Venditti P, Di Meo S
Dipartimento di Fisiologia Generale ed Ambientale, Università di Napoli Federico II, Italy.
Arch Biochem Biophys. 1996 Jul 1;331(1):63-8. doi: 10.1006/abbi.1996.0283.
It is well known that physical training permits an animal to respond successfully to exercise loads of various types, intensities, and durations. Furthermore, the trained animal can sustain the activity for a long period before the fatigue becomes limiting. The effects of physical training on the antioxidant defenses of tissues and on their susceptibility to damage induced by exhaustive exercise have been investigated. Therefore, untrained rats were sacrificed either at rest or immediately after swimming to exhaustion. Rats trained to swim for 10 weeks were also sacrificed, 48 hr after the last exercise, either at rest or after exhaustive swimming. Homogenates of liver, heart, and muscle were used for biochemical determinations. Mitochondrial and sarcoplasmic (SR) or endoplasmic (ER) reticulum integrity was assessed with measurements of respiratory control index and latency of alkaline phosphatase activity. Lipid peroxidation was measured by determination of malondialdehyde and hydroperoxides. Additionally, the effect of training on the antioxidant protection systems of tissues was examined by determining the glutathione peroxidase and glutathione reductase activity and the overall antioxidant capacity. Mitochondrial, SR, and ER integrity and lipid peroxidation were similar in trained and untrained at rest animals, whereas the glutathione peroxidase and glutathione reductase activity and the overall antioxidant capacity of tissues were greater in trained animals. The exhaustive exercise gave rise to tissue damage irrespective of the trained state, as documented by similar loss of SR and ER integrity, and by increase in lipid peroxidation found in exhausted trained and untrained rats. Because exercise endurance capacity was greatly increased by training, our results suggest that free radical-induced damage in muscle could be one of the factors terminating muscle effort. In effect, the greater antioxidant level should allow trained muscle to withstand oxidative processes more effectively, thus lengthening the time required so that the cell function is sufficiently damaged as to make further exercise impossible.
众所周知，体育训练能使动物成功应对各种类型、强度和持续时间的运动负荷。此外，经过训练的动物能够在疲劳成为限制因素之前长时间维持活动。人们已经研究了体育训练对组织抗氧化防御及其对力竭运动诱导损伤的易感性的影响。因此，未训练的大鼠在休息时或游泳至力竭后立即处死。经过10周游泳训练的大鼠在最后一次运动后48小时，同样在休息时或力竭游泳后处死。肝脏、心脏和肌肉的匀浆用于生化测定。通过测量呼吸控制指数和碱性磷酸酶活性的潜伏期来评估线粒体和肌浆网（SR）或内质网（ER）的完整性。通过测定丙二醛和氢过氧化物来测量脂质过氧化。此外，通过测定谷胱甘肽过氧化物酶和谷胱甘肽还原酶活性以及总抗氧化能力，研究了训练对组织抗氧化保护系统的影响。在休息状态下，训练组和未训练组动物的线粒体、SR和ER完整性以及脂质过氧化情况相似，而训练组动物组织的谷胱甘肽过氧化物酶和谷胱甘肽还原酶活性以及总抗氧化能力更高。无论训练状态如何，力竭运动都会导致组织损伤，这在力竭的训练组和未训练组大鼠中表现为相似的SR和ER完整性丧失以及脂质过氧化增加。由于训练极大地提高了运动耐力，我们的结果表明，自由基诱导的肌肉损伤可能是终止肌肉运动的因素之一。实际上，更高的抗氧化水平应使训练有素的肌肉更有效地抵抗氧化过程，从而延长细胞功能受到充分损伤以至于无法进行进一步运动所需的时间。
