Electrically-induced Muscle Contractions Attenuate Bone Loss After Spinal Cord Injury

Abstract

Within the first year after spinal cord injury (SCI), bone mineral density (BMD) of paralyzed extremities declines by 25–45% (Wilmet et al. 1995). An important predisposing factor is the loss of mechanical load delivered to the skeletal system via muscle contractions. PURPOSE We examined the extent to which an isometric plantar flexion training protocol attenuates bone loss longitudinally after SCI. METHODS Six individuals with complete paralysis began a unilateral plantar flexor muscle activation program within 4 months after SCI. The opposite limb served as a control. The plantar flexors were activated supra-maximally with a 15 Hz frequency train every 2 s for 667 ms. Subjects completed 4 bouts of 120 contractions on 5 days/week (compliance >80%) for over 1.5 years (mn = 2.1 yrs). Tibia compressive force, derived from plantar flexion torque output, was ∼70% of body weight (BW) initially but over 140% BW after 6 months of training. Proximal tibia, hip, and spine BMD were measured longitudinally using dual energy x-ray absorptiometry (DEXA). RESULTS The bilateral hip BMD and untrained tibia BMD declined significantly over the course of the training, while the lumbar spine BMD showed minimal change. There was a significant interaction between time and training for tibia BMD (P <0.05). The percent decline in BMD (from the baseline condition) for the trained tibia (∼10%) was significantly less than the untrained tibia (∼25 %) (P <0.05). Moreover, the trained limb percent decline in BMD remained steady (no additional decline from baseline occurred) over the first 1.5 years of the study (P <0.05). CONCLUSIONS This study supports that a compressive load of ∼1–2 times BW, induced by muscle contractions, can partially prevent the loss of BMD after SCI. Future studies establishing dose-response curves are necessary to delineate the precise loading dose and number of repetitions needed to attenuate bone loss after SCI. SUPPORT NIH R01 HD39445 (RKS) and the Foundation for Physical Therapy (SDJ)