Anders Karlsen1,2,3,4, Christopher Kjaer Cullum1,4, Kristoffer Larsen Norheim1,4,5, Frederik Ulrik Scheel1,4, Amanda Hempel Zinglersen1,4, Julie Vahlgren1,4, Peter Schjerling1,3, Michael Kjaer1,3, Abigail L Mackey1,2. 1. Institute of Sports Medicine Copenhagen, Department of Orthopaedic Surgery M, Bispebjerg Hospital, Copenhagen, DENMARK. 2. Center for Healthy Aging, Department of Biomedical Sciences, University of Copenhagen, Copenhagen, DENMARK. 3. Center for Healthy Aging, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, DENMARK. 4. Geriatric Department Q31, Bispebjerg Hospital, Copenhagen, DENMARK. 5. Sport Sciences, Department of Health Science and Technology, Faculty of Medicine, Aalborg University, Aalborg, DENMARK.
Abstract
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.
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.