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Abstract
High rates of muscle fatigue and vascular and muscle atrophy occur in spinal cord injured (SCI) individuals. The cause and effect of vascular atrophy in SCI individuals is not known. The purposes of this study were to determine if vascular atrophy was related to muscle atrophy and if increased muscle fatigue was related to altered blood flow in SCI individuals. Blood flow was measured in the femoral artery using Doppler ultrasound and muscle mass was determined by magnetic resonance imaging in nine complete, chronic SCI individuals and eight age- and weight-matched able bodied (AB) subjects. Blood flow was determined during cuff occlusion and three different electrical stimulation periods. Electrical stimulation of the quadriceps muscles was conducted to elicit similar activated muscle mass in both groups. Muscle fatigue was determined for each electrical stimulation period. SCI individuals had smaller muscle cross sectional areas (37%, p = 0.001) and volumes (38%, p = 0.001) than AB. SCI individuals had smaller diameter size (37%, p < 0.001) and maximal flows following cuff ischemia (40%, p < 0.001) than AB individuals. Vessel diameter and maximal flow responses to ischemia and exercise, when normalized to muscle volume, were not different between groups. Muscle fatigue was significantly greater (3-8 fold, p =0.001) in the SCI versus the AB individuals. A prolonged half time to peak blood flow at the beginning of exercise (5 fold, p = 0.001) was found in the SCI versus the AB group consistent with reduced oxidative capacity. Half time to recovery after cuff ischemia (p = 0.048) and exercise (p = 0.009) was prolonged in SCI compared to AB individuals consistent with impaired vascular control. In summary, vascular restructuring appears to be closely linked to muscle atrophy in SCI individuals. The magnitude of muscle blood flow to electrical stimulation did not explain muscle fatigue in SCI individuals. Blood flow response at the onset of exercise was delayed; suggesting the ability to increase blood flow to match demand may be a limiting factor, rather than the magnitude of the blood flow response. A prolonged time to recovery of blood flow may indicate decreased vessel reactivity.