Study Design: Cross-sectional study.Objective: (1) To quantify intramyocellular lipid (IMCL) content of the soleus muscle. (2) To assess the T-2 relaxation rates in the lower extremity skeletal muscles in persons with incomplete spinal cord injury (SCI).Setting: Academic Institution, Florida.Methods: Eight subjects (42 +/- 10 years old; 70 +/- 12 kg; 176 +/- 10 cm) with chronic (17 +/- 9 months post injury) motor SCI (C4-T12; ASIA C or D) and eight matched healthy controls were tested. Localized unsuppressed proton spectroscopy (H-MRS) was performed to estimate total lipid content and individual lipid components; IMCL and extramyocellular lipid (EMCL) from the soleus muscle. T-2-weighted imaging of lower extremity muscles yielded muscle T-2 rates.Results: The IMCL content of the soleus muscle was 3.3 times higher in the patient group as compared to controls (P = 0.002; 0.0401 (0.0234-0.0849) versus 0.0123 (0.0090-0.0175)). Similarly, EMCL measures were 4.5 times higher as compared to the controls (P 0.002). Significant differences were observed in the T-2 relaxation times of the soleus and gastrocnemius muscles (P < 0.05).Conclusion: The increased levels of IMCL might interfere with the glucose uptake in skeletal muscle; potentially predisposing persons with incomplete SCI to the development of peripheral insulin resistance. Marked elevations in the T-2 relaxation times of the locomotor muscles are reflective of an altered muscle composition.

Oxidative slow skeletal muscle contains carbonic anhydrase III in high concentration, but its primary function remains unknown. To determine whether its lack handicaps energy metabolism and/or acid elimination, we measured the intracellular pH and energy phosphates by (31)p magnetic resonance spectroscopy in hind limb muscles of wild-type and CA III knockout mice during and after ischemia and intense exercise (electrical stimulation). Thirty minutes of ischemia caused phosphocreatine (PCr) to fall and P-i to rise while pH and ATP remained constant in both strains of mice. PCr and P-i kinetics during ischemia and recovery were not significantly different between the two genotypes. From this we conclude that under neutral pH conditions resting muscle anaerobic metabolism, the rate of the creatine kinase reaction, intracellular buffering of protons, and phosphorylation of creatine by mitochondrial oxygen metabolism are not influenced by the lack of CA III. Two minutes of intense stimulation of the mouse gastrocnemius caused PCr, ATP, and pH to fall and ADP and P-i to rise, and these changes, with the exception of ATP, were all significantly larger in the CA III knockouts. The rate of return of pH and ADP to control values was the same in wild-type and mutant mice, but in the mutants PCr and Pi recovery were delayed in the first minute after stimulation. Because the tension decrease during fatigue is known to be the same in the two genotypes, we conclude that a lack of CA III impairs mitochondrial ATP synthesis.