No abstract

Alzheimer’s disease (AD) is the most common neurodegenerative disease, and numerous recent findings suggest that several pathologic signs, including loss of muscle strength and mass, are also detected in these patients. In the present study, we evaluated muscle cross-sectional area (CSA), myonuclear number, satellite cell (SC) content, and myosin heavy chain (MyHC) types in an animal model of AD and examined the possible role of resistance training in controlling skeletal muscle size in this disease. Fifty-eight male rats were randomly divided into four groups: healthy-control (H-C), healthy-exercise (H-Ex), Alzheimer-control (A-C), and Alzheimer-exercise (A-Ex). AD was induced by the single injection of 1–42 amyloid into the CA1 region of the hippocampus (1 μl/site). The rats in H-Ex and A-Ex groups performed a 5-week resistance training period (17 sessions). The results indicated that AD induces significant skeletal muscle atrophy and reduces the myonuclear number and SC content in gastrocnemius muscle in both whole muscle cross-sections and isolated myofibers. Interestingly, we did not find any significant differences in the different MyHC distributions of AD animals compared with controls, while resistance training significantly increased the CSA of MyHC IIb fibers in both AD and healthy animals. Altogether, these observations suggest that the skeletal muscle of AD animals are more prone to atrophy and loss of myonuclear number and satellite cell content, while resistance training successfully restores these impairments.

Background and Objectives Diabetic neuropathy is one of the most common complications of diabetes and no suitable drug treatment has been found for this complication. The aim of this study was to determine the effect of six weeks of aerobic exercise on KIF1B protein in the sensory part of the spinal cord in rats with diabetic neuropathy. Subjects and Methods In the present experimental study, 12 male Wistar rats were divided into 4 groups: healthy exercise, control exercise, healthy diabetes and control diabetes. The training program included 6 weeks of running training on the treadmill in 5 sessions per week. The dorsal part of the spinal cord was analyzed as sensory neurons. Results The results showed that aerobic exercise significantly reduced blood glucose in the diabetic group compared to the control diabetes group (P=0.002), but no significant difference was observed in the weight of rats. The results also showed that a significant increase (P=0.044) in KIF1B in healthy exercise group compared to healthy control group and a significant increase (P=0.027) in KIF1B in diabetic exercise group compared to control diabetes. Conclusion The results showed that aerobic exercise increases the amount of KIF1B protein in healthy and diabetic rats, and this increase in KIF1B motor protein can improve axonal transmission and thus improve nerve function.

No abstract

Alzheimer's disease (AD) is the most common neurodegenerative disease, and numerous recent findings suggest that several pathologic signs, including loss of muscle strength and mass, are also detected in these patients. In the present study, we evaluated muscle cross-sectional area (CSA), myonuclear number, satellite cell (SC) content, and myosin heavy chain (MyHC) types in an animal model of AD and examined the possible role of resistance training in controlling skeletal muscle size in this disease. Fifty-eight male rats were randomly divided into four groups: healthy-control (H-C), healthy-exercise (H-Ex), Alzheimer-control (A-C), and Alzheimer-exercise (A-Ex). AD was induced by the single injection of 1–42 amyloid into the CA1 region of the hippocampus (1 µl/site). The rats in H-Ex and A-Ex groups performed a 5-week resistance training period (17 sessions). The results indicated that AD induces significant skeletal muscle atrophy and reduces the myonuclear number and SC content in gastrocnemius muscle. Interestingly, we did not find any significant differences in the different MyHC distributions of AD animals compared with controls, while resistance training significantly increased the CSA of MyHC IIb fibers in both AD and healthy animals. Altogether, these observations suggest that the skeletal muscle of AD animals are more prone to atrophy and loss of myonuclear number and satellite cell content, while resistance training successfully restores these impairments.