minutes of recovery to peak exercise SBP of 0.9 or more, on the basis of the cutoff point with the highest sensitivity and specificity to predict cardiac events. An abnormal postexercise SBP response occurred in 90 patients (42%). Patients with an abnormal postexercise SBP response had more exercise-induced myocardial ischemia. more left ventricular impairment, and more extensive coronary artery lesions than those without. Cox proportional hazards model demonstrated that the abnormal postexercise SBP response was ranked first in ability to predict cardiac death (p = 0.025, relative risk 15.41). Bypass surgery was associated with an abnormal postexercise SBP ratio (p less than 0.05). Nonfatal reinfarction could not be predicted by any clinical or exercise variables. In conclusion, an abnormal postexercise SBP response could be useful for predicting cardiac death and the need for bypass surgery after myocardial infarction. This response is probably the result of myocardial ischemia and left ventricular impairment.

The significance of abnormal systolic blood pressure response during supine ergometer exercise and postexercise in ischemic heart disease, studied by exercise radionuclide ventriculography.

The prognostic value of abnormal postexercise systolic blood pressure (BP) response has not been investigated. Therefore, the significance of abnormal BP response during exercise and postexercise was examined in 169 patients with ischemic heart disease subjected to supine ergometer exercise gated equilibrium radionuclide ventriculography, coronary arteriography, and follow up averaging 3.6 years. Abnormal BP response during exercise (exertional "hypotension") was defined as 1) a failure of BP to rise by at least 11 mmHg or 2) an initial rise in BP but subsequent fall by more than 10 mmHg during exercise. Abnormal BP response during postexercise (postexercise "hypertension") was defined as an increase of more than 10 mmHg above the peak exercise BP. Of 169 patients, 51 (30%) had an abnormal BP response. Four types of BP response were identified: exertional "hypotension" (group 1a, n = 11), postexercise "hypertension" (group 1b, n = 30), exertional "hypotension" with postexercise "hypertension" (group 1c, n = 10) and normal BP response (group 2, n = 118). Both average exercise duration and peak heart rate were significantly lower in groups 1a, 1b and 1c than in group 2. The severity of exercise ST-segment depression was greater in groups 1b and 1c than in group 2. However, there was no significant difference in the severity of exercise ST-segment depression between group 1a and group 2. A decline in ejection fraction occurred more frequently in groups 1b and 1c than in group 2. Patients in groups 1a, 1b and 1c had more extensive coronary artery disease (CAD) than did patients in group 2. Medically treated patients with an abnormal BP response (groups 1a, 1b and 1c) had a poorer prognosis than did those with a normal BP response (group 2). These findings suggest that an abnormal BP response during supine exercise is infrequent, but is usually associated with impaired exercise tolerance and severe CAD. An abnormal postexercise BP response is also infrequent, but is more closely associated with evidence of myocardial ischemia and global left ventricular dysfunction than exertional "hypotension". In conclusion, postexercise "hypertension" has the same value as exertional "hypotension" as a predictor of poor prognosis.

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 < 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 < 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 < 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 < 0.05). No subject with hypotension experienced cardiovascular morbidity or mortality over a follow-up period averaging 4 years. Thus, in a general population, hypotension after treadmill exercise occurs primarily in younger persons with high maximal heart rates. It may be a cause for an ischemic electrocardiographic response but appears to have a benign prognosis.

Transcutaneous oxygen tension (TcPO2) during nonnutritive sucking (NNS) in preterm infants

There is evidence of hypertensive effects caused by anabolic androgenic steroids (AAS). A single exercise session promotes the acute reduction of blood pressure, but the effects of AAS on this phenomenon are unknown.To investigate the post-exercise blood pressure response in androgenic-anabolic steroid users.Thirteen AAS users (23.9 ± 4.3 years old) and sixteen controls (22.1 ± 4.5 years old) performed a session of aerobic exercise. Heart rate and blood pressure were assessed before exercise and during a 60 min post-exercise resting period. Repeated ANOVA measures were used to determine differences between the groups.While the control group had a significant reduction in post-exercise systolic blood pressure of up to 13.9 ± 11.6 mmHg at 40 min, this phenomenon was limited among AAS users who reached a maximum of 6.2 ± 11.5 mmHg at 60 min. The between groups comparison revealed significant higher post-exercise hypotension (PEH) for the control group at 30 min (−12.9 ± 14.1 mmHg versus −2.9 ± 7.6 mmHg), 40 min (−13.9 ± 11.6 mmHg versus −2.5 ± 8.3 mmHg), 50 min (−13.9 ± 13.9 mmHg versus −5.0 ± 7.9 mmHg) and 60 min (−12.5 ± 12.8 mmHg versus −6.2 ± 11.5 mmHg). There was no significant diastolic PEH in any of the groups.This study demonstrated impaired systolic post-exercise hypotension as a new adverse effect of AAS usage.

Lung function and treadmill performance of smoking and nonsmoking males receiving ascorbic acid supplements

Twelve cigarette smoking and 10 nonsmoking healthy human volunteers, 25 to 38 yr of age, performed lung function and treadmill performance tests over two periods of 3 wk duration while taking either ascorbic acid (300 mg daily) or placebo tablets in a cross-over design. The two exercise periods were separated by a one-month inactive phase. Tablets were administered in a random, double-blind manner. Plasma vitamin C levels were significantly increased after 3 wk of ascorbic acid supplementation in both smokers and nonsmokers as compared to initial levels in the same subjects. No differences between ascorbic acid and placebo treatments of smokers and nonsmokers were observed for 1-s forced expiratory volume, forced vital capacity, 1-s forced expiratory percent, resting heart rate, resting and postexercise systolic and diastolic blood pressures, treadmill workload, postexercise blood lactic acid, and ventilation measurements. The postexercise systolic blood pressure values of the nonsmokers were lower, although not quite significantly, after the ascorbic acid treatment than after the placebo. The 300-mg ascorbic acid supplement appeared to have little effect on the lung function and physical performance of healthy smoking and nonsmoking males.

Withdrawal of long-term therapy with atenolol in hypertensive patients.

1 The offset of effects on blood pressure and heart rate after cessation of long-term therapy (19 +/- 3.6 months) with atenolol (200 mg once/daily) was studied in six hypertensive patients. 2 Withdrawal of atenolol resulted in a gradual return of lying, standing and post-exercise systolic and diastolic blood pressure levels and heart rate towards the baseline value. The offset of effect greatly exceeded the time for elimination of atenolol. 3 No significant differences in the pharmacokinetic profile of atenolol were evident between the values obtained following chronic dosing and an acute single-dose study. 4 The lack of clinical evidence of increased cardiac adrenergic sensitivity or rebound hypertension following withdrawal of atenolol contrasts with reports of a withdrawal syndrome following cessation of therapy with propranolol. Nevertheless until the mechanism of the propranolol-withdrawal syndrome is better understood caution is required when stopped therapy with atenolol in patients with severe coronary artery disease.

A comparison of the effects of labetalol, bendrofluazide and their combination in hypertension.

1 Bendrofluazide (10 mg/day) or labetalol (300 mg and 600 mg/day) produced significant reductions in lying, standing, and post-exercise blood pressure in ten hypertensives. 2 Active treatments were approximately equivalent in anti-hypertensive effect. However, comparing lying and standing determinations, labetalol (600 mg/day) produced significantly greater additional postural falls in systolic blood pressure than during placebo or bendrofluazide treatment. 3 Systolic blood pressure rose after exercise during placebo or bendrofluazide treatment. However, on labetalol, mean changes in systolic blood pressure after exercise were negative and significantly different from those seen on placebo. 4 Greater reductions in lying and post-exercise systolic blood pressure were produced by combination treatment than by either individual drug. Additional postural and exercise-related falls in systolic blood pressure tended to be smaller with combination treatment than during treatment with labetalol alone. 5 Labetalol significantly reduced lying, standing, or post-exercise heart rate by comparison with placebo or bendrofluazide. 6 Labetalol significantly reduced lying, standing, or post-exercise heart rate by comparison with placebo or bendrofluazide. 6 Labetalol moderately reduced plasma renin activity, whereas bendrofluazide caused marked elevation. The effect of bendrofluazide predominated during combination treatment.

Acebutolol in hypertension: Relationships between drug concentration and effects

Relationships between plasma concentrations of acebutolol (Ac) and its N-acetyl metabolite (Am) and pharmacological effects were studied in patients with essential hypertension. In an acute study (N=7) 400 mg oral acebutolol produced similar peak plasma levels of Ac and Am but Am had a longer half life. Group mean pulse and blood pressure fell significantly, although the size of individual blood pressure fall varied five-fold. There was no significant change in plasma renin activity. Correlations were found between drug concentration and β-blockade, assessed as % reduction in exercise tachycardia, and between both of these and the fall in post exercise systolic blood pressure. Similar comparisons were made in a chronic optimum dose study (N=11) both pre-dose and three hours post-dose. Am concentration was consistently higher than Ac at both times. Blood pressure was lowered equally pre-and post-dose when compared to placebo and plasma renin activity (PRA) was reduced on active treatment. Correlations were again shown between drug concentrations and β-blockade but none were found with changes in blood pressure or PRA. Between subject differences in blood pressure response could not be fully explained in terms of the other measurements but it is unlikely that pharmacokinetic differences are the major source of this variability.

Pulse Wave and Blood Pressure Changes Occurring during a Physical Training Program

Abstract Members of the Santa Barbara basketball team were tested periodically during and after the 1957–58 season of play. The changes in physical conditioning were estimated using a step test. During this period of time the blood pressure and pulse wave measurements were studied to investigate the effects of basketball conditioning on these measurements. The resting and postexercise systolic blood pressure measurements decreased significantly during training. These changes were significant after 16 weeks, while the pulse rate changes indicated conditioning had changed in six weeks. During de-training these measurements reversed and made significant changes in ten weeks. The pulse wave measurements more closely followed those of the step test. They changed significantly in six weeks, leveled off, and finally reversed to the starting level during de-training.