Abstract
Exercise is known to improve cardiac recovery following coronary occlusion. However, whether short-term exercise can improve cardiac function and hypoxia tolerance ex vivo independent of reperfusion injury and the possible role of calcium channels in improved hypoxia tolerance remains unknown. Therefore, in the current study, heart function was measured ex vivo using the Langendorff method at different oxygen levels after a 4-week voluntary wheel-running regimen in trained and untrained male mice (C57Bl/6NCrl). The levels of cardiac Ca2+-channels: L-type Ca2+-channel (CACNA1C), ryanodine receptor (RyR-2), sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA2), and sodium-calcium exchanger were measured using western blot. Trained mice displayed lower cardiac afterload pressure generation capacity (rate and amplitude), but unaltered hypoxia tolerance when compared to untrained mice with similar heart rates. The level of CACNA1C positively correlated with the pressure generation rate and amplitude. Furthermore, the CACNA1C-RYR-2 ratio also positively correlated with the pressure generation rate. While the 4-week training period was not enough to alter the intrinsic cardiac hypoxia tolerance, interestingly it decreased pressure generation capacity and slowed pressure decreasing capacity in the mouse hearts ex vivo. This reduction in pressure generation rate could be linked to the level of channel proteins in sarcolemmal Ca2+-cycling in trained mice. However, the Ca2+-channel levels did not differ significantly between the groups, and thus, the level of calcium channels cannot fully explain all the functional alterations, despite the detected correlations. Therefore, additional studies are warranted to reveal further mechanisms that contribute to the reduced intrinsic capacity for pressure production in trained mouse hearts.
Highlights
Exercise is well known to benefit cardiac health and function
The perfusion pressure was not affected by the oxygen level and there was no interaction between the oxygen level and test group
We demonstrated that a 4-week period of voluntary running wheel training is insufficient to improve intrinsic murine cardiac hypoxia tolerance
Summary
Exercise is well known to benefit cardiac health and function. There is strong evidence indicating that exercise decreases the risk of many diseases, such as coronary artery disease [12]. Several studies have shown that long-term endurance exercise can increase the ischemic tolerance of ex vivo isolated rat hearts [4, 30, 31]. The coronary flow is occluded for a set duration and the recovery of the heart is monitored after reperfusion. These studies measure both hypoxia tolerance and tolerance to reperfusion injury. To our knowledge, it has not previously been studied whether short-term exercise can improve hypoxia tolerance of the heart independent of reperfusion injury by using an experimental design that investigates heart function ex vivo in multiple levels of hypoxia
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