Exercise training alters an anoxia-induced, glibenclamide-sensitive current in rat ventricular cardiocytes.

The effect of training on properties of a sarcolemmal ATP-sensitive K+ current (I(K(ATP))) was examined in left ventricular cardiocytes isolated from sedentary (Sed) and trained (Tr) female Sprague-Dawley rats. Whole cell patch-clamp techniques were used to characterize I(K(ATP)), an anoxia-inducible, glibencamide-sensitive current. An anoxic condition was induced by superfusing cells with a buffer that was equilibrated with 100% N(2), maintained under a layer of argon, and that contained 2-deoxy-D-glucose. Over a 1-h period of anoxia, 59% of Tr cells and 85% Sed cells expressed I(K(ATP)). In those cells that did express I(K(ATP)), the time to expression of the current during the anoxic period occurred significantly later in cells from the Tr group compared with the Sed. Peak I(K(ATP)) density was significantly lower in the Tr cells compared with the Sed cells. These results indicate that the onset and magnitude of I(K(ATP)) were altered by training. These alterations in I(K(ATP)) may be reflective of processes that contribute to training-induced cardioprotection against ischemia-reperfusion damage.