Publication | Open Access
Prolonged muscle vibration reducing motor output in maximal voluntary contractions in man.
239
Citations
14
References
1990
Year
Muscle FunctionMotor ControlKinesiologyMuscle InjuryMotor OutputExerciseMaximal Voluntary ContractionsApplied PhysiologySustained VibrationMuscle VibrationMotor BehaviorHealth SciencesProlonged Muscle VibrationRehabilitationNeuromuscular PhysiologyPhysiologyExercise PhysiologyMotor SystemElectromyographyMusculoskeletal InteractionHuman Movement
1. We observed in a previous study on the human foot dorsiflexor muscles that the fatigue-induced decline in motor output during sustained maximal voluntary contractions (MVCs) was temporarily counteracted during the initial phase of superimposed high-frequency (150 Hz) muscle vibration, whereas prolonged muscle vibration seemed to accentuate the fatigue-induced decline in gross EMG activity and motor unit firing rates. A more extensive investigation of this late effect of muscle vibration on MVCs was performed in the present study. 2. Prolonged periods of superimposed muscle vibration caused a reduction of EMG activity, motor unit firing rates and contraction force in both intermittent and sustained MVCs. This vibration-induced effect had the following main characteristics: (i) it developed slowly during the course of about 1 min of sustained vibration and subsided within 10-20 s after the end of vibration; (ii) it was much more pronounced in some subjects than in others (not age-dependent) and it was accentuated by preceding muscle exercise; (iii) it affected primarily the subject's ability to generate and/or maintain high firing rates in high-threshold motor units. 3. Since the effect developed while vibration at the same time exerted a tonic excitatory influence on the alpha-motoneurone pool (as evidenced by the presence of a tonic vibration reflex) it is argued that the vibration-induced suppression of motor output in MVCs probably does not depend on alpha-motoneurone inhibition, but on a reduced accessibility of these neurones to the voluntary commands. It is suggested that contributing mechanisms might be vibration-induced presynaptic inhibition and/or 'transmitter depletion' in the group Ia excitatory pathways which constitute the afferent link of the gamma-loop.
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