Siobhan M Schabrun1, Ryan E Stafford, Paul W Hodges. 1. NHMRC Centre of Clinical Research Excellence in Spinal Pain, Injury and Health, School of Health and Rehabilitation Science, The University of Queensland, St Lucia, Brisbane, Queensland, Australia. s.schabrun@uq.edu.au
Abstract
AIMS: Striated muscles of continence appear to exhibit marked fatigue during voluntary efforts. This is counterintuitive considering the high proportion of slow twitch muscle fibers. One explanation is that fatigue is due to central, rather than peripheral mechanisms. Here we examined the contribution of reduced voluntary activation (central fatigue) to the decline in anal sphincter (AS) and elbow flexor muscle force during voluntary contractions. METHODS:Ten healthy subjects participated. Fatigue was induced using 10 maximal voluntary contractions sustained for 20 s. During each fatiguing contraction, transcranial magnetic stimulation (TMS) was delivered over the motor cortex at 5 s intervals. Central fatigue was assessed using the superimposed twitch force elicited by TMS. Peripheral fatigue was measured using brachial plexus (elbow flexors) or sacral plexus (AS) stimulation during contraction and at rest. RESULTS: Ability to maximally activate AS (75.9%) was less than for the elbow flexors at baseline (91.6%). Voluntary activation declined in both muscles, but the decline was greater in AS (AS 28%; elbow flexors 12%). There was no change in the amplitude of the twitch evoked by peripheral nerve stimulation in either muscle. CONCLUSIONS: AS exhibits a greater decline in voluntary activation during fatiguing contractions than elbow flexor muscles. This is not accompanied by peripheral changes, which implies central mechanisms are responsible. Thus, we conclude that AS is susceptible to central fatigue during maximal voluntary activations. We propose this may be a protective mechanism to conserve contractile potential of the anal sphincter for function.
RCT Entities:
AIMS: Striated muscles of continence appear to exhibit marked fatigue during voluntary efforts. This is counterintuitive considering the high proportion of slow twitch muscle fibers. One explanation is that fatigue is due to central, rather than peripheral mechanisms. Here we examined the contribution of reduced voluntary activation (central fatigue) to the decline in anal sphincter (AS) and elbow flexor muscle force during voluntary contractions. METHODS: Ten healthy subjects participated. Fatigue was induced using 10 maximal voluntary contractions sustained for 20 s. During each fatiguing contraction, transcranial magnetic stimulation (TMS) was delivered over the motor cortex at 5 s intervals. Central fatigue was assessed using the superimposed twitch force elicited by TMS. Peripheral fatigue was measured using brachial plexus (elbow flexors) or sacral plexus (AS) stimulation during contraction and at rest. RESULTS: Ability to maximally activate AS (75.9%) was less than for the elbow flexors at baseline (91.6%). Voluntary activation declined in both muscles, but the decline was greater in AS (AS 28%; elbow flexors 12%). There was no change in the amplitude of the twitch evoked by peripheral nerve stimulation in either muscle. CONCLUSIONS: AS exhibits a greater decline in voluntary activation during fatiguing contractions than elbow flexor muscles. This is not accompanied by peripheral changes, which implies central mechanisms are responsible. Thus, we conclude that AS is susceptible to central fatigue during maximal voluntary activations. We propose this may be a protective mechanism to conserve contractile potential of the anal sphincter for function.