Influence of alprenolol on hemodynamic and metabolic responses to prolonged exercise in subjects with hypertension

Frisk-Holmberg, M; Jorfeldt, L.; Juhlin-Dannfeldt, Anders

doi:10.1002/cpt1977216675

Cited by 42 publications

(14 citation statements)

References 11 publications

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“…Other studies have not demonstrated a reduction in Q with PB during submaximal exercise (Frisk-Holmberg et al 1977;Wilmore et al 1985).…”

Section: Introductionmentioning

confidence: 93%

“…PB has been found to have variable effects on plasma Lametabolism during submaximal exercise. Some studies have demonstrated no change in plasma [La-] (Frisk-Holmberg et al 1977;Lundborg et al 1981;Van Baak et al 1987); other studies have found a decrease (Verstappen and Van Baak 1987). Muscle [La-] during submaximal exercise does not appear to be significantly altered by @B (Kaiser et al 1985;Frisk-Holberg et al 1979).…”

Section: Eflects On Glycolysismentioning

confidence: 99%

“…The associated increase in stroke volume prevents large decreases in 0 during exercise (Frisk-Holmberg et al 1977;Reybrouck et al 1977;Wilmore et al 1985). An increase in end-diastolic volume and a decrease in akerload are probably responsible for the larger stroke volume observed during exercise with PB (Anderson and Vik-Mo 1982;Reybrouck et al 1977).…”

Section: Introductionmentioning

confidence: 99%

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Factors contributing to increased muscle fatigue with β-blockers

McKelvie¹,

Jones²,

Heigenhauser³

1991

Can. J. Physiol. Pharmacol.

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beta-Adrenoceptor blockers are widely used clinically and can be classified as nonselective (beta 1 and beta 2) or selective (beta 1). Impairment of exercise performance is a well-known side effect of this group of drugs. This paper reviews mechanisms that could potentially be responsible for this impairment. In addition to cardiovascular and metabolic effects, beta-blockade inhibits Na(+)-K+ ATPase pumps controlling ion movement between muscle and plasma and thus may contribute to muscle fatigue through this mechanism. To investigate the relationship between the change in plasma [K+] and exercise performance, we studied healthy male subjects taking propranolol. Eight subjects performed maximal incremental cycle ergometer exercise tests during control (no drug), low dose (LD) (40 mg daily), and high dose (HD) (265 +/- 4.3 (SE) mg daily) of propranolol. The control plasma [K+] (5.8 +/- 0.12 mequiv./L) during exercise was significantly lower than either the LD (6.4 +/- 0.05 mequiv./L) or HD (6.1 +/- 0.16 mequiv./L) values. There was no significant difference between plasma [K+] for the LD and HD of propranolol. However, maximum oxygen uptake was reduced only while taking the HD of propranolol. Six of the subjects also performed three 30-s bouts of high intensity exercise on an isokinetic cycle ergometer while taking the LD and HD of propranolol. There was no significant difference between doses for the increase in plasma [K+] (LD, 7.8 +/- 0.35 mequiv./L vs. HD, 7.6 +/- 0.36 mequiv./L) during exercise. However, exercise performance was significantly reduced during HD compared with LD. These results suggest that the increases in plasma [K+] with propranolol did not play a direct significant role in the reduced performance observed during the HD.

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“…Other studies have not demonstrated a reduction in Q with PB during submaximal exercise (Frisk-Holmberg et al 1977;Wilmore et al 1985).…”

Section: Introductionmentioning

confidence: 93%

Section: Eflects On Glycolysismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Factors contributing to increased muscle fatigue with β-blockers

McKelvie¹,

Jones²,

Heigenhauser³

1991

Can. J. Physiol. Pharmacol.

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“…p-adrenoceptor antagonists are believed to decrease glycogenolysis in skeletal muscle by inhibiting phosphorylase activity (Haugaard & Hess, 1965). Decreased glycogenolysis can explain the reduced release of lactate from skeletal muscle during p-adrenoceptor blockade (Trap-Jensen, Clausen, Noer, Larsen, Krogsgaard & Christensen, 1976;Frisk-Holmberg, Jorfeldt & Juhlin-Dannfeldt, 1977;Juhlin-Dannfeldt & Astrom, 1979;Hartling et al, 1980). Furchgott (1959) felt unable to classify the receptors for catecholamine-induced glycogenolysis as either a-or p-adrenoceptors and proposed that the adrenoceptor responsible for glycogenolysis should be denoted the 'yreceptor'.…”

Section: Discussionmentioning

confidence: 97%

Systemic and Forearm Haemodynamic and Metabolic Effects of Racemic Propranolol or d-Propranolol in Healthy Subjects

Trap‐Jensen

1981

Clinical Science

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1. The immediate haemodynamic and metabolic effects of intravenous administration of DL-propranolol and D-propranolol were studied in healthy male subjects at rest and during dynamic forearm exercise. The dose of DL-propranolol and of D-propranolol was 0.1 and 1.0 mg/kg body weight respectively. 2. DL-Propranolol reduced heart rate significantly at rest, during forearm exercise and post-exercise, whereas D-propranolol had a lesser effect on heart rate which was significant only at the end of the exercise period. Arterial blood pressure and forearm blood flow were unchanged after either drug. 3. Both drugs reduced the release of lactate from the exercising forearm. Forearm exchange of oxygen, glucose, free fatty acids and triglycerides remained unchanged. 4. The arterial blood glucose concentration increased after D-propranolol, but was unchanged after DL-propranolol. The arterial serum free fatty acid concentration decreased after DL-propranolol, but was not changed after D-propranolol. Arterial concentrations of lactate and triglycerides were not influenced by the drugs. 5. The chronotropic response to beta-adrenoceptor blockade appears to be stereoselective, suggesting specific blockade of beta-adrenoceptors. Metabolic responses to beta-adrenoceptor blockade are difficult to explain in terms of the known adrenoceptor system and may be due to non-specific actions of beta-adrenoceptor antagonists. An exception is inhibition of lipolysis, which is probably mediated via beta-adrenoceptors.

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“…Thus impaired tissue lipolysis, by Pl-adrenoceptor blockade, may reduce the availability of free fatty acids for aerobic glycolysis (Trap-Jensen etal., 1976), this being reflected by reductions in the respiratory quotient (Epstein et al, 1965;Kaiser, 1984) indicating that carbohydrate metabolism may become predominant. Impairment of hepatic and muscle glycogenolysis by P2-adrenoceptor blockade (Arnold et al, 1968) may also reduce anaerobic glycolysis and explain the reported reductions of plasma lactate (Trap-Jensen et al, 1976;Frisk-Holmberg et al, 1977). Muscle lactate, however, is unaltered during 13-adrenoceptor blockade indicating that impaired performance is not the result of lactate accumulation .…”

mentioning

confidence: 99%

Absence of excess peripheral muscle fatigue during beta‐adrenoceptor blockade.

Cooper

Stokes

Edwards

et al. 1988

Brit J Clinical Pharma

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1 In eight normal volunteers, the adductor pollicis (AP) was fatigued using intermittent trains of programmed, supramaximal stimulation at 1, 10, 20, 50, 100 and 1 Hz. Activity protocols were performed both with and without circulatory occlusion, both without and during propranolol 80 mg thrice daily in order to investigate the effects of ,-adrenoceptor blockade on 'peripheral' fatigue mechanisms. 2 The degree of 13-adrenoceptor blockade was assessed by the reduction of exercise tachycardia during cycle ergometry, e.g. pulse rates at 210 watts were reduced from 190 ± 15 to 127 ± 5 beats min-' (mean ± 1 s.d.) indicating that ,3-adrenoceptor blockade was substantial and highly significant (P < 0.001). 3 Before, during and following fatiguing activity with circulatory occlusion force declines were identical during and without P-adrenoceptor blockade. During and following activity without occlusion, there were slight declines in force which were questionably significantly different at 20 Hz (P < 0.05). 4 The compound muscle action potential (CMAP) amplitude, measured from the skin surface over the muscle, was unaltered by 3-adrenoceptor blockade before, during or after activity whether with or without circulatory occlusion.5 The maximal relaxation rate (MRR) was not significantly reduced in previously unfatigued muscle during ,-adrenoceptor blockade. During activity, both with and without circulatory occlusion, there was no evidence that MRR was reduced significantly more during ,3-adrenoceptor blockade. 6 The absence of a convincing effect of 13-adrenoceptor blockade on peripheral fatigue mechanisms may indicate that central mechanisms are involved or that impairments of peripheral force production, of a specific nature or as a result of exacerbation of limitations of circulatory oxygen transport, though small are detected during voluntary exercise and give rise to increases in motor unit recruitment and/or firing rates, and hence increased perception of fatigue.

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Influence of alprenolol on hemodynamic and metabolic responses to prolonged exercise in subjects with hypertension

Cited by 42 publications

References 11 publications

Factors contributing to increased muscle fatigue with β-blockers

Factors contributing to increased muscle fatigue with β-blockers

Systemic and Forearm Haemodynamic and Metabolic Effects of Racemic Propranolol or d-Propranolol in Healthy Subjects

Absence of excess peripheral muscle fatigue during beta‐adrenoceptor blockade.

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