Tomita T, Murakami T, Iwase T, Nagai K, Fujita J, Sasayama S
Department of Internal Medicine, Kyoto University Hospital, Japan.
Circulation. 1994 Feb;89(2):836-45. doi: 10.1161/01.cir.89.2.836.
The effects of chronic exercise training on myocardial contractility and beta-adrenergic signal transduction in hearts with left ventricular dysfunction have not been determined.
Fourteen-week-old cardiomyopathic BIO 53.58 and normal F1B Syrian hamsters underwent 10 weeks of treadmill training and were compared with 24-week-old BIO 53.58 and F1B untrained controls. Left ventricular isovolumic maximum positive dP/dt and peak developed pressure were significantly lower in BIO 53.58 than in F1B controls. Exercise training improved left ventricular contractile indices in BIO 53.58 but not F1B hamsters. The left ventricular beta-adrenergic receptor number (Bmax) was similar in BIO 53.58 and F1B controls. Basal adenylate cyclase activity (ACA) and ACAs stimulated by isoproterenol, 5'-guanylylimidodiphosphate (GppNHp), sodium fluoride, and forskolin were significantly lower in BIO 53.58 than in F1B controls. The functional activity of stimulatory guanine nucleotide-binding protein (Gs), as determined by reconstitution with S49 lymphoma cyc- cell membranes, was significantly lower in BIO 53.58 controls. After 10 weeks of exercise training, Bmax and basal and isoproterenol-stimulated ACAs were unchanged in either BIO 53.58 or F1B hamsters compared with controls. However, in F1B hamsters, training decreased ACAs stimulated by GppNHp, sodium fluoride, and forskolin, with a reduced functional activity of Gs. In contrast, these ACAs increased significantly in association with an enhanced Gs activity in cardiomyopathic BIO 53.58 hamsters after training.
Chronic exercise training does not change receptor-mediated beta-adrenergic responsiveness in either F1B or BIO 53.58 hamsters. However, exercise training reduces Gs activity in normal F1B hamsters and improves the functional abnormality of Gs in cardiomyopathic BIO 53.58 hamsters. This improvement may potentially contribute to augmented left ventricular contractility in BIO 53.58 after training.
慢性运动训练对左心室功能不全心脏的心肌收缩力和β-肾上腺素能信号转导的影响尚未明确。
14周龄的心肌病BIO 53.58和正常F1B叙利亚仓鼠进行10周的跑步机训练，并与24周龄未训练的BIO 53.58和F1B对照仓鼠进行比较。BIO 53.58仓鼠的左心室等容最大正dP/dt和最大舒张压力峰值显著低于F1B对照仓鼠。运动训练改善了BIO 53.58仓鼠的左心室收缩指标，但对F1B仓鼠无效。BIO 53.58仓鼠和F1B对照仓鼠的左心室β-肾上腺素能受体数量（Bmax）相似。BIO 53.58仓鼠的基础腺苷酸环化酶活性（ACA）以及由异丙肾上腺素、5'-鸟苷酰亚胺二磷酸（GppNHp）、氟化钠和福斯高林刺激的ACA均显著低于F1B对照仓鼠。通过与S49淋巴瘤cyc-细胞膜重组测定刺激型鸟嘌呤核苷酸结合蛋白（Gs）的功能活性，BIO 53.58对照仓鼠的该活性显著降低。经过10周的运动训练后，与对照相比，BIO 53.58或F1B仓鼠的Bmax以及基础和异丙肾上腺素刺激的ACA均未改变。然而，在F1B仓鼠中，训练降低了由GppNHp、氟化钠和福斯高林刺激的ACA，Gs功能活性降低；相反，在训练后的心肌病BIO 53.58仓鼠中，这些ACA显著增加，同时Gs活性增强。
慢性运动训练在FIB或BIO 53.58仓鼠中均不会改变受体介导的β-肾上腺素能反应性。然而，运动训练降低了正常F1B仓鼠的Gs活性，并改善了心肌病BIO 53.58仓鼠Gs的功能异常。这种改善可能有助于训练后BIO 53.58仓鼠左心室收缩力增强。
