Frisk-Holmberg M, Juhlin-Dannfelt A, Aström H
Clin Physiol. 1985 Jun;5(3):231-42.
The influence of chronic beta 1-adrenoceptor blockade on haemodynamic and metabolic responses was examined in eight young hypertensive subjects during a 40 min submaximal bicycle test at 50% of maximal capacity. The patients were randomly allocated to one placebo and one treatment period of 6 weeks. During treatment atenolol (Tenormin, 100 mg) was given twice daily. Arterial pressure, cardiac output, leg blood flow, oxygen uptake and different metabolites in the blood were determined. The heart rate was reduced by beta 1-adrenoceptor blockade by 30% during exercise, and the decrease was related to plasma concentration of the drug. Cardiac output was decreased by approximately 10%, but the negative chronotropic effect was partly compensated for by a higher stroke volume. Blockade leg blood flow was reduced by 10%, but more oxygen was extracted, giving an unchanged oxygen uptake. Blood concentration and leg uptake of glucose were not influenced by the treatment, but plasma free fatty acids were reduced by 30-40%. Leg lactate release was decreased to half the value in the unblocked situation. Plasma renin activity did not increase at the beginning of exercise, but after 40 min an increase was seen, though only to half of the pretreatment value. It is concluded that beta 1-adrenoceptor blockade during submaximal exercise reduces blood flow to the working muscles and that this reduction is the result of a lower cardiac output. Aerobic metabolism is unchanged as a result of increased oxygen extraction, but less fat is used as lipolysis is inhibited. Glucose uptake by the working muscles is unchanged by beta 1-blockade, but there is evidence for an increased carbohydrate metabolism. As for non-selective blockade, atenolol decreases lactate release but this could be the result of non-specific action on the beta 1-receptor and/or increased carbohydrate oxidation. Furthermore, the beta 1-adrenoceptors seem to have a major influence on the renin release during exercise.
在8名年轻高血压患者进行40分钟最大运动能力50%的次极量自行车测试期间，研究了慢性β1肾上腺素能受体阻滞剂对血流动力学和代谢反应的影响。患者被随机分配到一个安慰剂期和一个为期6周的治疗期。治疗期间，阿替洛尔（天诺敏，100毫克）每日服用两次。测定动脉压、心输出量、腿部血流量、摄氧量和血液中的不同代谢产物。运动期间，β1肾上腺素能受体阻滞剂使心率降低30%，且这种降低与药物的血浆浓度有关。心输出量降低约10%，但负性变时作用部分被较高的每搏输出量所代偿。阻断后腿部血流量减少10%，但更多的氧气被摄取，从而使摄氧量保持不变。血液中葡萄糖浓度和腿部对葡萄糖的摄取不受治疗影响，但血浆游离脂肪酸减少30% - 40%。腿部乳酸释放降至未阻断状态时的一半。运动开始时血浆肾素活性未增加，但40分钟后有所增加，不过仅为治疗前值的一半。结论是，次极量运动期间β1肾上腺素能受体阻滞剂减少了流向工作肌肉的血流量，这种减少是心输出量降低的结果。由于氧气摄取增加，有氧代谢未改变，但由于脂解受到抑制，脂肪利用减少。β1受体阻滞剂未改变工作肌肉对葡萄糖的摄取，但有证据表明碳水化合物代谢增加。与非选择性阻断一样，阿替洛尔减少乳酸释放，但这可能是对β1受体的非特异性作用和/或碳水化合物氧化增加的结果。此外，β1肾上腺素能受体似乎对运动期间的肾素释放有主要影响。
