Journal
JOURNAL OF APPLIED PHYSIOLOGY
Volume 115, Issue 5, Pages 756-764Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.00122.2013
Keywords
spinal cord injury; skeletal muscle; glucose uptake signaling; neuromuscular electrical stimulation; resistance exercise
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Funding
- VA Merit Award
- University of Alabama Birmingham (UAB) Center for Exercise Medicine, Department of Physical Medicine and Rehabilitation [5T32 DK-62710]
- UAB Center for Clinical and Translational Science [UL1 TR000165]
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The mechanisms underlying poor glucose tolerance in persons with spinal cord injury (SCI), along with its improvement after several weeks of neuromuscular electrical stimulation-induced resistance exercise (NMES-RE) training, remain unclear, but presumably involve the affected skeletal musculature. We, therefore, investigated skeletal muscle signaling pathways associated with glucose transporter 4 (GLUT-4) translocation at rest and shortly after a single bout of NMES-RE in SCI (n = 12) vs. able-bodied (AB, n = 12) men. Subjects completed an oral glucose tolerance test during visit 1 and approximate to 90 NMES-RE isometric contractions of the quadriceps during visit 2. Muscle biopsies were collected before, and 10 and 60 min after, NMES-RE. We assessed transcript levels of GLUT-4 by quantitative PCR and protein levels of GLUT-4 and phosphorylated-and total AMP-activated protein kinase (AMPK)-alpha, CaMKII, Akt, and AS160 by immunoblotting. Impaired glucose tolerance in SCI was confirmed by higher (P < 0.05) plasma glucose concentrations than AB at all time points after glucose ingestion, despite equivalent insulin responses to the glucose load. GLUT-4 protein content was lower (P < 0.05) in SCI vs. AB at baseline. Main group effects revealed higher phosphorylation in SCI of AMPK-alpha, CaMKII, and Akt (P < 0.05), and Akt phosphorylation increased robustly (P < 0.05) following NMES-RE in SCI only. In SCI, low skeletal muscle GLUT-4 protein concentration may, in part, explain poor glucose tolerance, whereas heightened phosphorylation of relevant signaling proteins (AMPK-alpha, CaMKII) suggests a compensatory effort. Finally, it is encouraging to find (based on Akt) that SCI muscle remains both sensitive and responsive to mechanical loading (NMES-RE) even approximate to 22 yr after injury.
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