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Am J Physiol Endocrinol Metab 284: E655-E662, 2003; doi:10.1152/ajpendo.00343.2002
0193-1849/03 $5.00
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Vol. 284, Issue 4, E655-E662, April 2003

TRANSLATIONAL PHYSIOLOGY
Altered energetic properties in skeletal muscle of men with well-controlled insulin-dependent (type 1) diabetes

Gregory J. Crowther2, Jerrold M. Milstein4, Sharon A. Jubrias1, Martin J. Kushmerick1,2,3, Rodney K. Gronka1, and Kevin E. Conley1,2,3

Departments of 1 Radiology, 2 Physiology and Biophysics, and 3 Bioengineering, University of Washington Medical Center, Seattle 98195; and 4 Department of Neurology, Children's Hospital and Regional Medical Center, Seattle, Washington 98105

This study asked whether the energetic properties of muscles are changed by insulin-dependent diabetes mellitus (or type 1 diabetes), as occurs in obesity and type 2 diabetes. We used 31P magnetic resonance spectroscopy to measure glycolytic flux, oxidative flux, and contractile cost in the ankle dorsiflexor muscles of 10 men with well-managed type 1 diabetes and 10 age- and activity-matched control subjects. Each subject performed sustained isometric muscle contractions lasting 30 and 120 s while attempting to maintain 70-75% of maximal voluntary contraction force. An altered glycolytic flux in type 1 diabetic subjects relative to control subjects was apparent from significant differences in pH in muscle at rest and at the end of the 120-s bout. Glycolytic flux during exercise began earlier and reached a higher peak rate in diabetic patients than in control subjects. A reduced oxidative capacity in the diabetic patients' muscles was evident from a significantly slower phosphocreatine recovery from a 30-s exercise bout. Our findings represent the first characterization of the energetic properties of muscle from type 1 diabetic patients. The observed changes in glycolytic and oxidative fluxes suggest a diabetes-induced shift in the metabolic profile of muscle, consistent with studies of obesity and type 2 diabetes that point to common muscle adaptations in these diseases.

glycolysis; mitochondrial oxidative phosphorylation; tibialis anterior muscle


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