Tate C A, McMurray R G, Riggs C E, Setaro F, Horvath S M
Eur J Appl Physiol Occup Physiol. 1980;43(2):167-72. doi: 10.1007/BF00422447.
To examine the effects of exhaustive swimming in normal and myopathic hamsters on muscle mitochondrial Ca2+ metabolism, sedentary normal and BIO 14.6 dystrophic Syrian hamsters swam individually in 35 degree C water until exhaustion occurred. Although the normal hamsters swam three times longer than did the BIO 14.6 hamsters, both swimming groups had a comparable two-fold increase in blood lactate. Contrary to exhaustive running, exhaustive swimming did not significantly affect mitochondrial Ca2+ uptake in either cardiac or skeletal muscle, regardless of the disease state. However, in general, the coefficients of variation for mitochondrial Ca2+ metabolism increased as a function of exercise, with the BIO 14.6 swimmers more variable than the normal swimmers. This suggests that the mitochondrial Ca2+ uptake process may be affected in some manner by exhaustive swimming, so that deviations from the norm are more apparent. The results provide further evidence that mitochondrial Ca2+ metabolism adapts to the specific type of exercise utilized to produce exhaustion.
为研究力竭游泳对正常和患肌病仓鼠肌肉线粒体Ca2+代谢的影响,将久坐不动的正常叙利亚仓鼠和BIO 14.6营养不良叙利亚仓鼠分别置于35摄氏度水中游泳直至力竭。虽然正常仓鼠的游泳时间比BIO 14.6仓鼠长三倍,但两个游泳组的血乳酸均有类似的两倍增长。与力竭跑步不同,无论疾病状态如何,力竭游泳对心肌或骨骼肌线粒体Ca2+摄取均无显著影响。然而,总体而言,线粒体Ca2+代谢的变异系数随运动而增加,BIO 14.6游泳组比正常游泳组的变异更大。这表明力竭游泳可能以某种方式影响线粒体Ca2+摄取过程,从而使与正常情况的偏差更加明显。结果进一步证明线粒体Ca2+代谢会适应导致力竭的特定运动类型。