Int J Sports Med 1997; 18(7): 497-502
DOI: 10.1055/s-2007-972671
Physiology and Biochemistry

© Georg Thieme Verlag Stuttgart · New York

Effect of Training on Antioxidant Capacity, Tissue Damage, and Endurance of Adult Male Rats

P. Venditti, S. Di Meo
  • Dipartimento di Fisiologia Generale ed Ambientale, Università di Napoli, Napoli, Italy
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09. März 2007 (online)

We studied the effects of physical training on antioxidant defences and susceptibility to damage induced by exhaustive exercise in tissues of adult (12 mo) rats. Therefore, untrained animals were sacrificed either at rest (n = 8) or immediately after swimming to exhaustion (n = 8). Rats trained to swim for 10 weeks were also sacrificed, 48 hr after the last exercise, either at rest (n = 8) or after exhaustive swimming (n = 8). Integrity of mitochondria and sarcoplasmic (SR) or endoplasmic (ER) reticulum of liver, heart, and muscle was assessed by measuring mitochondrial respiratory control and latency of alkaline phosphatase activity. Lipid peroxidation was measured by determination of malondialdehyde and hydroperoxides. Additionally, the effect of training on tissue antioxidant systems was examined by determining the glutathione peroxidase (GPX) and glutathione reductase (GR) activity and the overall antioxidant capacity (CA). Membrane integrity was unaffected by training in liver and muscle, and improved in heart of at rest animals, whereas lipid peroxidation was reduced in both liver and heart. Glutathione peroxidase and glutathione reductase activity, and overall antioxidant capacity were increased (p < 0.05) by training in liver and muscle. In heart, antioxidant capacity was increased from 0.21 ± 0.01 to 0.33 ± 0.02 (p < 0.05), but glutathione peroxidase activity remained unchanged (p > 0.05), and glutathione reductase activity was decreased from 3.56 ± 0.08 to 2.27 ± 0.10 ?mol × min-1 x g-1 (p < 0.05). The exhaustive exercise gave rise to tissue damage irrespective of trained state, as documented by similar loss of SR and ER integrity, and increase (p < 0.05) in lipid peroxidation found in exhausted trained and untrained rats. However, the above changes were elicited by exercise of greater duration in trained than in untrained rats (340 ± 17 min and 233 ± 6 min, respectively). These findings support the view that free radical-induced damage in muscle could be one of the factors involved in muscle fatigue. If so, the increased endurance in trained rats should reflect lengthening of the time required for the oxidative processes to sufficiently impair cell functions so as to make further exercise impossible.