title: Decreased muscle endurance associated with diabetic neuropathy may be attributed partially to neuromuscular transmission failure.
abstract: Diabetic polyneuropathy (DPN) can cause muscle atrophy, weakness, contractile slowing, and neuromuscular transmission instability. Our objective was to assess the response of the impaired neuromuscular system of DPN in humans when stressed with a sustained maximal voluntary contraction (MVC). Baseline MVC and evoked dorsiflexor contractile properties were assessed in DPN patients (n = 10) and controls (n = 10). Surface electromyography was used to record tibialis anterior evoked maximal compound muscle action potentials (CMAPs) and neuromuscular activity during MVCs. Participants performed a sustained isometric dorsiflexion MVC for which task termination was determined by the inability to sustain ≥60% MVC torque. The fatigue protocol was immediately followed by a maximal twitch, with additional maximal twitches and MVCs assessed at 30 s and 2 min postfatigue. DPN patients fatigued ∼21% more quickly than controls (P < 0.05) and featured less relative electromyographic activity during the first one-third of the fatigue protocol compared with controls (P < 0.05). Immediately following fatigue, maximal twitch torque was reduced similarly (∼20%) in both groups, and concurrently CMAPs were reduced (∼12%) in DPN patients, whereas they were unaffected in controls (P > 0.05). Twitch torque and CMAP amplitude recovered to baseline 30 s postfatigue. Additionally, at 30 s postfatigue, both groups had similar (∼10%) reductions in MVC torque relative to baseline, and MVC strength recovered by 2 min postfatigue. We conclude DPN patients possess less endurance than controls, and neuromuscular transmission failure may contribute to this greater fatigability.
authors: School of Medicine, Queen's University, Kingston, Ontario, Canada; School of Kinesiology and Health Studies, Queen's University, Kingston, Ontario, Canada; School of Kinesiology, Faculty of Health Sciences, The University of Western Ontario, London, Ontario, Canada; mallen@qmed.ca.
authors: Matti D
authors: http://orcid.org/0000-0002-0755-3164
authors: MD
authors: Allen
authors: Department of Clinical Neurological Sciences, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada;
authors: Kurt
authors: K
authors: Kimpinski
authors: School of Kinesiology, Faculty of Health Sciences, The University of Western Ontario, London, Ontario, Canada; Department of Clinical Neurological Sciences, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada; Department of Physical Medicine and Rehabilitation, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada; and.
authors: Timothy J
authors: TJ
authors: Doherty
authors: School of Kinesiology, Faculty of Health Sciences, The University of Western Ontario, London, Ontario, Canada; Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, The University of Western Ontario, London, Ontario, Canada.
authors: Charles L
authors: CL
authors: Rice
mesh_terms: D000368:Aged; D016022:Case-Control Studies; D003928:Diabetic Nephropathies / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009119:Muscle Contraction; D018763:Muscle Fatigue; D009469:Neuromuscular Junction / Q000503:physiopathology*; D010807:Physical Endurance; D009435:Synaptic Transmission
keywords: compound muscle action potential; diabetes; electromyography; fatigue; weakness