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.

PURPOSE/HYPOTHESIS: Incomplete spinal cord injury (ISCI) results in varying degrees of sensory and motor dysfunction distal to the level of lesion. Degradation of the musculoskeletal system is a major secondary complication associated with this injury. Improving the deconditioned distal skeletal musculature is a significant goal within the province of current rehabilitative therapies. Locomotor Training (LT), incorporating body weight support and treadmill as a modality to retrain the capacity to step, has shown considerable potential in improving the overall functional ability in persons with ISCI. However it is important to understand the extent to which skeletal muscle function covary as result of LT and how it relates to the positive alterations seen as a result of the training. Thus, the purpose of this study was to quantify lower extremity muscle function in a group of persons with ISCI who underwent LT. NUMBER OF SUBJECTS: Three individuals (3614 yrs, 1614 cm, and 7020 kg) with ISCI (C5T8, ASIA C or D) underwent LT for nine weeks. MATERIALS/METHODS: Peak isometric torque (PT), time to develop torque (T2080), and voluntary activation deficits (AD) of the quadriceps femoris (QF) and triceps surae (TS) muscle groups were determined at 0 weeks and at 5 weeks of LT (total training 9 weeks). LT consisted of nine weeks of daily sessions, 2030 minutes of stepping on the treadmill at walking speeds approximating normal using body weight supported training and manual assistance, followed by immediate over ground training. Measurements of PT were assessed at 90 degrees of knee flexion (QF) and 0 degrees of plantar flexion (TS) using a Biodex system 3 dynamometer. AD was quantified using the twitch interpolation technique. RESULTS: Following LT, PT increased 19% and 22% for the QF and TS muscle groups respectively in the less involved side, while torque increased 4.5% (QF) and 15.5% (TS) in the more involved side. In contrast, T2080 decreased 6% (QF) and 24% (TS) in the less involved side QF and TS, while it decreased 21.5% (QF) and 23.2% (TS) in the more involved side. AD decreased by 23% (QF) and 12% (TS) in the less involved side, while they decreased 10% (QF) and 14.72% (TS) in the more involved side. CONCLUSIONS: These preliminary results indicate that muscles in persons with ISCI tend to generate more torque, use less time to generate peak torque and show signs of greater voluntary activation after five weeks of LT. CLINICAL RELEVANCE: Changes in muscle function in these lower extremity muscles could translate to improvements in functional ability following Locomotor Training. Support Contributed by: NIH RO1 HD037645/ NIH KO1 HD01348