Eccentric Exercise Elicits Elevation of Resting Calcium in Skeletal Muscle. Periodic Acceleration Enhanced the Recovery

Abstract

Eccentric exercise (EC) can cause transient muscle damage, including muscle injury, muscle protein release into the plasma, an acute-phase immune response, and a decrease of muscle performance. Periodic acceleration (pGz) is a novel treatment that stimulates nitric oxide (NO) production by cNOS. Male mice (25-32 g) were divided in 4 groups (5/group). Group A: non-exercised (control); Group B: EC (45 min downhill exercise); Group C: EC followed by 30 min of pGz at 480 cpm daily starting on day 0 for 10 days; Group D: EC followed by 30 min of pGz, treated with L-NAME, 4 days prior and 10 days after EC. Resting intracellular Ca2+ concentration ([Ca2+]rest) was measured in vivo using Ca2+ selective microelectrodes on days 0, 2, 4, 6, 8, and 10 after EC. In group A the average [Ca2+]rest was 1113.8 nM on day 0 and did not change on subsequent days. On days 0, 2, 4, 6, 8 and 10 [Ca2+]rest (in nM) in polarized-exercised muscle fibers in group B was 395±38, 381±35, 334±23, 295±39, 268±27, and 223±27. In group C (EC+pGz) [Ca2+]rest was 402±46, 304±26, 260±35, 145±16, 121±10 nM and 113±6, showing a significant difference from group B by day 2 and reached control by day 10. In group D (EC+pGz+LNAME) the beneficial effect of pGz on [Ca2+]rest was abolished. We conclude that EC induced a chronic elevation of [Ca2+]rest in skeletal muscle that lasted up to 10 days and that pGz was able to accelerate the return to normal [Ca2+] homeostasis following EC induced muscle injury. The salutary effect of pGz on [Ca2+]rest appears to be mediated by an increase in NO generation, since the NOS blocker, L-NAME, eliminated the effect of pGz on [Ca2+]rest after EC.