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TRANSLATIONAL PHYSIOLOGY

Body-weight-support treadmill training improves blood glucose regulation in persons with incomplete spinal cord injury

¹Department of Kinesiology, Exercise and Metabolism Research Group and Centre for Health Promotion and Rehabilitation, ²Department of Medicine, Neurology and Pediatrics, and ³Department of Gastroenterology, McMaster University, Hamilton, Ontario, Canada L8S 4K1

Submitted 13 February 2004 ; accepted in final form 21 April 2004

The impact of a 6-mo body-weight-supported treadmill training program on glucose homeostasis and muscle metabolic characteristics was investigated. Nine individuals (31 ± 3 yr, 8.1 ± 2.5 yr postinjury; means ± SE) with incomplete spinal cord injury trained three times weekly for a total of 6 mo. Training session duration and intensity (velocity) increased by 54 ± 10% (P < 0.01) and 135 ± 20%, respectively. Muscle biopsies and a modified glucose tolerance test (100 g glucose with [U-¹³C]glucose) were performed before (Pre) and after training (Post). Training resulted in a reduction in area under the curve of glucose x time (–15 ± 4%) and insulin x time (–33 ± 8%; both P < 0.05). Oxidation of exogenous (ingested) glucose increased as a result of training (Pre = 4.4 ± 0.7 g/h, Post = 7.4 ± 0.6 g/h; P < 0.05), as did oxidation of endogenous (liver) glucose (Pre = 3.8 ± 0.3 g/h, Post = 5.2 ± 0.3 g/h; P < 0.05). Training resulted in increased muscle glycogen (80 ± 23%; P < 0.05) and GLUT-4 content and hexokinase II enzyme activity (126 ± 34 and 49 ± 4%, respectively, both P < 0.01). Resting muscle phosphocreatine content also increased after training (Pre = 62.1 ± 4.3, Post = 78.7 ± 3.8, both mmol/kg dry wt and P < 0.05). Six months of thrice-weekly body-weight-supported treadmill training in persons with an incomplete spinal cord injury improved blood glucose regulation by increasing oxidation and storage of an oral glucose load. Increases in the capacity for transport and phosphorylation glucose in skeletal muscle likely play a role in these adaptations.

GLUT-4; non-insulin-dependent diabetes mellitus; insulin action; glucose control

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