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Excerpt
Loss of contractile area does not entirely explain torque deficits after limb disuse, emphasizing the need to examine the role of other factors. PURPOSE: To assess how changes in plantarflexor cross-sectional area (CSA) and phosphate metabolites, specifically inorganic phosphate (Pi), together, account for torque loss after immobilization. METHODS: Twenty-two patients with surgically stabilized, unilateral ankle malleolar fractures and nine healthy subjects participated in the study. Patients were immobilized for eight weeks followed by ten weeks of rehabilitation. Data were collected at 1 week (1w-R), 5 weeks (5w-R), and 10 weeks (10w-R) of rehabilitation. CSA of the lower limb was assessed with Magnetic Resonance Imaging performed at a 1.5 Tesla magnet. Pi content and Pi/PCr (PCr = phosphocreatine) ratio were measured (n = 8) from the medial gastrocnemius with an oblong surface coil (6 × 8 cm) using 31P Magnetic Resonance Spectroscopy performed at a 2.0 Tesla magnet. Isometric plantarflexor torque was assessed at 0 degree of plantarflexion using a dynamometer. Independent sample t-tests were used for comparisons between patients and healthy subjects for the 1w-R and 10w-R time points. Linear regression was used to examine how CSA and Pi content explain changes in muscle torque. RESULTS: Following immoblization, patients had significant plantarflexor atrophy (p < 0.01), elevated Pi levels and Pi/PCr ratios (p < 0.01), and decreased torque (p < 0.01) compared to controls. Rehabilitation resulted in significant hypertrophy of the plantarflexors (p < 0.01) with a progressive decrease in Pi content and Pi/PCr ratio (p < 0.01), and a concurrent increase in torque (p < 0.01). During rehabilitation, CSA only accounted for 39% of the variance in torque (p < 0.01), while CSA and Pi together accounted for 52% (p < 0.01). CONCLUSION: These results support in vitro findings that elevated Pi levels contribute to decreased force production. Metabolic alterations with disuse may help explain some of the torque deficits that are not entirely accounted for by changes in CSA. Other factors, such as altered neural drive, may account for the remaining, unexplained torque deficits. Supported by NIH-RO1HD37645, NIH-RO1HD40850, 2P41RR02305.
