Long-Term Antihypertensive Therapy with Beta-Blockers: Submaximal Exercise Capacity and Metabolic Effects During Exercise

Abstract

The effects of long-term (6 months) antihypertensive treatment with three different types of beta-blockers (propranolol, nonselective without ISA; pindolol, nonselective with ISA; metoprolol, beta 1-selective without ISA) on submaximal exercise capacity and metabolic variables during submaximal endurance exercise were studied in seven subjects with essential hypertension. Exercise tests were performed on a bicycle ergometer at 70% of estimated VO2 max. Similar reductions of resting and exercise blood pressure and exercise heart rate were obtained with the three beta-blockers. Exercise time was significantly reduced by all three beta-blockers during chronic antihypertensive therapy. The reduction tended to be more pronounced after 5-6 months of treatment than after 1 week (P = 0.06). During exercise, the plasma glycerol and nonesterified fatty acid concentrations were reduced. Plasma glucose concentration was reduced at the end of the exercise test during propranolol treatment only. Plasma lactate concentrations tended to be increased, but the difference was significant during pindolol treatment only. Oxygen uptake tended to decrease and respiratory exchange ratio to increase. Plasma potassium concentrations during exercise were significantly increased with all three beta-blockers. The effects on the metabolic variables during exercise were similar after 1 week and during long-term (20/24 weeks) beta-blocker treatment. The study shows that submaximal endurance exercise capacity is impaired in patients with essential hypertension on beta-blocker therapy and that the impairment is maintained during long-term antihypertensive beta-blocker treatment.

Exercise haemodynamics and maximal exercise capacity during beta‐ adrenoceptor blockade in normotensive and hypertensive subjects.

“…We cannot be sure that our results are also valid for patients with higher levels of blood pressure. Although in most studies, treatment periods were longer than in our study, we do not consider this a very likely explanation for the discrepancies, since in normotensive subjects it has been shown that there is no difference in effect between a single dose and a chronic (Smyth et al, 1984;Van Baak et al, 1985). Based on the results obtained we have to reject the hypothesis that the effect of 1-adrenoceptor blocker administration on exercise haemodynamics differs between normotensive and hypertensive subjects.…”

“…In this study, we confirmed the finding of previous studies (Anderson etal., 1979;Folgering & Van Bussel, 1980;Hughson & MacFarlane, 1981;Tesch & Kaiser, 1983;Smyth et al, 1984;Van Baak et al, 1985 , 1982Lijnen etal., 1979;Leenen et al, 1980;Losment et al, 1986). One possible explanation for the discrepant findings is that most of the studies mentioned above may have suffered from methodological bias.…”

“…In many studies, acute as well as chronic administration of nonselective and p1-selective ,Badrenoceptor blocking agents has been shown to reduce maximal exercise capacity in normotensive subjects (Anderson et al, 1979;Folgering & Van Bussel, 1980;Hughson & MacFarlane, 1981; Tesch & Kaiser, 1983;Smyth et al, 1984;Van Baak et al, 1985. On the other hand, the majority of studies in hypertensive subjects suggests that maximal exercise capacity is not affected during ,-adrenoceptor blockade (Hansson et al, 1977;Reybrouck et al, 1977;Franz et al, 1979Franz et al, , 1982Franz et al, , 1985Lijnen et al, 1979;Leenen et al, 1980;Losment et al, 1986).…”

Hypothesis: β-Adrenergic Receptor Blockers and Weight Gain

“…Several investigators have shown that total energy expenditure may be reduced 4% to 9% with ␤-blocker treatment. [15][16][17][18][19][20] In a recent study, we showed that ␤-blockade reduces the basal metabolic rate by 12% in obese hypertensive patients, compared with obese hypertensive patients receiving other antihypertensive agents. 21 Astrup et al 22 provided evidence for a ␤ 2 -adrenergic receptor-mediated facultative thermogenic component in skeletal muscle and a ␤ 1 -adrenergic receptor-mediated component in nonmuscle tissue.…”

Evaluating Symptoms to Improve Quality of Life in Patients with Chronic Stable Angina

“…Therefore, beta-blockers should be avoided or used with caution in patients with hypotension and they are contraindicated in patients with significant sinus bradycardia and partial atrioventricular block [4]. Therapy with beta-blockers can also reduce exercise capacity and impair sexual function in some patients [49, 50]. Similar to beta-blockers, CCBs also exert their effects by lowering blood pressure and heart rate; therefore, nondihydropyridine CCBs are contraindicated in patients with left ventricular systolic dysfunction with or without heart failure and in patients with heart block and disorders of the sinus node [4].…”