ABSTRACT
In the present study, an attempt has been made to investigate the possible mechanisms involved in skeletal muscle fatigue by using electrical stimulation in STZ-induced diabetes in albino rats. Animals were randomly classified into three main groups: Normal Non-treated Group, Diabetic Group [in which rats were intraperitoneally injected with a single dose of streptozotocin [STZ] solution 50 mg/Kg body wt.] and Insulin-treated Group [in which diabetic rats were injected subcutaneously with insulin]. All experimental muscles are stimulated at 10Hz frequency. Each group of the three main groups was further subdivided into the following subgroups: early fatigue subgroup: in which stimulation was immediately terminated at early fatigue [10% force decline], mid Fatigue Subgroup: in which stimulation was immediately terminated at mid fatigue [50% force decline] and late Fatigue Subgroup, in which stimulation was immediately terminated at late fatigue ll. 90% force decline]. Immediately after the end of the stimulation protocol, circulation was cut to prevent recovery of the metabolite levels. The muscles were excised, frozen in liquid nitrogen [N2] and then kept at -80 c[degree] for determination of glycogen content lactate, nitric oxide [NO] and antioxidant status. Stimulation of experimental caused a gradual and progressive decrease in muscle power [i.e. fatigue] recorded at 10, 50 and 90% force decline. The loss of power was accompanied with significant progressive increase in lactic acid levels, reaching its maximal level at to 90% of force decline with a corresponding decrease in glycogen content that reached its minimal level also at 90% of force decline compared to CC [controlled contralateral] limb. It also caused a significant increase in NO level that reached its maximal level at 90% of force decline. This was accompanied with a significant progressive reduction in GSH level with a corresponding increase in GPX activity. In STZ-induced diabetic rats, marked acceleration of fatigue was observed evidenced by a significant decrease in the time required to achieve fatigue at every level recorded compared to normal non-treated rats. This was .accompanied with a significant reduction in lactate, glycogen and NO levels. The antioxidant defense was also attenuated evidenced by a significant reduction in GSH concentration with a marked increase in GPX activity. Insulin treatment delayed the onset of fatigue in stimulated rats, evidenced by a significant improvement in the time required to achieve fatigue at every level recorded compared to the corresponding diabetic rats but still significantly accelerated compared to .the corresponding normal rats. This improvement was accompanied with a significant increase in lactate, glycogen and NO levels as well as antioxidant status compared to the corresponding diabetic rats
In Conclusion, there is a causal relationship between DM and accelerated fatigability in muscles tested. Insulin treatment failed to restore the normal contractile status. It is probably that diabetes induces changes in the contractile filaments that accelerate the onset of fatigue, and these structural changes could not be corrected by insulin treatment. Reduced NO synthesis as well as GSH depletion as causal factors for fatigue in the present work are quite evident in diabetic rats