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Correspondence: Rocio Montoya-Perez Coordinacion General de Estudios de Posgrado, Universidad Michoacana de San Nicolas de Hidalgo, Francisco J Mujica s/n Ciudad Universitaria, Edif C5, Col Felicitas del Rio 58030, Morelia, Michoacan, Mexico Tel +52 44 3322 3500 ext 4157 Email biochio@yahoo.com.mx Background: Fatigue in skeletal muscle is defined as a reduction in the physical power needed to execute a function or as an inability to maintain mitochondrial ATP production. The mitochondrial potassium channel (mitoK ATP ) participates in combating fatigue in skeletal muscle. In this work, we evaluated the role of the mitoK ATP channel activator (diazoxide) and inhibitors of the signaling routes (protein kinase C, staurosporine; protein kinase G, KT5823; and nitric oxide synthase, metil N-Nitro-L-arginine ester, L-NAME), on muscle fatigue tension. In addition, we evaluated the main signaling routes used by the nitric oxide synthase protein and protein kinase C and G, in the presence of their specific activators. Methods: We used the anterior latissimus dorsi skeletal muscle of 2–3-week-old chicks. This muscle consists of slow muscle fibers. Tension was achieved by applying repetitive electrical stimulation that induced fatigue in an in vitro model. Results: Diazoxide significantly reduced muscle fatigue (P = 0.0002 in peak tension, P = 0.2 in maximum tension) by increasing post-fatigue tension, in spite of the fact that 5-hydroxydecanoate, a selective inhibitor of mitoK ATP , did not suppress post-fatigue tension. Conclusion: Our results suggest a lack of direct interaction in inhibition of the signaling routes during fatigue-induced mitoK ATP activation. This effect is possibly due to the type of skeletal muscle fibers (slow), the stimulation protocols (twitch), and the animal (avian) model used in the study.

Mitochondrial KATP channels in skeletal muscle: are protein kinases C and G, and nitric oxide synthase involved in the fatigue process?