Muscle mass is not significantly lost during short-term hospitalization of relatively high functioning and active geriatric patients although our findings are potentially affected by changes in hydration status. Resistance training during hospitalization increases skeletal muscle mass, and patients with high levels of systemic inflammation demonstrate less ability to increase or preserve muscle mass in response to resistance training during illness.
Aim This study aimed to examine changes in lean mass during hospitalization in geriatric patients and the effect of muscle activation by neuromuscular electrical stimulation. Methods Thirteen patients (69–94 yr) at a geriatric ward completed tests at hospital admission (days 2–3) and discharge (days 8–10). One leg received daily stimulation of the knee extensors, whereas the other leg served as a control leg. Lean mass was evaluated by dual-energy x-ray absorptiometry scans and muscle thickness by ultrasound scans. Muscle biopsies were collected from both legs at admission and discharge in nine patients and analyzed for fiber size, satellite cell number, and activation and expression of genes associated with muscle protein synthesis and breakdown, connective tissue, and cellular stress. Results The relative decline in leg lean mass and midthigh region lean mass was larger in the control (−2.8% ± 1.5%) versus the stimulated leg (−0.5% ± 1.4%, P < 0.05). Although there were no changes in fiber size or satellite cell number, the mRNA data revealed that, compared with control, the stimulation resulted in a downregulation of myostatin (P < 0.05) and a similar trend for MAFbx (P = 0.099), together with an upregulation of Collagen I (P < 0.001), TenascinC (P < 0.001), CD68 (P < 0.01), and Ki67 (P < 0.05) mRNA. Conclusion These findings demonstrate a moderate decline in leg lean mass during a hospital stay in geriatric patients, whereas leg lean mass was preserved with daily neuromuscular electrical muscle activation. At the cellular level, the stimulation had a clear influence on suppression of atrophy signaling pathways in parallel with a stimulation of connective tissue and cellular remodeling processes.
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