Endurance Exercise Increases Force Production in Mouse Fast-Twitch Muscles

Abstract

Endurance exercise is known to induce mitochondrial biogenesis and improve the ability to utilize oxygen. Here we show that endurance training also can improve force production in mouse fast-twitch extensor digitorium longus (EDL) muscles under non stressed conditions. Wild-type mice had unlimited access to running wheels for 7 weeks. Mice ran in average a distance of 3.500 meters per 24-hour. Control group were mice with non-rotating running wheels in their cages. After 7 weeks mice were sacrificed and force and fatigue was measured in isolated, intact EDL muscles. No difference was observed in the rate of fatigue between exercised and non-exercised mice, which might be due to deficient oxygen diffusion into deeper parts of the isolated muscles. However, the maximal force production in EDL was increased by ∼ 30% in exercised compared with non-exercised mice. Reduced FKBP12 binding to the major intracellular Ca2+-release channel (ryanodine receptor type 1 (RyR1)) has been associated with muscle weakness induced by high-intensive exercise. We have indications that the exercised muscles showing increased force have decreased FKBP12 binding compared to the control group. This suggests that decrease in FKBP12 binding to RyR1 might not only be deteriorating for the muscle function. Instead our results indicate a more complex modulation where decreased FKBP12 binding to RyR1 in response to exercise could be either beneficial (training) or detrimental (overtraining) for muscle function.