Biomedical subjects

L Gullestad

Publications and source records attributed to L Gullestad.

At least 73 records · Page 4Linked to original sources

PubMed1997

Effect of bolus injection versus continuous infusion of furosemide on diuresis and neurohormonal activation in patients with severe congestive heart failure.

Previous studies have demonstrated that continuous infusion of furosemide results in increased diuresis and natriuresis compared with bolus administration of the drug in patients with severe heart failure. We reasoned that continuous infusion of furosemide caused less activation of neurohumoral mechanisms, since other studies have shown that bolus administration of furosemide may activate this system. We therefore tested the hypothesis that continuous administration of furosemide would increase water and sodium excretion due to less activation of neurohormones. Eight patients with severe heart failure were studied during continuous infusion over 24 h and bolus injections of furosemide twice daily in a randomized cross-over study. Bolus administration of furosemide increased diuresis and natriuresis significantly in the first 4 h after administration compared with continuous administration, but this was later reversed, resulting in similar 24 h total output. The neurohormones measured at baseline were all markedly elevated. Neither regimens of furosemide caused any further significant changes in neurohumoral response except that pro-ANF decreased more during the first 8 h after bolus administration compared to continuous infusion. This study has demonstrated that bolus administration of furosemide in conventional doses is equally effective as continuous intravenous infusion in patients with severe heart failure. This may be due to maximal neurohormonal activation in severe heart failure (NYHA III-IV) which could not be further activated by bolus administration.

Atrial Natriuretic Factor↗

PubMed1997

Methotrexate or total lymphoid radiation for treatment of persistent or recurrent allograft cellular rejection: a comparative study.

BACKGROUND: Methotrexate and total lymphoid irradiation (TLI) have been used successfully for treatment of recurrent and persistent rejection in orthotopic heart transplant recipients; however, there has been no comparison of these two modalities. METHODS: We retrospectively compared the efficacy of methotrexate (n = 29) versus TLI (n = 28) in heart transplant recipients with recurrent or persistent rejection. All patients received induction therapy (rabbit anti-thymocyte globulin or OKT3) and standard triple immunosuppressive therapy. Methotrexate (7.5 mg to 22.5 mg per wk) or TLI (80 cGy x 10 fractions) was used for the treatment of recurrent or persistent rejection on the basis of clinical indications. Average biopsy scores (International Society of Heart and Lung Transplantation biopsy score/total number of biopsies performed) calculated over 3-month periods, daily maintenance prednisone dose before and after methotrexate or TLI treatment, and actuarial survival and freedom from angiographic coronary artery disease and infection were compared. To control for the general decrease in prednisone with increased time from transplantation, a control group matched for time from transplantation was selected. RESULTS: Recipient sex and age at transplant, donor age, and donor ischemic time were similar in both groups. Days after transplantation to start of therapy was longer in patients receiving methotrexate; however, this did not reach statistical significance. Patients receiving TLI had received more cumulative corticosteroids and OKT3 before the start of TLI therapy (p < 0.001). There were no differences in actuarial freedom from infection or coronary artery disease between the two groups and between the treatment groups and the control group. Actuarial survival was reduced in patients receiving TLI 3 years after transplantation (p < 0.05). Maintenance prednisone doses from 3 months before until 9 months after therapy (mg/kg) were not different between patients receiving TLI and methotrexate and were significantly greater than the prednisone doses in the control group. Four months after treatment initiation, the prednisone dose was significantly reduced in both treatment groups compared with the pretherapy dose (methotrexate 0.28 +/- 0.16 to 0.22 +/- 0.13, p = 0.05; TLI 0.36 +/- 0.16 to 0.22 +/- .07, p < 0.001). The average biopsy score was significantly reduced by both methotrexate and TLI therapy (methotrexate 1.8 +/- 0.7 to 0.83 +/- 0.9, p = 0.0001; TLI 2.1 +/- 0.8 to 1.0 +/- 0.9, p = 0.0001). CONCLUSION: Methotrexate and TLI are both effective for the treatment of recurrent or persistent rejection after heart transplantation, reducing average biopsy scores and daily maintenance prednisone doses. There was a reduction in actuarial survival rates in patients treated with TLI, possibly reflecting the greater rejection therapy received before TLI initiation. Because both agents are effective, the choice of methotrexate or TLI may be based on clinical indications, as well as other issues, such as cost, compliance, and availability.

Actuarial Analysis↗

PubMed1997

Importance of decreased heart rate in predicting transplant coronary artery disease.

Studies in animals and humans have demonstrated that an increased heart rate is a predictor for the development of coronary atherosclerosis and overall cardiovascular mortality. In contrast, we have previously reported that the need for pacemaker implantation because of bradycardia in heart transplant recipients is associated with an increased prevalence of transplant coronary artery disease (TxCAD). Hence, the relevance of changes in heart rate to the development of TxCAD remains unclear. Intra-coronary ultrasound examinations (ICUS) were therefore analyzed in 130 heart transplant recipients (age 50 +/- 11 yr) studied at annual evaluations (3.7 +/- 3.0 yr after transplantation). Quantitative ultrasound measurements were obtained by calculating mean coronary artery intimal thickness (MIT) obtained by examination of the left anterior descending artery. The presence of TxCAD was defined as MIT > 0.3 mm. Resting heart rates (HR) were recorded with the patients in the supine position during routine echocardiography. Based on HR recordings, two groups were defined: group 1, HR below; or group 2, HR above the median. TxCAD was detected in 40% of the ICUS studies overall. The prevalence of TxCAD was higher in group 1 (49%) compared with group 2 (33%), p < 0.05. There was no significant difference in donor ischemic time or donor gender, recipient age, gender, body weight, CMV status, creatinine, total cholesterol, use of lipid lowering drugs or diltiazem. Donor age and use of beta-blockers were higher in group 1 compared with group 2 (29 +/- 10 vs. 25 +/- 9 yr, and 15% vs. 5%, for donor age and beta-blocker use, respectively). By multivariate regression analysis only donor age and years after transplantation were independently correlated with TxCAD. After excluding patients taking beta-blockers and diltiazem, the prevalence of CAD was still higher in group 1 (50%) vs. group 2 (34%). In conclusion, transplant coronary artery disease is more prevalent in patients with lower, rather than higher, heart rates. The reason for this is unclear, but may reflect impaired blood flow to the sinoatrial node.

Adult↗

PubMed1996

Early Doppler echocardiographic dysfunction is associated with an increased mortality after orthotopic cardiac transplantation.

BACKGROUND: Doppler echocardiographic (DE) diastolic dysfunction has been correlated with rejection after orthotopic cardiac transplantation (Tx). However, the relationship of early diastolic dysfunction to late outcome is unknown. The purpose of this study was to assess the correlation between early DE diastolic dysfunction and outcome after heart Tx. METHODS AND RESULTS: Of 133 patients undergoing heart Tx between October 1990 and April 1994, 83 were identified with > or = 4 routine DE performed during the first 6 months. Assessment of diastolic function included measurement of isovolumic relaxation time (IVRT), pressure half-time (PHT), and peak early mitral inflow velocity (M1). Diastolic dysfunction was defined as a decrease of 15% from baseline (IVRT and PHT) or an increase of 20% (M1). A mean dysfunction score (MDS) was calculated for each patient (number of episodes of dysfunction by Doppler total number of echocardiograms performed). The population diastole MDS was determined and two groups established (group 1, MDS < mean; group 2, MDS > mean). Actuarial survival, rejection, and transplant coronary artery disease (TxCAD) were compared between groups. Actuarial survival was significantly reduced in patients with greater early diastolic dysfunction (P < .05). There were 17 deaths overall: 5 in group 1 (mean, 786 days) and 12 in group 2 (mean, 384 days). There were no significant differences in treated rejection episodes, actuarial freedom from rejection or TxCAD, immunosuppression, sex, donor age, donor ischemic time, or cytomegalovirus between the two groups. CONCLUSIONS: Diastolic dysfunction within 6 months of transplant was associated with an increased late mortality.

Adult↗

PubMed1996

The effect of acute vs chronic treatment with beta-adrenoceptor blockade on exercise performance, haemodynamic and metabolic parameters in healthy men and women.

1. Variable results have been reported on the effect of beta-adrenoceptor blockers on maximal oxygen uptake (VO2 max) and exercise endurance. This may in part be due to different subject populations, but it could also be due to an adaption of metabolic and haemodynamic responses to exercise during chronic treatment with beta-adrenoceptor blockers. The present study was therefore carried out to examine the effect of acute and chronic administration of the non-selective beta-adrenoceptor blocker propranolol on both peak VO2 and exercise performance in the same subjects. Since the effect of beta-adrenoceptor blockade has not been properly investigated in women, eight healthy women were compared with seven men. Progressive bicycle exercise to exhaustion was performed after propranolol 0.15 mg kg-1 i.v. (acute) or 80 mg three times daily for 2 weeks (chronic) or placebo given according to a double-blind crossover design. 2. Mean (s.e. mean) peak VO2, was significantly reduced from 42.3 (1.6) ml min-1 kg-1 during placebo to 40.3 (1.2, P < 0.05) ml min-1 kg-1 after acute and 39.1 (1.2, P < 0.001) ml min-1 kg-1 after chronic propranolol treatment. No significant difference in peak VO2 between the two propranolol treatment regimens was observed (mean difference 1.2, 95% CI -0.1 to 2.4 ml min-1 kg-1). There was no treatment interaction with gender. 3. Cumulative work, 163 (9.3) kJ, was significantly reduced by acute, 148 (7.7, P < 0.001) kJ, and chronic, 147 (7.6, P < 0.001) kJ, administration of propranolol since the time to exhaustion was reduced by 5.3% and 5.3%, respectively. There was no significant difference between the two regimens of propranolol (mean difference 0.2, 95% CI -6.7 to 7.0 kJ) or between the sexes. Maximal knee extensor and handgrip strengths were not affected by propranolol. 4. Whereas sex did not influence ventilatory, haemodynamic or metabolic parameters, some differences were observed between acute and chronic propranolol treatment. During submaximal exercise oxygen uptake was reduced by approximately 2% and RER values increased by 0.04-0.05 after chronic treatment in contrast to no effect of acute propranolol treatment. Heart rate and systolic blood pressure were reduced significantly more after chronic compared with acute propranolol treatment; peak heart rate being 186 (2.2), 147 (2.3) and 134 (2.3) beats min-1, and peak systolic blood pressure being 189 (7), 171 (4) and 161 (4) mmHg after placebo, acute and chronic propranolol administration, respectively. Also the exercise induced rise in potassium and lactate levels were modified differentially; the rise in potassium concentration was less after chronic compared with acute propranolol treatment and lactate levels were reduced only after chronic administration of propranolol. In contrast, ventilation, which was unchanged after propranolol during submaximal exercise, was reduced to similar extent at exhaustion from 108 (6.4) to 97 (7.2) and 96 (5.9) l min-1 after acute and chronic propranolol administration, respectively. Diastolic blood pressure and subjective perception of fatigue were similar across the treatment regimens. 5. The study has demonstrated that acute and chronic administration of propranolol result in different haemodynamic and metabolic response to exercise, although endurance and peak oxygen consumption were reduced to the same extent. The response to propranolol was not significantly different between men and women.

Adrenergic beta-Antagonists↗

PubMed1996

Analysis of deaths in patients awaiting heart transplantation: impact on patient selection criteria.

OBJECTIVE: To analyse the clinical characteristics of patients who died on the Stanford heart transplant waiting list and to develop a method for risk stratifying status 2 patients (outpatients). METHODS: Data were reviewed from all patients over 18 years, excluding retransplants, who were accepted for heart transplantation over an eight year period from 1986 to 1994. RESULTS: 548 patients were accepted for heart transplantation; 53 died on the waiting list, and 52 survived on the waiting list for over one year. On multivariate analysis only peak oxygen consumption (peak VO2: 11.7 (SD 2.7) v 15.1 (5.2) ml/kg/min, P = 0.02) and cardiac output (3.97 (1.03) v 4.79 (1.06) litres/min, P = 0.04) were found to be independent prognostic risk factors. Peak VO2 and cardiac index (CI) were then analysed in the last 141 consecutive patients accepted for cardiac transplantation. All deaths and 88% of the deteriorations to status 1 on the waiting list occurred in patients with either a CI < 2.0 or a VO2 < 12. In those with a CI < 2.0 and a VO2 < 12, 38% died or deteriorated to status 1 in the first year on the waiting list. Patients with CI > or = 2.0 and a VO2 > or = 12 all survived throughout follow up. Using a Cox's proportional hazards model with CI and peak VO2 as covariates, tables were constructed predicting the chance of surviving for (a) 60 days and (b) 1 year on the waiting list. CONCLUSIONS: These data provide a basis for risk stratification of status 2 patients on the heart transplant waiting list.

Cardiac Output↗

PubMed1996

Diabetes mellitus and morbidity and mortality risks after coronary artery bypass surgery.

Of 1025 patients (912 men, 113 women) who underwent coronary artery bypass grafting and were followed up for a mean of 7.4 years, 45 (4.4%) had diabetes mellitus. Norwegian population is 1.8-2%). Early mortality was not significantly greater among diabetics than in non-diabetics (2.2 vs. 3.1%, odds ratio--OR-0.44, confidence interval--CI- 0.05-3.56). Diabetic patients had no increased risk of perioperative myocardial infarction (OR = 0.87, CI 0.36-2.10) or of low-output syndrome necessitating intraortic balloon pumping (OR = 0.42, CI 0.55-3.05), and no excess incidence of late non-fatal myocardial infarction (relative risk = 0.69, CI 0.10-1.28) or late chronic heart failure (OR = 2.50, CI 0.5-11.0). Long-term mortality was increased in the diabetic patients (relative risk 1.87, CI 1.60-2.14). Thus diabetes did not entail heightened risk of early mortality, perioperative myocardial infarction or low-output syndrome. Nor was there excess risk of recurrent angina pectoris, late non-fatal myocardial infarction or chronic heart failure among the diabetic patients, but the late mortality risk was increased.

Angina Pectoris↗

PubMed1996

Influence of the exercise protocol on hemodynamic, gas exchange, and neurohumoral responses to exercise in heart transplant recipients.

BACKGROUND: A gradual accommodation to increasing exercise loads has been recommended for exercise testing in denervated posttransplantation heart recipients. However, how the exercise protocol influence the hemodynamic, gas exchange, and hormonal response to exercise in this not been studied. METHODS: Nine heart transplant recipients tests incremental maximal bicycle ergometry tests in random order. Exercise stages of 1 and 3 minute durations were compared with matched work rate increments ranging between 30 and 40 W. Expiratory gas was measured continuously and arterial blood was sampled at each of the matched work rates. RESULTS: Total exercise duration was 6.4 +/- and 15.3 +/- 0.7 minutes for the 1-minute and 3-minute protocols, respectively. Maximal workload was significantly higher during the 1-minute versus the 3-minute protocol (238 +/- 9 versus 200 +/- 11 W, p < 0.001), but maximal oxygen uptake was not significantly different (25.5 +/- 1.1 versus 26.5 +/- 1.2 ml. min-1.kg-1). Hemodynamic, metabolic, and some hormonal parameters showed marked differences between the two protocols, with significantly higher responses observed during the 3-minute protocol for heart rate, ventilation, lactate, atrial natriuretic factor, and growth hormone. Catecholamine (epinephrine and norepinephrine) and insulin responses did not differ between the two tests. If expressed as a relative exercise intensity (percentage of maximal oxygen uptake) no differences in hormonal responses were observed between the two protocols, except for growth hormone response which remained higher during the 3-minute protocol. CONCLUSIONS: Although maximal oxygen uptake was independent of the exercise protocol in these heart transplant recipients, the exercise protocol has a major influence on the hormonal and metabolic response. The delayed response observed for oxygen uptake and hormonal responses suggests a significant physiologic lag time during the more rapidly incremental protocol. These differences should be taken into account when exercise is used as a method to evaluate the heart transplant recipient.

Adult↗

PubMed1996

Exercise capacity of heart transplant recipients: the importance of chronotropic incompetence.

BACKGROUND: Maximal exercise capacity is limited in patients after heart transplantation. The extent to which chronotropic incompetence contributes to this intolerance has not been well defined. METHODS: This prospective cross-sectional study examined the heart rate response to exercise and its relation to exercise capacity in 159 heart transplant recipients during progressive, symptom-limited, upright exercise. All prior exercise studies of heart transplant recipients that reported peak oxygen uptake and peak heart rate were also evaluated. RESULTS: Peak oxygen uptake was closely correlated with peak heart rate (r = 0.39, p < 0.001) and maximum increase in heart rate (r = 0.49, p < 0.001) during exercise by our patients. Similar correlations were found in the published studies for peak oxygen uptake versus maximal heart rate (r = 0.54, p < 0.05) and peak oxygen uptake versus increase in heart rate (r = 0.63, p < 0.02). The current study showed that the increase in heart rate from rest to peak exercise was significantly higher and the decline in heart rate after exercise significantly faster for patients 2 or more years after transplantation than for patients less than 2 years after transplantation (46 +/- 2 versus 38 +/- 1.9 beats/min, p < 0.05); the decline in heart rate 4 minutes after exercise was 27 +/- 1.8 versus 16 +/- 1.8 beats/min, respectively ( p < 0.001). CONCLUSION: The reduction in peak oxygen consumption, particularly during the first 2 years, appears to be related in part to chronotropic incompetence. Late after transplantation the heart rate response to exercise is greater and the decline in heart rate after exercise faster, suggesting possible autonomic reinnervation in some patients. Chronotropic incompetence may be an inadequate explanation of oxygen uptake impairment seen late after transplantation, when other factors such as myocardial dysfunction and intrinsic skeletal muscle abnormalities are of increasing importance.

Analysis of Variance↗

PubMed1995

[Drug therapy of angina pectoris. Are the possibilities exploited well enough?].

A retrospective comparative study of the use of antianginal drugs in 1987 and 1992/93 has been carried out in unselected series of patients admitted for angiographic evaluation. Compared with the patients in 1987 the patients in 1992/93 were treated with approximately 50% of the doses of beta-blockers and isosorbide dinitrate. There was also a considerable reduction of the proportion of patients who received doses of beta-blockers of a similar level as used in large multicentre studies showing improved survival after myocardial infarction. The explanation of this change in therapy may be due, at least partly, to a general fear of side-effects.

Adrenergic beta-Antagonists↗

PubMed1995

[Intermittent claudication and beta-blockaders. An unfortunate combination?].

beta-adrenergic blockers have been considered relatively contraindicated in patients with peripheral arterial disease because of reports claiming that these drugs may worsen intermittent claudication. The authors review the published randomized controlled trials and discuss the results of comparisons of this treatment with treatment with alternative drugs. None of the studies of beta-blockade in patients with intermittent claudication showed a reduction of walking distance or impairment of peripheral flow compared with patients given placebo, except one study using a beta-blocker with intrinsic sympathomimetic activity. Alternative drugs are included in only few trials and do not seem to be beneficial. There is a lack of evidence to suggest that beta-blockers adversely effect walking capacity or worsen symptoms in mild to moderate intermittent claudication. beta-blockers should not be avoided if considered in other respects to be the optimal therapy for associated atherosclerotic disease.

Adrenergic beta-Antagonists↗

PubMed1995

[Treatment of terminal heart failure].

Heart transplantation is one treatment for terminal heart failure. To assure a good result it is important to give optimal treatment while waiting for a suitable donor organ. We review the treatment received by patients on the waiting list for heart transplantation at our hospital from 1983 to 1994. On the basis of our experience from 183 patients, we discuss the routine and intensive care of severe heart failure, as well as the practice of anticoagulation and antiarrhythmic treatment.

Adolescent↗

PubMed1995

[Hypercholesterolemia--a clinical problem in heart transplantation. A therapeutic trial with low-dose lovastatin].

One year after heart transplantation, serum total cholesterol had increased by 24% in 103 recipients on prednisolon, cyclosporin A, and azathioprin immuno-suppression, and was above 5.2 mmol/l in 84 of them. Incremental small dose lovastatin treatment up to 20 mg per day safely reduced total cholesterol by 19% and LDL-cholesterol by 24% in 14 patients with serum cholesterol above 7.5 mmol/l. Serum concentration of lovastatin did not increase further after three weeks treatment with 20 mg. It is concluded that hypercholesterolaemia in heart recipients treated with cyclosporin A can be treated safely with small dose lovastatin. Drug therapy should be individualized and conducted by physicians experienced in transplantation medicine.

Adult↗

PubMed1995

[Reduced physical tolerance in patients with heart failure. Mechanisms and therapeutic effects].

Physical performance is markedly reduced in patients with congestive heart failure, but the reason has not been precisely defined. It has been generally assumed that reduced exercise performance is related to ventricular systolic performance, or as more recently suggested, to impaired left ventricular diastolic function. However, there is no clear relationship between the indices of left ventricular performance and exercise capacity, and there is a dissociation between improvement in haemodynamic parameters and exercise performance. Recent studies suggest that peripheral changes may be major determinants of exercise performance. This may involve reduced blood flow to the exercising limbs because of impaired vasodilatory capacity or intrinsic changes in the skeletal muscle itself. In this review, these factors are considered, and the impact of different therapeutic strategies is discussed.

Exercise↗

PubMed1995

[Beta 3-receptors: incidence and properties, possible clinical significance].

Beta 3-adrenoceptors is a term used for atypical beta-adrenoceptors which do not fit into either the beta 1- or beta 2-receptor as classified by pharmacological methods. The receptor has been cloned and is thus also genetically defined. Beta 3-adrenoceptors appear to be widely distributed. Until now their importance has been based on studies using agonists with high potency, but yet not selective for beta 3-adrenoceptors. The distribution and functional importance in humans are unclear, and will probably not be clarified before selective antagonists and labelled ligand are developed. Agonists for the beta 3-adrenoceptors may be of clinical value in the treatment of obesity, non-insulin dependent diabetes mellitus, gastrointestinal disorders like irritable colon, inflammatory lung diseases and depression.

Adrenergic beta-Agonists↗

PubMed1995

K+ balance of the quadriceps muscle during dynamic exercise with and without beta-adrenoceptor blockade.

The effect of propranolol (0.15 mg/kg body wt) on K+ fluxes was investigated in seven healthy males performing 8-min two-legged knee-extension exercise at two different powers. K+ concentration was measured in the femoral vein by a K(+)-selective electrode, and leg blood flow was measured by the dye-dilution technique. During control bouts, rates of change in femoral venous K+ concentration were 38 +/- 10 and 53 +/- 8 mumol.l-1.s-1 at onset of exercise (K+ efflux) and -14 +/- 3 and -34 +/- 3 mumol.l-1.s-1 at cessation of exercise (K+ reuptake) at low and high powers, respectively. This mismatch between K+ efflux and reuptake rates fits with the steady-state K+ loss rate of 0.14 +/- 0.04 and 0.32 +/- 0.09 mmol/min. Propranolol raised K+ efflux rate, did not modify K+ reuptake rate or steady-state K+ loss, but caused transiently increased K+ loss rate at the onset of exercise, thus accentuating the rise of arterial K+ concentration. In conclusion, the continuous muscle K+ loss during steady-state exercise with a small muscle mass is not due to lack of catecholamine stimulation, but beta-adrenoceptor blockade increased the Na(+)-K+ pump lag so that the initial K+ loss at onset of exercise was increased.

Adrenergic beta-Antagonists↗

PubMed1994

K+ shifts of skeletal muscle during stepwise bicycle exercise with and without beta-adrenoceptor blockade.

1. K+ efflux rate and control of K+ reuptake rate in exercising muscle cells was examined in six healthy female volunteers. 2. A K(+)-selective electrode in the femoral vein continuously monitored K+ concentration ([K+]fv) during bicycling. Power was increased stepwise 5-6 times by 30-40 W every fourth minute until exhaustion before and after I.V. administration of propranolol. Leg blood flow was measured by bolus injections of Cardiogreen. 3. [K+]fv increased from about 4.3 to 6.8 mmol l-1 at exhaustion both before and after propranolol administration, but after drug infusion endurance was reduced from 22.2 +/- 0.6 to 19.7 +/- 1.1 min, so [K+]fv rose more rapidly. 4. The exercise-induced efflux rate of K+ from the muscle cells was estimated to be about 11 mumol kg-1s-1 at exhaustion both before and after propranolol administration. 5. As an indicator of rate of net loss of K+ from the leg, veno-arterial concentration differences ([K+]fv-a) during first, fourth and fifth power increments were high after 15 and 40 s, but declined toward the end of each power step. Propranolol accentuated [K+]fv-a only after 15 and 40 s of the first and fourth increments. 6. The exercise-induced increase in reuptake rate of K+ in the muscle, estimated at exhaustion, was not significantly changed by propranolol and was about 10 mumol kg-1s-1, corresponding to about 15% of maximum Na(+)-K+ pump capacity in man. 7. Extracellular accumulation and loss of K+ from muscle during bicycle exercise is due to Na(+)-K+ pump lag. The higher [K+]fv during propranolol is mainly due to impaired redistribution outside the exercising muscles. In addition at low powers, beta-adrenoceptor blockade caused a transiently increased net loss due to an accentuated Na(+)-K+ pump lag.

Adult↗

PubMed1994

Effect of beta-adrenoceptor blockade on post-exercise oxygen consumption.

In the recovery period after strenuous exercise, there is an increase in O2 uptake termed the excess post-exercise O2 consumption (EPOC), consisting of a rapid and a prolonged component. Mechanisms regulating the prolonged component of EPOC are not completely understood, but an effect of catecholamines has been suggested. The purpose of this study was to investigate the effect of beta-adrenoceptor blockade on EPOC. Six healthy young men were randomized to one control experiment and two exercise experiments, one with and one without nonselective beta-adrenoceptor blockade. In the exercise experiments, they exercised for 60 minutes at 78% +/- 3% (mean +/- SD) of maximal O2 uptake (VO2max) on a cycle ergometer followed by 6.5 hours' bedrest. In the beta-adrenoceptor blockade experiment, propranolol (0.1 mg.kg-1 body weight [BW]) was administered intravenously immediately after the exercise bout and again 3.5 hours after exercise. The control experiment was performed without exercise or beta-adrenoceptor blockade. EPOC was calculated as the difference in O2 uptake between the exercise and control experiments. A supplementary study on 15 subjects showed resting O2 uptake to be unaffected by propranolol. O2 uptake was significantly increased during the recovery period after exercise when no beta-adrenoceptor blocker was administered. After 6.5 hours of bedrest, the mean increase (+/- SE) in O2 uptake was 19 +/- 4 mL.min-1. In contrast, when propranolol was administered during recovery from exercise, O2 uptake was significantly increased for only the first 2 hours. Propranolol decreased total EPOC (+/- SE) by about one third, from 14.4 +/- 1.9 to 9.5 +/- 2.5 L.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗