White F C, McKirnan M D, Breisch E A, Guth B D, Liu Y M, Bloor C M
J Appl Physiol (1985). 1987 Mar;62(3):1097-110. doi: 10.1152/jappl.1987.62.3.1097.
Cardiac functional and structural adaptations to exercise-induced hypertrophy were studied in 68 pigs. Pigs were exercise trained on a treadmill for 10 wk. Sequential measurements were made of cardiac dimensions, [left ventricular end-diastolic diameter (EDD), changes in diameter (delta D%), wall thickness (WTh), wall thickening (WTh%), left ventricular pressure (LVP), time derivative of pressure (dP/dt), stroke volume, total body O2 consumption (VO2), blood gases, and systemic hemodynamics] at rest and during moderate and severe exercise. Postmortem studies included morphometric measurements of capillary density, arteriolar density, mitochondria, and myofibrils. All of the exercise-trained pigs showed significant increases in aerobic capacity. Maximum O2 consumption (VO2 max) increased by 37.5% in group 1 (moderate exercise training) and 34% in group 3 (heavy exercise training). Cardiac hypertrophy ranged from less than 15% in a group (n = 8) subjected to moderate exercise training to greater than 30% in a group (n = 11) subjected to heavy exercise training. Before training, exercise was characterized by a decreasing EDD during progressive exercise; this was reversed after exercise training. Stroke volume and end-diastolic volumes during exercise showed a highly significant increase after exercise training and hypertrophy. Morphometric measurements showed that mitochondria and cell membranes increased with increasing myocyte growth in all exercise groups, but there was only a partially compensated adaptation of capillary proliferation. Arteriolar number and length increased in all exercise groups. Intrinsic contractility as measured by delta D%, WTh%, or left ventricular dP/dt did not increase with exercise training and in some instances decreased. Therefore, left ventricular adaptation to strenuous exercise in the pig heart is primarily one of changes in left ventricular dimensions and a compensated hypertrophy. Exercise-induced increases in EDD and stroke volume can be accounted for by decreases in peripheral resistance and increased cardiac dimensions.
在68头猪身上研究了心脏功能和结构对运动诱导的肥大的适应性。猪在跑步机上进行了10周的运动训练。在休息以及中度和重度运动期间，对心脏尺寸[左心室舒张末期直径（EDD）、直径变化（δD%）、壁厚（WTh）、壁增厚（WTh%）、左心室压力（LVP）、压力时间导数（dP/dt）、每搏输出量、全身耗氧量（VO₂）、血气和全身血流动力学]进行了连续测量。死后研究包括对毛细血管密度、小动脉密度、线粒体和肌原纤维的形态测量。所有接受运动训练的猪的有氧能力均显著提高。第1组（中度运动训练）的最大耗氧量（VO₂ max）增加了37.5%，第3组（重度运动训练）增加了34%。心脏肥大范围从接受中度运动训练的一组（n = 8）中的小于15%到接受重度运动训练的一组（n = 11）中的大于30%。训练前，运动的特点是在渐进性运动期间EDD下降；运动训练后这种情况得到了逆转。运动训练和肥大后，运动期间的每搏输出量和舒张末期容积显著增加。形态测量表明，在所有运动组中，线粒体和细胞膜随着心肌细胞生长的增加而增加，但毛细血管增殖仅部分得到代偿性适应。所有运动组中小动脉数量和长度均增加。通过δD%、WTh%或左心室dP/dt测量的内在收缩力并未随运动训练增加，在某些情况下反而下降。因此，猪心脏对剧烈运动的左心室适应主要是左心室尺寸的变化和代偿性肥大。运动诱导的EDD和每搏输出量增加可归因于外周阻力降低和心脏尺寸增加。
