Effect of T3 treatment on the response to ischemia-reperfusion of heart preparations from sedentary and trained rats.

We investigated whether swim training modifies the effect of T(3) treatment on rat heart response to ischemia-reperfusion. Homogenates of Langendorff preparations perfused for 25 min after 20-min ischemia were used for biochemical determinations and isolation of mitochondrial fractions. Oxidative damage and antioxidant levels of homogenates, O(2) consumption and H(2)O(2) release rates, oxidative damage, and susceptibility to Ca(2+)-induced swelling of mitochondria were determined. During reperfusion, hyperthyroid hearts displayed significant tachycardia and low inotropic recovery. This pattern was improved by training, which also attenuated tissue oxidative damage and glutathione depletion. Similar training effects were shown in euthyroid preparations. Moreover, training reduced mitochondrial H(2)O(2) production and oxidative damage in hyperthyroid and euthyroid hearts and susceptibility to Ca(2+)-induced swelling only in the hyperthyroid ones. Rates of mitochondrial O(2) consumption were not different in sedentary and trained hyperthyroid rats. However, determination of the oxidative capacity suggested that, in the sedentary rats, O(2) consumption was conditioned by oxidative damage mitochondria have suffered, whereas in trained rats, it was due to changes in mitochondrial characteristics. The above results suggest that moderate training is able to reduce hyperthyroid heart susceptibility to oxidative damage and dysfunction modifying mitochondrial population.