Melo Ronaldo Meira, Martinho Eduardo, Michelini Lisete Compagno
Department of Physiology and Biophysics, Biomedical Sciences Institute, University of Sao Paulo, Av. Prof. Lineu Prestes, 1524, 05508-900, São Paulo, SP, Brazil.
Hypertension. 2003 Oct;42(4):851-7. doi: 10.1161/01.HYP.0000086201.27420.33. Epub 2003 Aug 11.
We showed that the training-induced, pressure-lowering effect correlates with decreased arteriole wall/lumen ratio and venule growth in the gracilis muscle. To investigate whether these beneficial changes are tissue-specific or occur in other muscles and tissues, we analyzed the effects of hypertension and training on microcirculatory profile of locomotor/nonlocomotor muscles and another nonmuscular tissue. Spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats were submitted to low-intensity training (50% to 60% maximal exercise capacity, 13 weeks); age-matched control rats were kept sedentary. Trained and sedentary rats were instrumented for pressure and heart rate measurements at rest. Morphometric analyses (arterioles, capillaries, venules) were performed in all tissues. Training attenuated pressure and heart rate only in SHR. Arterioles (inner diameter <30 microm) were markedly hypertrophied in sedentary SHR, but wall/lumen ratio was equally reduced (approximately 30%) and normalized by training in locomotor (soleus, gastrocnemius, gracilis) and nonlocomotor skeletal muscles (temporalis) in the myocardium and diaphragm, without changes in the renal cortex. Training also increased venule density (approximately 2-fold) only in locomotor and nonlocomotor muscles of SHR. Capillary density was similarly increased in all exercised muscles of both groups, with no change in temporalis and kidneys. Data suggest that growth/proliferation of small venules and regression of hypertrophied arteriole wall/lumen ratio are generalized tissue-specific (skeletal muscle) and group-specific (SHR) adjustments to training to reduce local resistance and augment physical capacity of circulation, thus contributing to training-induced pressure-lowering effect. They are accompanied by remodeling of myocardium (cardiac output) and diaphragm arterioles (ventilatory adjustments), stressing the importance of training as a nonpharmacological therapy to control pressure levels in hypertension.
我们发现，训练诱导的降压效果与股薄肌中细动脉壁/管腔比值降低和小静脉生长有关。为了研究这些有益变化是组织特异性的，还是发生在其他肌肉和组织中，我们分析了高血压和训练对运动/非运动肌肉以及另一种非肌肉组织微循环特征的影响。将自发性高血压大鼠（SHR）和Wistar-Kyoto大鼠进行低强度训练（最大运动能力的50%至60%，持续13周）；年龄匹配的对照大鼠保持 sedentary 状态。对训练和 sedentary 大鼠进行静息时血压和心率测量。对所有组织进行形态计量分析（细动脉、毛细血管、小静脉）。训练仅使SHR的血压和心率降低。久坐的SHR中，内径<30微米的细动脉明显肥厚，但壁/管腔比值同样降低（约30%），并通过训练在运动（比目鱼肌、腓肠肌、股薄肌）和非运动骨骼肌（颞肌）、心肌和膈肌中恢复正常，肾皮质无变化。训练还仅使SHR的运动和非运动肌肉中的小静脉密度增加（约2倍）。两组所有运动肌肉中的毛细血管密度均同样增加，颞肌和肾脏无变化。数据表明，小静脉的生长/增殖以及肥厚的细动脉壁/管腔比值的恢复是针对训练的全身性组织特异性（骨骼肌）和组特异性（SHR）调整，以降低局部阻力并增强循环的物理能力，从而促成训练诱导的降压效果。它们伴随着心肌（心输出量）和膈肌细动脉（通气调整）的重塑，强调了训练作为控制高血压患者血压水平的非药物疗法的重要性。
