Colin W Moore1, Matti D Allen1,2, Kurt Kimpinski1,3, Timothy J Doherty1,3,4, Charles L Rice1,5. 1. School of Kinesiology, Faculty of Health Sciences, The University of Western Ontario, London, Ontario, N6G 1H1, Canada. 2. School of Medicine, Queen's University, Kingston, Ontario, Canada. 3. Department of Clinical Neurological Sciences, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada. 4. Department of Physical Medicine and Rehabilitation, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada. 5. Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada.
Abstract
INTRODUCTION: The aim of this study was to determine whether diabetic polyneuropathy (DPN) is associated with reduced muscle quality using MRI. METHODS: MRIs of the tibialis anterior (TA) muscle were recorded from 9 individuals (5 men) with DPN (∼65 years) and 8 (4 men) age- and gender-matched controls. A magnetization transfer ratio (MTR) and T2 relaxation times of the TA were calculated. RESULTS: Despite equal voluntary activation, the DPN group was ∼37% weaker than controls, with a significantly lower proportion (∼8%) of contractile tissue and lower MTR (0.28 ± 0.03 vs. 0.32 ± 0.02 percent units). T2 relaxation time was significantly longer in the DPN group (77 ± 16 ms) compared with controls (63 ± 6 ms). CONCLUSIONS: These findings indicate a reduction in the structural integrity and myocellular protein density in the TA of those with DPN. Thus, muscle weakness in DPN is likely due to both a loss of muscle mass and a reduction in contractile quality.
INTRODUCTION: The aim of this study was to determine whether diabetic polyneuropathy (DPN) is associated with reduced muscle quality using MRI. METHODS: MRIs of the tibialis anterior (TA) muscle were recorded from 9 individuals (5 men) with DPN (∼65 years) and 8 (4 men) age- and gender-matched controls. A magnetization transfer ratio (MTR) and T2 relaxation times of the TA were calculated. RESULTS: Despite equal voluntary activation, the DPN group was ∼37% weaker than controls, with a significantly lower proportion (∼8%) of contractile tissue and lower MTR (0.28 ± 0.03 vs. 0.32 ± 0.02 percent units). T2 relaxation time was significantly longer in the DPN group (77 ± 16 ms) compared with controls (63 ± 6 ms). CONCLUSIONS: These findings indicate a reduction in the structural integrity and myocellular protein density in the TA of those with DPN. Thus, muscle weakness in DPN is likely due to both a loss of muscle mass and a reduction in contractile quality.
Authors: Jean Farup; Jesper Just; Frank de Paoli; Lin Lin; Jonas Brorson Jensen; Tine Billeskov; Ines Sanchez Roman; Cagla Cömert; Andreas Buch Møller; Luca Madaro; Elena Groppa; Rikard Göran Fred; Ulla Kampmann; Lars C Gormsen; Steen B Pedersen; Peter Bross; Tinna Stevnsner; Nikolaj Eldrup; Tune H Pers; Fabio M V Rossi; Pier Lorenzo Puri; Niels Jessen Journal: Cell Metab Date: 2021-10-21 Impact factor: 31.373