Neuromuscular adaptations to muscle fatigue during submaximal isometric contractions in man

Abstract: During a sustained contraction, the force producing capacity of a muscle gradually decreases. In order to maintain a constant force output, the neuromuscular system has to adapt to the contractile fatigue process. The aim of the present work was to study these adaptations during short- and long-lasting contractions by analysing voluntary and reflex myoelectric activities, muscle twitch responses and force tremor. During brief isometric handgrips, a linear relationship between the amplitude of the surface electromyogram (EMG) and the force output was found, while tremor increased initially and then decreased at high contraction levels. Both EMG and tremor changes reflected effort related modulations of motor unit recruitment and motor unit firing rates. The maximal voluntary and involuntary EMG amplitude was reduced at decreased gastrocnemius muscle lengths. This reduction originated from either an impairment of neuromuscular transmission or changes in the geometry of muscle fibres, the latter resulting in a reduced number of fibres located within the pick-up volume of the recording electrode. During isometric contractions of the triceps surae, sustained at 30% of a maximum voluntary contraction until endurance limit, the net excitatory drive to the a-motoneuron pool increased, as assessed by twitch occlusion and H-reflexes. In parallel, EMG and tremor amplitude increased, which appeared to predominantly result from recruitment of unfatigued motor units and bursting EMG activity. The increased excitatory drive was found to additionally modulate Renshaw interneurons, as recurrent inhibition of soleusa-motoneurons, evaluated by paired H-reflexes, was reduced after ten minutes of a fatiguing plantar flexion. Toward endurance limit of a long-lasting submaximal plantar flexion, tremor amplitude increased in a non-linear fashion. When la-afferent input to the a-motoneuron pool was reduced by either tendon vibration or an ischemic block, the tremor increase was significantly diminished. This demonstrates the significance of stretch reflex activity for the enhancement of tremor. It appears that la-afferent input triggers oscillations in the stretch reflex arc during a fatiguing contraction, which result in bursting EMG activity and augmented tremor. At endurance limit, EMG and twitch occlusion results indicated that central fatigue had occurred, as complete muscle activation was not achievable. However, after one minute of electrical stimulation to the same torque level, subjects were able to voluntarily continue the contraction and finally achieve full muscle activation. As the electrical stimulation allowed for muscle spindle, supraspinal and motoneuronal recovery, while metabolic stress and contractile fatigue continued, it appeared that central fatigue was not caused by metabo-receptor or nociceptor mediated peripheral reflex inhibition of the a-motoneuron pool. In conclusion, during a long-lasting submaximal constant-force contraction of the triceps surae, the neuromuscular system adapts to contractile fatigue mainly by recruitment of new motor units, facilitated by an increased excitatory drive to the a-motoneuron pool and by a reduction of Renshaw inhibition. The increase in excitatory drive seems to additionally increase the probability of oscillations in the stretch reflex loop, resulting in enhancement of tremor during fatigue. Despite this increase, excitatory drive fails to reach its maximum at endurance limit. Thus, central fatigue occurs, which appears to be independent of peripheral reflex inhibition, but due to fatigue at the muscle spindle, the motoneuronal and/or the supraspinal level.