Reduced Skeletal Muscle Capillarization and Glucose Intolerance

Abstract

Objective: Reduced capillarization in hemiparetic skeletal muscle of chronic stroke patients can limit insulin, glucose, and oxygen supply to muscle, thereby contributing to impaired glucose metabolism and cardiovascular deconditioning. We hypothesized that compared to sedentary controls, stroke subjects have reduced skeletal muscle capillarization that is associated with glucose intolerance and reduced peak oxygen consumption (Vo_2peak). Methods: Twelve chronic stroke subjects (ages, 62.1±2.8 years), and matched sedentary controls with impaired (n=12) or normal (n=12) glucose tolerance underwent oral glucose tolerance tests, exercise tests, and vastus lateralis biopsies. Results: Stroke subjects had lower capillarization in hemiparetic muscle than in nonparetic muscle and normal glucose tolerant controls (∼22 and ∼28%, respectively; P<0.05) and had similar bilateral capillarization, compared to controls with impaired glucose tolerance. Capillary density in hemiparetic muscle inversely correlated with 120-minute glucose (r=−0.70, P<0.01) and glucose area under the curve (r=−0.78, P<0.01). Vo_2peak was ∼40% lower in stroke subjects, compared to controls (P<0.001), but did not correlate with capillarization (P=n.s.). Conclusions: Hemiparetic muscle capillarization is reduced after stroke, and reduced capillarization is associated with glucose intolerance in stroke and control subjects. Interventions to increase skeletal muscle capillarization may prove beneficial for improving glucose metabolism in chronic stroke patients.

• diabetes
• insulin resistance
• capillaries
• hemiparesis
• skeletal muscle

Acknowledgements

The authors’ appreciation is extended to the men and women who participated in this study. They are grateful to the clinicians, students, nurses, laboratory technicians, and exercise physiologists who assisted with this study. This research was supported, in part, by the Baltimore Veterans Affairs Maryland Exercise and Robotics Center of Excellence (R.F.M.), the Baltimore Veterans Affairs Research Enhancement Award Program (R.F.M.), Veterans Affairs Merit Awards (C.E.H.-M. and A.S.R.), the Baltimore Veterans Affairs Medical Center Geriatric Research, Education and Clinical Center (GRECC), the University of Maryland Claude D. Pepper Center (P30-AG-12583; A.P.G.), and NIH grant R01-AG-019310 (A.S.R.). Dr. Prior is supported by NIH T32-AG-000219, Dr. Joseph is supported by NIH K01-AG-021457, and Dr. Ryan is supported by a VA Research Career Scientist Award.