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.

Keywords: compound muscle action potential; diabetes; electromyography; fatigue; weakness.

Fig. 1.

Sample torque, tibialis anterior root-mean-squared electromyography (RMS EMG), and plantar flexor RMS EMG during a sustained, isometric dorsiflexion maximal voluntary contraction (MVC) fatigue protocol and subsequent recovery at 30 s and 2 min post-task termination.

Fig. 2.

Mean (±SD) absolute dorsiflexion torque [N·m (A); % (B)] produced during a sustained, isometric dorsiflexion MVC fatigue protocol in controls (○; time to task termination = 71 s) and diabetic polyneuropathy (DPN) patients (●; time to task termination = 56 s). *Significant difference between groups in time to task termination (P < 0.05). Controls produced significantly greater torque throughout the protocol (P < 0.05).

Fig. 3.

Tibialis anterior relative RMS EMG during a sustained, isometric dorsiflexion MVC fatigue protocol in controls (○) and DPN patients (●). Values are means ± SD. *Significant difference between groups (P < 0.05).

Fig. 4.

Electrically evoked dorsiflexion relative twitch torques (A) and relative peak-to-peak compound muscle action potential (CMAP) amplitudes (mV; B) at baseline and immediately, 30 s, and 2 min post-task termination in controls (○) and DPN patients (●). Values are means ± SD. §Significant difference from baseline (P < 0.05). *Significant difference between groups (P < 0.05).