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Biomedical subjects

L Gullestad

Publications and source records attributed to L Gullestad.

97 records · Page 6Linked to original sources
PubMed1988

Difference between beta-1-selective and non-selective beta-blockade during continuous and intermittent exercise.

Limiting factors of maximal exercise performance are not clearly defined. In order to differentiate between various factors, maximal exercise was studied during continuous (n = 12) and intermittent (n = 9) exercise. The non-selective beta-blocker timolol (10 mg b.i.d. for 5 days) was compared double-blind and placebo controlled with the beta-1-selective beta-blocker metoprolol (100 mg b.i.d. for 5 days), with respect to effect on maximal exercise tolerance. Total cumulated work was comparable during continuous and intermittent exercise. Timolol and metoprolol reduced maximal exercise performance. No difference was observed between the two beta-blockers during intermittent exercise. The non-selective beta-blocker caused a greater reduction in exercise performance (10.4%) than the beta-1-selective beta-blocker (4.7%) (P less than 0.05) during continuous exercise. Maximal heart rate was higher with metoprolol than timolol during continuous exercise. The non-selective beta-blocker caused a slightly greater inhibition of lipolysis than the beta-1 selective one. No significant differences in glucose concentrations were observed between the treatment regimens. Exercise caused a marked increase in serum potassium concentrations. Beta-blockade caused further increase in potassium at any given workload. This study indicates that maximal working capacity is comparable during continuous and intermittent exercise. Beta-1-selective and non-selective beta-blockade reduce the maximal working capacity, non-selective more than beta-1-selective. Substrate availability was not responsible for the beta-blocker induced reduction of the working capacity. The rate of rise in serum potassium was significantly higher during beta-blockade and may, therefore, be a limiting factor for the maximal working capacity.

Administration, Oral↗
PubMed1987

The effects of naloxone and timolol on plasma catecholamine levels during short-term dynamic exercise.

In order to study the role of opioid- and betareceptors on exercise-induced catecholamine responses, the effects of acute intravenous administration of 1 and 4 mg naloxone and of the non-selective betablocker timolol 2 mg of on circulating concentrations of adrenalin, noradrenaline and dopamine during exercise to exhaustion were examined in eight normal, healthy young men, using a double-blind, randomized, placebo-controlled design. During maximal exercise, adrenalin levels increased from 71 +/- 17 to 821 +/- 235 pg/ml (p less than 0.05), noradrenaline from 355 +/- 58 to 4235 +/- 1031 pg/ml (p less than 0.05), and dopamine from 72 +/- 20 to 178 +/- 44 pg/ml (p less than 0.05). Naloxone did not influence basal or exercise-induced noradrenaline responses. Timolol clearly augmented peak adrenalin concentration at maximal exercise capacity (1543 +/- 510 pg/ml, p less than 0.05). Basal noradrenaline level was increased (546 +/- 86 pg/ml, p less than 0.05), while exercise-induced noradrenaline level was reduced (2954 +/- 594 pg/ml, p less than 0.05) in proportion to the reduction in maximal exercise capacity during timolol treatment. Neither naloxone nor timolol affected dopamine levels. No additive effect was seen with the combination of naloxone and timolol. It is concluded that the opioid peptides are probably not involved in noradrenaline and dopamine responses, whereas betablockers change the catecholamine response to short-term maximal exercise.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Oral versus intravenous magnesium supplementation in patients with magnesium deficiency.

The efficacy of oral magnesium supplementation in correcting magnesium deficiency was examined in a group of 40 elderly patients with suspected magnesium deficiency. The patients were randomized in a double-blind, placebo-controlled fashion to oral magnesium-lactate-citrate for 6 weeks. Magnesium status was assessed by an intravenous magnesium-loading test at baseline and after treatment. For comparison, another group of 23 patients received 30 mmol magnesium sulfate intravenously daily for 7 days. A group of 30 patients without known predisposition to magnesium deficiency and a group of 27 young healthy subjects served as controls. The initial magnesium-loading test in the placebo group reduced magnesium retention from a mean 41% (95% confidence intervals 34-49) to 22% (15-29) (p less than 0.01). In the group receiving oral magnesium supplementation for 6 weeks, magnesium retention decreased from 39% (31-47) to 10% (2-18) (p less than 0.01), which was significantly better than with placebo treatment (p less than 0.01). The magnesium retention after oral magnesium supplementation was comparable to that observed after parenteral administration of magnesium for 7 days, 6% (-4 to 16), and to that in the reference groups of patients 4% (-2 to 10) and healthy control subjects 3% (-2 to 8). The study suggests that the bioavailability of orally given magnesium-lactate-citrate is satisfactory, and that oral administration of magnesium for 6 weeks may restore magnesium depots in patients with magnesium deficiency.

Administration, Oral↗