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Gazzetta Medica Italiana Archivio per le Scienze Mediche 2012 December;171(6):693-701


language: English

Effects of acute and chronic exercise on cardiac metallothionein in rats

Dabidi Roshan V. 1, Jolazadeh T. 1, Hosseinzadeh M. 2, Myers J. 3

1 College of Physical Education and Sport Sciences, Department of Sport Physiology, University of Mazandaran, Babolsar, Iran; 2 Center for Sensory-Motor Interaction (SMI), Aalborg University, Aalborg, Denmark; 3 Cardiology Division, VA Palo Alto Health Care System, Stanford University, Palo Alto, CA, USA


AIM: Exercise increases oxygen free radicals that cause oxidative stress. Metallothioneins (MTs) are increased in states of oxidative stress and ameliorate the damaging effects of free radicals.
METHODS: We measured MT levels and oxidative markers in heart tissue of rats exposed to acute training (2 days) or chronic (8 weeks) aerobic training. Thirty-two male rats were divided into four groups; sedentary, acute untrained, acute trained, acute and 8-wk regularly trained groups. The training programs were performed for 8 weeks, 5 times a week.
RESULTS: Acute groups were subjected to running on a treadmill until exhaustion. The MT, TBARS, glutathione peroxidase (GPx) activity, zinc (Zn), and CPK-MB levels were analyzed by standard methods. MT level after 8-wk of training remained unaltered as compared to the sedentary group. MT, GPx and TBARS levels significantly increased after acute exercise, whereas 8-wk of exercise training did not alter any of the indices of oxidative stress. In untrained rats, acute exercise induced increases in CPK-MB, while in the rats exposed to 8-weeks of training there were smaller changes in CPK-MB, as compared to the untrained rats.
CONCLUSION: The current results suggest that the increased cardiac MT level in response to exhaustive exercise may represent a protective mechanism against oxidative stress and consequent damage to cardiac cells, which are susceptible to ischemic injury. In addition, increased cardiac MT level may also contribute to a limitation related to intrinsic oxidant status in heart tissue.

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