Pierce G N, Sekhon P S, Meng H P, Maddaford T G
Division of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Winnipeg, Manitoba, Canada.
J Appl Physiol (1985). 1989 Apr;66(4):1715-21. doi: 10.1152/jappl.1989.66.4.1715.
Cardiac contractile function is dependent on the integrity and function of the sarcolemmal membrane. Swimming exercise training is known to increase cardiac contractile performance. The purpose of the present study was to examine whether a swimming exercise program would alter sarcolemmal enzyme activity, ion flux, and composition in rat hearts. After approximately 11 wk of exercise training, cardiac myosin and actomyosin Ca2+-adenosinetriphosphatase (ATPase) activity was significantly higher in exercised rat hearts than in sedentary control rat hearts. Glycogen content was increased in plantaris and gastrocnemius muscles from exercised animals as was succinic dehydrogenase activity in gastrocnemius muscle of exercised rats in comparison to sedentary rat preparations. Sarcolemmal vesicles were isolated from hearts of exercise-trained and control rats. Sarcolemmal Na+-K+-ATPase and K+-p-nitrophenylphosphatase activities, Na+-Ca2+ exchange, and passive Ca2+ binding did not differ between the two groups. ATP-dependent Ca2+ uptake and 5'-nucleotidase activity were elevated in the cardiac sarcolemmal vesicles isolated from exercised animals compared with sedentary control rats. Sarcolemmal phospholipid composition was not altered by the exercise training. Our results demonstrate that swimming training in rats does not affect most parameters of cardiac sarcolemmal function or composition. However, the elevated sarcolemmal Ca2+ pump activity in exercised rats may help to reduce intracellular Ca2+ and augment cardiac relaxation rates. The enhanced 5'-nucleotidase activity may stimulate adenosine production, which could affect myocardial blood flow. The present results further our knowledge on the subcellular response of the heart to swimming training in the rat.
心脏收缩功能依赖于肌膜的完整性和功能。已知游泳运动训练可提高心脏收缩性能。本研究的目的是检验游泳运动计划是否会改变大鼠心脏的肌膜酶活性、离子通量和组成。经过约11周的运动训练后,运动大鼠心脏中的心肌肌球蛋白和肌动球蛋白钙 - 腺苷三磷酸酶(ATP酶)活性显著高于久坐不动的对照大鼠心脏。与久坐不动的大鼠相比,运动动物的比目鱼肌和腓肠肌中的糖原含量增加,运动大鼠腓肠肌中的琥珀酸脱氢酶活性也增加。从运动训练大鼠和对照大鼠的心脏中分离出肌膜囊泡。两组之间的肌膜钠 - 钾 - ATP酶和钾 - 对硝基苯磷酸酶活性、钠 - 钙交换以及被动钙结合没有差异。与久坐不动的对照大鼠相比,从运动动物分离出的心脏肌膜囊泡中的ATP依赖性钙摄取和5'-核苷酸酶活性升高。运动训练未改变肌膜磷脂组成。我们的结果表明,大鼠的游泳训练不会影响心脏肌膜功能或组成的大多数参数。然而,运动大鼠中升高的肌膜钙泵活性可能有助于减少细胞内钙并提高心脏舒张速率。增强的5'-核苷酸酶活性可能刺激腺苷生成,这可能影响心肌血流量。目前的结果进一步加深了我们对大鼠心脏对游泳训练的亚细胞反应的认识。