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CAN LOWER-LIMB EXERCISE INTERVENTION PARTIALLY REVERSE BONE LOSS IN CHRONIC SPINAL CORD INJURY?



Abstract

After spinal cord injury (SCI) rapid muscle atrophy and extensive bone loss occur in the paralysed limbs resulting in increased fracture incidence (mostly at the epiphyses in the distal and proximal tibia and distal femur). We investigated whether re-introducing mechanical loading of the lower-limb bones in chronic SCI through exercise could induce bone formation, in accordance with Wolff’s Law.

We present cross-sectional data from the Scottish paraplegic population illustrating the time course of bone loss after SCI, and review case studies describing musculoskeletal changes following lower-limb exercise interventions in chronic SCI. Reference data were obtained from 47 subjects with SCI at neurological levels T2 to L2, ranging from 6 months to 40 years post-injury. We used peripheral Quantitative Computed Tomography (XCT3000, Stratec, Germany) to scan 4 sites in the tibia and 2 in the femur, and evaluated trabecular, cortical, and total bone data, and soft-tissue parameters. Here, we focus on trabecular bone mineral density (BMDtrab) at the epiphyses, which provides an indicator of bone integrity. The same scans were performed pre- and post-training in chronic paraplegics who undertook a period of lower-limb exercise training (body-weight-supported treadmill training (BWSTT) or electrically-stimulated leg cycle (FES-cycle) training); these results are reviewed.

The temporal pattern of bone loss is characterised by exponential decline in BMDtrab, reaching steady-state at 100 mg/cm3 in the distal tibia after 7 years and at 130 mg/cm3 in the distal femur after 3 years. A subject with incomplete SCI (18 years post-injury) showed an increase in BMDtrab in the distal tibia following 5-months BWSTT. In a separate study, subjects with complete SCI had varying responses to FES-cycle training.

Bone loss appears to plateau after 7 years post-SCI. The effectiveness of physical interventions aimed at reversing bone loss in chronic SCI seemingly depends on the details of the associated bone-loading patterns.

Correspondence should be addressed to Editorial Secretary Mr ML Costa or Assistant Editorial Secretary Mr B.J. Ollivere at BOA, 35–43 Lincoln’s Inn Fields, London WC2A 3PE, England; Email: mattcosta@hotmail.com or ben@ollivere.co.uk