Physical activity is probably the only physiological source of increased production of ROS. How can we reconcile this evidence with the known beneficial effects of exercise? We will present here some of the results obtained in a multicentric study carried out on rats undergoing aerobic exercise training on a treadmill. Exercise – even moderate - led to the formation of long-lasting circulating lipid peroxidation products and to DNA damage in male germ cells. On the other hand, exercise training protected rat heart from ischemia/reperfusion (I/R) injury; both oxidative stress and cardioprotection were proportional to the intensity of the exercise protocol. Training-induced cardioprotection was accompained by the upregulation of Mn-SOD, HSP70 and HO-1 in the heart, along with the upregulation of other proteins, such as Caveolin-3, probably unrelated to the anti-oxidant defence. A 10-wk exercise training led to the sprouting of new capillaries in the myocardium. Both heart resistance to I/R injury, and increase in HSP70 protein and in cardiac vascularization were rather persistant over a detraining period. Moreover, physical training induced paraoxonase-3 upregulation, thus contributing to reduce cholesterol oxidation. Some of the biochemical pathways leading to these beneficial effects were elucidated in our work. Noteworthy, physical activity appeared to exert an hormetic effect, with chronic moderate exercise upregulating protective proteins, and single bursts of stressing exercise leading to cell injury, expecially in untrained animals. The contribute of ROS to the signaling pathways leading to the upregulation of cell defences as well as to cell damage is paramount.

Exercise: friend and foe

MARINI, MARINA;
2009

Abstract

Physical activity is probably the only physiological source of increased production of ROS. How can we reconcile this evidence with the known beneficial effects of exercise? We will present here some of the results obtained in a multicentric study carried out on rats undergoing aerobic exercise training on a treadmill. Exercise – even moderate - led to the formation of long-lasting circulating lipid peroxidation products and to DNA damage in male germ cells. On the other hand, exercise training protected rat heart from ischemia/reperfusion (I/R) injury; both oxidative stress and cardioprotection were proportional to the intensity of the exercise protocol. Training-induced cardioprotection was accompained by the upregulation of Mn-SOD, HSP70 and HO-1 in the heart, along with the upregulation of other proteins, such as Caveolin-3, probably unrelated to the anti-oxidant defence. A 10-wk exercise training led to the sprouting of new capillaries in the myocardium. Both heart resistance to I/R injury, and increase in HSP70 protein and in cardiac vascularization were rather persistant over a detraining period. Moreover, physical training induced paraoxonase-3 upregulation, thus contributing to reduce cholesterol oxidation. Some of the biochemical pathways leading to these beneficial effects were elucidated in our work. Noteworthy, physical activity appeared to exert an hormetic effect, with chronic moderate exercise upregulating protective proteins, and single bursts of stressing exercise leading to cell injury, expecially in untrained animals. The contribute of ROS to the signaling pathways leading to the upregulation of cell defences as well as to cell damage is paramount.
S91
S91
Marini M.; Veicsteinas A.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11585/81418
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