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Biomedical subjects

H L Brammell

Publications and source records attributed to H L Brammell.

At least 19 recordsLinked to original sources
PubMed1990

Plasma catecholamine responses to exercise after training with beta-adrenergic blockade.

Exercise training has been shown to decrease plasma norepinephrine (NE) and epinephrine (EPI) levels during absolute levels of submaximal exercise, which may reflect alterations in sympathetic tone as a result of training. To determine if beta-adrenergic blockade altered these changes in the plasma concentration of catecholamines with exercise conditioning, we studied the effects of beta-adrenergic blockade on NE and EPI at rest and during exercise in 24 healthy, male subjects after a 6-wk exercise training program. The subjects were randomized to placebo (P), atenolol 50 mg twice daily (A), and nadolol 40 mg twice daily (N). There were no changes in resting NE and EPI compared with pretraining values in any subject group. During the same absolute level of submaximal exercise NE decreased in P and A but was unchanged in N, whereas EPI decreased only in P. At maximal exercise all three groups developed significant increases in NE after training that paralleled increases in systolic blood pressure. EPI at maximal exercise increased after training with N but was unchanged with P or A. These training-induced changes in plasma catecholamine levels were masked or blunted when the A and N groups were studied while still on medication after training. Thus beta-adrenergic blockade has important effects on adaptations of the sympathetic nervous system to training, especially during submaximal exercise.

Adrenergic beta-Antagonists↗
PubMed1989

Exercise haemodynamic effects of beta-blockade and intrinsic sympathomimetic activity.

Beta-adrenergic blockade with intrinsic sympathomimetic activity (ISA) causes less depression of resting and submaximal heart rate (HR) than non-ISA beta-blockers. The effects of these drugs on exercise haemodynamics have not been well studied. We evaluated effects of pindolol, propranolol and placebo during rest and steady-state exercise on cardiac output, oxygen consumption, calf blood flow, HR and blood pressure in 18 healthy subjects. Pindolol 5 mg and propranolol 80 mg given twice daily, reduced maximal exercise HR by 50 and 52 beats.min-1 respectively, confirming similarity of beta 1-blockade. Resting cardiac output was unchanged in all three groups after one week of therapy. Cardiac output, measured during steady-state exercise decreased in the propranolol group (18.3 vs 15.6 l.min-1) with no significant changes in pindolol (15.7 vs 16.01.min-1) or placebo (18.6 vs 17.3 l.min-1). The rise in cardiac output, from rest to exercise, was similarly attenuated by propranolol but not by pindolol or placebo. Exercise stroke volume increased 12% on pindolol (123-140 cc) and decreased 7% on propranolol (143-133 cc). Neither drug had a detrimental effect on exercise calf blood flow compared to placebo. Thus, unlike propranolol, pindolol with ISA, maintains a normal cardiac output during submaximal exercise.

Adult↗
PubMed1986

Effects of selective and nonselective beta-adrenergic blockade on mechanisms of exercise conditioning.

Exercise conditioning involves adaptations in the heart, peripheral circulation, and trained skeletal muscle that result in improved exercise capacity. Since the specific influence of beta-adrenergic stimulation on these various adaptations has not been clear, we studied the effect of beta 1-selective and nonselective beta-adrenergic blockade on the exercise conditioning response of 24 healthy, sedentary men after an intensive 6 week aerobic training program. Subjects randomly assigned to receive placebo, 50 mg bid atenolol, or 40 mg bid nadolol were tested before and after training both on and off drugs. Comparable reductions in maximal exercise heart rate occurred with atenolol and nadolol, indicating equivalent beta 1-adrenergic blockade. Vascular beta 2-adrenergic selectivity was maintained with atenolol as determined by calf plethysmography during intravenous infusion of epinephrine. All subjects trained at greater than 85% of maximal heart rate and 80% of VO2 max determined on drug. VO2 max increased after training 16 +/- 2% (p less than .05) in the placebo group and 6 +/- 2% (p less than .05) in the atenolol group, while there was no change in the nadolol group. At maximal exercise, subjects receiving placebo increased their exercise duration and oxygen pulse significantly greater than those receiving atenolol or nadolol. During submaximal exercise there were reductions in heart rate and heart rate-blood pressure product in all three groups, but these reductions were greater with placebo than with either drug. Leg blood flow during submaximal exercise decreased 24 +/- 2% (p less than .01) in the placebo group but was unchanged in the atenolol and nadolol groups. Lactates in arterialized blood during submaximal exercise were reduced equivalently in all three groups after training. Capillary/fiber ratio in vastus lateralis muscle biopsy specimens increased 31 +/- 6% in the placebo group and 21 +/- 6% in the atenolol group (both p less than .05) and tended to increase in the nadolol group. Succinic dehydrogenase and cytochrome oxidase activities in muscle biopsy specimens increased equivalently in all three groups, especially during submaximal exercise, these changes were less marked than that with placebo. While beta-adrenergic blockade attenuated the exercise conditioning response, skeletal muscle adaptations including increases in oxidative enzymes, capillary supply, and decreases in exercise blood lactates were unaffected. Cardiac and peripheral vascular adaptations do appear to be affected by beta-adrenergic blockade during training. Cardioselectivity does not seem to be important in modifying these effects.

Adrenergic beta-Antagonists↗
PubMed1985

beta-2 Adrenergic blockade evaluated with epinephrine after placebo, atenolol, and nadolol.

Vascular beta 2-adrenergic blocking effects of the water-soluble drugs atenolol (beta 1-selective) and nadolol (nonselective) were evaluated. Twenty-four healthy young men were studied in three dosing groups (eight subjects per group) before and after 1 wk on placebo, atenolol (50 mg twice a day), or nadolol (40 mg twice a day). Maximal treadmill exercise heart rates were reduced to a similar degree by atenolol (-48 +/- 3 bpm) and nadolol (-48 +/- 4 bpm) but were not affected by placebo. Trough blood levels were 226 +/- 9 ng/ml for atenolol and 43 +/- 9 ng/ml for nadolol. Calf blood flow was measured with a plethysmograph and calf vascular resistance was calculated from blood pressure and flow. beta 2-Adrenergic blockade was determined at rest with epinephrine infused intravenously in graded doses from 0.001 to 0.032 micrograms/kg/min. Mean arterial pressure and calf vascular resistance rose markedly after nadolol but not after atenolol or placebo. Marked bradycardia developed after nadolol, probably by baroreceptor stimulation. Thus at an equivalent, substantial degree of beta 1-adrenergic blockade, nadolol blocks vascular beta 2-adrenergic receptors and atenolol does not. Measurement of the peripheral vascular response to epinephrine infusion is an effective means of assessing the impact of beta-adrenergic blockers on vascular beta 2-adrenergic receptors.

Adrenergic beta-Antagonists↗
PubMed1984

Effect of beta blockade and intrinsic sympathomimetic activity on exercise performance.

Beta-adrenergic receptor blocking drugs with intrinsic sympathomimetic activity may have the advantage of not depressing myocardial function and pulse rate at rest. Little is known about their effects during exercise. Thus, the effects of small and large doses of pindolol, a nonselective beta-adrenergic blocking drug with intrinsic sympathomimetic activity, were compared with the effects of small and large doses of propranolol in 13 normal men during treadmill exercise. Compared with placebo, all drug regimens decreased exercise duration (p less than 0.001). There were no significant differences in duration between pindolol and propranolol, or between the small and large dose of each drug. Maximal oxygen consumption tended to be lower with all preparations compared with placebo (p less than 0.10). With smaller doses, decrements of maximal heart rate (HR) and HR-blood pressure (BP) product were equivalent for pindolol and propranolol (decreases of 46 vs 43 beats/min, and 13,000 vs 12,000 units). The HR-BP product decreased more with high-dose propranolol than high-dose pindolol (decrease of 18,000 vs 14,800 units) due to a greater decrement in HR with propranolol (decrease of 65 +/- 3 vs 53 +/- 3 beats/min). At both submaximal levels, for both low- and high-dose preparations, HR, BP and HR-BP product were lower for propranolol than for pindolol. Thus, in healthy subjects, pindolol and propranolol at doses that produced equivalent reductions in maximal oxygen consumption, exercise duration and, for the smaller dose, HR, had different effects on submaximal HR-BP product, an index of myocardial oxygen consumption, as a result of a higher HR and BP with pindolol.

Adult↗
PubMed1984

Nifedipine and the conditioning response.

The effect of nifedipine (N) on conditioning was studied in 14 healthy sedentary men, aged 20 to 34 years. Subjects were ranked according to maximal oxygen consumption (VO2 max), paired, and 1 of each pair randomly assigned to take N, 20 mg, or placebo (C) 3 times daily. Exercise conditioning was 5 times/week for 6 weeks at greater than 85% of maximal heart rate for both groups. Adherence to exercise was 81% for the N and 82% for the C group. After training, the N group improved VO2 max from 41.4 +/- 1.4 to 51.6 +/- 2.0 ml/kg/min (p less than 0.05) and exercise time from 22 +/- 1 to 28 +/- 1 minutes (p less than 0.05). Heart rate (HR) at rest and the product of heart rate and systolic blood pressure both decreased (p less than 0.05): 70 +/- 6 to 55 +/- 4 beats/min; 9,300 +/- 900 to 6,800 +/- 700 beats/min X mm Hg. In the C group, VO2 max increased from 43.2 +/- 2.5 to 49.9 +/- 2.5 ml/kg/min (p less than 0.05); exercise duration improved from 24 +/- 2 to 29 +/- 2 minutes (p less than 0.05), and the rate-pressure product at rest decreased from 8,000 +/- 400 to 6,700 +/- 400 (p less than 0.05). Differences between N and C were not significant. Thus, N, unlike propranolol, does not inhibit the response to exercise conditioning.

Adaptation, Physiological↗
PubMed1984

Effect of aerobic conditioning on the peripheral circulation during chronic beta-adrenergic blockade.

The relation of peripheral circulatory adjustments to exercise training during long-term beta-adrenergic blockade has not been investigated. In 12 healthy men aged 22 to 34 years, blood flow in the calf was evaluated with submaximal exercise before and after a 6 week aerobic conditioning program. During conditioning, six subjects received no drug and six received propranolol, 80 to 120 mg/day in divided doses. Treated and control subjects were studied on entry and at the conclusion of a conditioning program, 72 hours after drug withdrawal in subjects given propranolol. The training was intensive and equivalent in both groups. Control subjects increased maximal oxygen uptake from 47.5 +/- 1.1 to 51.4 +/- 0.4 ml/kg per min (p less than 0.05), whereas those on propranolol did not improve. Immediately after exercise, blood flow in the calf was measured with strain gauge plethysmography after 3 minutes of supine exertion on a cycle ergometer. In control subjects, flow decreased from 15.7 +/- 1.6 to 14.0 +/- 1.4 ml/100 ml per min at 300 kg-m/min of exertion (p less than 0.05) and from 26.5 +/- 3.8 to 21.8 +/- 2.3 ml/100 ml per min at 700 kg-m/min (p less than 0.05). Vascular resistance was unchanged in these subjects at 300 kg-m/min (6.1 +/- 0.8 to 6.7 +/- 1.0 pru) (p = NS), but increased at 700 kg-m/min (4.2 +/- 0.8 to 4.8 +/- 0.7 pru) (p less than 0.05). In subjects given propranolol, no change in flow or resistance occurred after training at either work load.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Effect of beta-adrenergic blockade on circulating catecholamines and dopamine-beta-hydroxylase activity during exercise in normal subjects.

We investigated the effects of beta-adrenergic blockade with propranolol (P) on circulating catecholamines at rest and during isometric and dynamic exercise. By means of a radioenzymatic assay, we measured plasma norepinephrine (NE) and epinephrine (E) concentrations in nine normal, sedentary men, aged 22 to 34 years. Measurements were made during resting conditions, at 3 minutes of 30% maximal isometric handgrip exercise (IHE), and during submaximal and maximal dynamic treadmill exercise. Measurements were repeated one week later after the subjects received P in doses ranging from 40 to 80 mg four times a day (plasma P levels at the time of exercise ranged from 96 to 303 ng/ml with a mean of 178 ng/ml). We also measured serum dopamine-beta-hydroxylase (DBH) activity to detect changes in chronic sympathetic tone. Changes in NE from rest to exercise were significant (p less than 0.01) at all exercise loads with or without P. Changes in E from rest to exercise were significant (p less than 0.01) at all exercise loads with or without P except for submaximal dynamic exercise during the control study (p greater than 0.05). For NE, there were no significant differences between the control and P values either at rest or during any form of exercise. For E, there were no significant changes between the control and p values at rest or at maximal dynamic exercise, although there were mild increases (p less than 0.05) with IHE and submaximal dynamic exercise. DBH activity increased significantly (p less than 0.01) from rest to exercise for all exercise points with and without P, but there were no significant differences between the control and p values either at rest or during any form of exercise. In conclusion, we have demonstrated that competitive blockade of beta-adrenergic receptors at the tissue level does not alter neural release of NE or DBH and has little effect on adrenal release of E.

Adult↗
PubMed1983

Attenuation of exercise conditioning by low dose beta-adrenergic receptor blockade.

Because it has been shown that high doses of propranolol (40 to 80 mg orally, four times daily) markedly attenuate cardiovascular response to exercise training in healthy subjects, the effects of lower doses of this nonselective beta-adrenergic receptor antagonist on the conditioning response were investigated. Twelve normal men underwent maximal treadmill testing before and after a 6 week intensive exercise program. After an initial test, six men were randomized in a paired fashion to receive low dose propranolol and the others received no drug. The average propranolol dose +/- standard error was 22 +/- 4 mg four times daily, and the average decrease in maximal heart rate due to propranolol was 32 +/- 4 beats/min. Both groups trained at comparable intensities. At the end of the training period, propranolol was stopped and testing was repeated so that the effect of beta-receptor blockade was no longer present but the training effects still persisted. Maximal oxygen consumption increased in control subjects from 47.5 +/- 1.1 to 51.4 +/- 0.4 ml/kg per min (p less than 0.05) but was unchanged in those receiving propranolol (47.2 +/- 1.9 versus 47.4 +/- 1.5). Exercise duration increased in both groups but the increment was greater in the control group (+2.4 versus +1.1 min, p less than 0.05). It is concluded that low level beta-receptor blockade attenuates cardiovascular conditioning in normal subjects in exercise training programs. High levels of sympathetic stimulation during training appear to be important, if not essential, to the conditioning process.

Adrenergic beta-Antagonists↗
PubMed1982

Effect of aerobic conditioning on cardiovascular response to isometric exercise.

The response to isometric handgrip exercise (IHE) and isometric quadriceps exercise (IQE) (30% maximum voluntary contraction held 3 min) was studied before and after 5 wk of aerobic training. Training exercises involved only the lower extremities. Seventeen healthy unconditioned males aged 21--35 yr were subjects. During training nine subjects received propranolol in doses that provided a high degree of beta-adrenergic blockade; eight received a placebo. All subjects were tested before training or drug and after training, 3--5 days off drug. With IGE after training, the placebo group had lower maximum heart rate (91 +/- 4 to 79 +/- 5 beats/min, P less than 0.05), systolic blood pressure (151 +/- 5 to 139 +/- 4 mmHg, P less than 0.05), and double product (heart rate x systolic blood pressure) (138 +/- 10 x 10(2) to 110 +/- 7 x 10(2), P less than 0.05). The response to IQE in the propranolol group was unchanged after training. Heart rate, systolic blood pressure, and double product with IHE was unchanged in either group after training. Aerobic conditioning can modify the hemodynamic response to isometric exercise. This effect is specific for the trained muscle group and is prevented by beta-adrenergic blockade.

Adult↗
PubMed1982

The effects of a cardioselective (metoprolol) and a nonselective (propranolol) beta-adrenergic blocker on the response to dynamic exercise in normal men.

We compared the effects of a cardioselective beta-adrenergic blocking drug, metoprolol, with a nonselective beta-adrenergic blocker, propranolol, on the response of 10 normal men to dynamic treadmill exercise. The volunteers underwent a standard graded exercise test to exhaustion while receiving placebo; propranolol, 40 mg every 6 hours; propranolol, 80 mg every 6 hours; metoprolol, 50 mg every 6 hours; or metoprolol, 100 mg every 6 hours. The drugs were given in a double-blind fashion for 48 hours before exercise. Five days were allowed between successive drug administrations and the order of drug administration was randomized. Heart rate, arterial pressure, oxygen consumption, minute ventilation and CO2 production were monitored. Plasma drug concentrations were measured at the time of exercise. Judged by plasma levels, propranolol was about three times more potent than metoprolol in attenuating heart rate. Both drugs produced a wide variation in plasma levels after a given oral dose, and both drugs attenuated the systolic blood pressure response to exercise. Neither drug affected diastolic blood pressure or maximum oxygen consumption, maximum minute ventilation or the anaerobic threshold. We conclude that there is no evidence that the cardioselective drug metoprolol is superior to propranolol in terms of the ability to perform or respond to short-term maximal exercise. In addition, the fact that maximal oxygen consumption and the anaerobic threshold were unaffected implies that fatigue during exercise while on beta-adrenergic blocking drugs is not due to an effect of these drugs in limiting blood flow to the exercising extremities.

Adult↗
PubMed1976

A program for rehabilitation in coronary heart disease.

A practical, easily applied approach to coronary heart disease rehabilitation has been reviewed. Good rehabilitation is nothing more than total patient care that begins on admission to hospital and continues for the remainder of the patient's life. Optimization of medical care, psychosocial and vocational adjustment, activity progression, reconditioning, and patient education must be constantly sought at all stages of the program. Consistency and thoroughness can be assured through the use of a few helpful forms and handouts. The real and potential benefits of a comprehensive cardiac rehabilitation program amply justify the effort in all clinical settings.

Activities of Daily Living↗
PubMed1976

A physiologic approach to cardiac rehabilitation.

Rehabilitation of the patient with atherosclerotic coronary heart disease is a longitudinal, comprehensive care program that ends only on the death of the patient. Although much remains to be learned about cardiac rehabilitation, there is a rational basis predicated upon causes of disability, healing of myocardial damage, energy cost of activities, a rational approach to the activity and exercise prescription, and the potential benefits from exercise to justify a concerted national rehabilitation effort. The potential benefits in terms of more rapid return to work, maintenance of the patient's psychosocial integrity, and modification of natural history of the disease make the institution of a cardiac rehabilitation program a prudent activity for a practitioner, clinic, or hospital.

Adaptation, Physiological↗
PubMed1973

Pharmacodynamic studies of beta adrenergic antagonism induced in man by propranolol and practolol.

The pharmacodynamic activities of two beta adrenergic antagonists, propranolol and practolol, were compared in eight hypertensive patients. The activity of each antagonist was established in relation to its blood concentration at maximal and submaximal adrenergic blockade defined by inhibition of exercise tachycardia. Maximal inhibition of exercise tachycardia was comparable with both drugs and averaged 74+/-7% of the control value during drug treatment. This inhibition was achieved with a blood concentration of 2.5+/-0.4 mug/ml practolol and 0.10+/-0.08 mug/ml propranolol. The antagonist activities of these drugs against adrenergic stimulation with isoproterenol infusion indicated a much greater relative potency of propranolol against this stimulus, and in vivo estimates of PA(2) values differed by more than 600-fold. Relative antagonist activity of practolol during isoproterenol stimulation was equivalent both at cardiac (inotropic and chronotropic) and at vascular adrenergic receptors, whereas greater antagonist activity of propranolol was observed at vascular receptors than at cardiac receptors. Thus, the activity of practolol was not limited to cardiac receptors as previously suggested. Practolol did not reduce cardiac output at any dose level and the effect on resting blood pressure was small. Both practolol and propranolol had much greater hypotensive activity during exercise. These studies have defined the differing pharmacodynamic activities on the cardiovascular system of two effective beta adrenergic receptor antagonists and have established the blood levels of these antagonists necessary to achieve effective adrenergic blockade.

Acetanilides↗