Abstract
Background: Stroke patients experience functional changes resulting from muscle atrophy related to disuse, lack or limited neuronal stimulation, and undernutrition. Acute ischemic stroke is assumed to induce muscle atrophy. However, there is little information regarding muscle changes after acute stroke.
Objective: The purpose of this study was to examine the effect of inactivity and undernutrition after acute stroke on mass, myofibrillar protein content, and Types I and II fiber cross-sectional areas of rat hindlimb muscles.
Methods: Adult male Sprague-Dawley rats (body weight, 240-270 g) were randomly assigned to one of three groups: a stroke group (n = 7) that had occlusion of the right middle cerebral artery, a control group (n = 7) that underwent a sham right middle cerebral artery procedure, and an undernourished group (n = 9) that was pair-fed to match the intake of stroke rats. Food and water intake as well as body weight were measured daily. The rats were anesthetized 7 days after occlusion or sham occlusion, after which the soleus (Type I), plantaris (Type II), and gastrocnemius (Type II) muscles were dissected from both the affected and unaffected sides. The brain was sectioned to identify cerebral infarction in the stroke group. Body weight, food intake, muscle weight, fiber type distribution, cross-sectional area, and myofibrillar protein content of the dissected muscles were determined.
Results: The stroke group at 7 days after ischemic stroke showed significant decreases (p < .05), as compared with the control rats, in diet intake and body weight, muscle weight of affected gastrocnemius, Type I fiber cross-sectional area of the affected soleus muscle, Types I and II fiber cross-sectional areas and Type II fiber distribution of the unaffected soleus muscle, and myofibrillar protein content of both the affected and unaffected soleus muscles. As compared with the control group, the undernourished group showed significant decreases (p < .05) in diet intake and body weight, Type I fiber cross-sectional area of the affected soleus muscle, Types I and II fiber cross-sectional areas and Type II fiber distribution of the unaffected soleus muscle, Type I fiber distribution of the affected gastrocnemius muscle, and myofibrillar protein content of both the affected and unaffected soleus muscles. As compared with the undernourished group, the stroke group showed significant decreases (p < .05) in muscle weight and Type II fiber distribution of the affected gastrocnemius muscle. There were no differences in muscle characteristics between the affected and unaffected hindlimb muscles at 7 days after ischemic stroke.
Conclusions: Hindlimb muscle atrophy occurs in both affected and unaffected sides after acute stroke, with Type I muscle changes more apparent than Type II changes.