Subjects quickly fatigue when they perform maximal voluntary contractions (MVCs). Much of the loss of force is from processes within muscle (peripheral fatigue) but some occurs because voluntary activation of the muscle declines (central fatigue). The role of central fatigue during submaximal contractions is not clear. This study investigated whether central fatigue developed during prolonged low-force voluntary contractions. Subjects (n = 9) held isometric elbow flexions of 15% MVC for 43 min. Voluntary activation was measured during brief MVCs every 3 min. During each MVC, transcranial magnetic stimulation (TMS) was followed by stimulation of either brachial plexus or the motor nerve of biceps brachii. After nerve stimulation, a resting twitch was also evoked before subjects resumed the 15% MVC. Perceived effort, elbow flexion torque and surface EMG from biceps, brachioradialis and triceps were recorded. TMS was also given during the sustained 15% MVC. During the sustained contraction, perceived effort rose from ∼2 to ∼8 (out of 10) while ongoing biceps EMG increased from 6.9 ± 2.1% to 20.0 ± 7.8% of initial maximum. Torque in the brief MVCs and the resting twitch fell to 58.6 ± 14.5 and 58.2 ± 13.2% of control values, respectively. EMG in the MVCs also fell to 62.2 ± 15.3% of initial maximum, and twitches evoked by nerve stimulation and TMS grew progressively. Voluntary activation calculated from these twitches fell from ∼98% to 71.9 ± 38.9 and 76.9 ± 18.3%, respectively. The silent period following TMS lengthened both in the brief MVCs (by ∼40 ms) and in the sustained target contraction (by ∼18 ms). After the end of the sustained contraction, the silent period recovered immediately, voluntary activation and voluntary EMG recovered over several minutes while MVC torque only returned to ∼85% baseline. The resting twitch showed no recovery. Thus, as well as fatigue in the muscle, the prolonged low-force contraction produced progressive central fatigue, and some of this impairment of the subjects' ability to drive the muscle maximally was due to suboptimal output from the motor cortex. Although caused by a low-force contraction, both the peripheral and central fatigue impaired the production of maximal voluntary force. While central fatigue can only be demonstrated during MVCs, it may have contributed to the disproportionate increase in perceived effort reported during the prolonged low-force contraction.
SUMMARY1. The effect of magnetic stimulation of the human motor cortex on the excitability of soleus, tibialis anterior and flexor carpi radialis motoneurones was investigated by H reflex testing in ten healthy subjects.2. At rest, an early facilitation of the flexor carpi radialis and tibialis anterior H reflexes was always seen, whereas a similar early facilitation of the soleus H reflex was seen in only two out of seven subjects. For all three motoneuronal pools the facilitation was curtailed 1-5 ms later by an inhibition which lasted for another 3-4 ms. In five subjects an inhibition without any evidence of an earlier facilitation was seen for the soleus H reflex.3. The. intensity of the magnetic stimulation was subsequently decreased so that it had no effect on the H reflex at rest. When the subject then performed a voluntary agonist contraction a facilitatory effect with an early onset and a duration of 20-25 ms was observed for all three muscles. When the subject performed a voluntary antagonist contraction an inhibition was seen for the soleus H reflex with an onset 1-3 ms later than the facilitation. This is interpreted as resulting from the excitation by the magnetic stimulus of corticospinal neurones voluntarily activated in relation to the given motor task.4. The initial part of the facilitation was significantly smaller during cocontraction of both agonists and antagonists than during isolated agonist contraction.5. Whereas the early part of the facilitation always occurred during plantarflexion when the H reflex was conditioned by magnetic stimulation, this was never the case when it was conditioned by electrical stimulation of the cortex with the stimulus regimes used in these experiments.6. It is suggested that the early part of the facilitation observed during agonist contraction is caused by activation of corticomotoneuronal cells projecting to the agonist motoneuronal pool and that the inhibition observed during antagonist contraction is caused by activation of corticospinal cells projecting both to the antagonist motoneuronal pool and I a inhibitory interneurones to the agonist
Activation of descending corticospinal tracts with transmastoid electrical stimuli has been used to assess changes in the behaviour of motoneurones after voluntary contractions. Stimuli were delivered before and after maximal voluntary isometric contractions (MVCs) of the elbow flexor muscles. Following a sustained MVC of the elbow flexors lasting 5–120 s there was an immediate reduction of the response to transmastoid stimulation to about half of the control value. The response recovered to control levels after about 2 min. This was evident even when the size of the responses was adjusted to accommodate changes in the maximal muscle action potential (assessed with supramaximal stimuli at the brachial plexus). To determine whether the post‐contraction depression required activity in descending motor paths, motoneurones were activated by supramaximal tetanic stimulation of the musculocutaneous nerve for 10 s. This did not depress the response to transmastoid stimulation. Following a sustained MVC of 120 s duration, the response to transcranial magnetic stimulation of the motor cortex gradually declined to a minimal level by about 2 min and remained depressed for more than 10 min. Additional studies were performed to check that the activation of descending tracts by transmastoid stimulation was likely to involve excitation of direct corticospinal paths. When magnetic cortical stimuli and transmastoid stimuli were timed appropriately, the response to magnetic cortical stimulation could be largely occluded. This study describes a novel depression of effectiveness of corticospinal actions on human motoneurones. This depression may involve the corticomotoneuronal synapse.
. Changes in segmental and motor cortical output with contralateral muscle contractions and altered sensory inputs in humans. J Neurophysiol 90: 2451-2459, 2003; 10.1152/jn.01001.2002. Motor or sensory activity in one arm can affect the other arm. We tested the hypothesis that a voluntary contraction can affect the motor pathway to the contralateral homologous muscle and investigated whether alterations in sensory input might mediate such effects. Responses to transcranial magnetic stimulation [motor-evoked potentials (MEPs)], stimulation of the descending tracts [cervicomedullary MEPs (CMEPs)], and peripheral nerve stimulation (H-reflex) were recorded from the relaxed right flexor carpi radialis (FCR), while the left arm underwent unilateral interventions (5 s duration) that included voluntary contraction, muscle contraction evoked through percutaneous stimulation, tendon vibration, and cutaneous and mixed nerve stimulation. During moderate to strong voluntary wrist flexion on the left, MEPs in the right FCR increased, CMEPs were unaffected, and the H-reflex was depressed. These results are consistent with an increase in excitability of the motor cortex, no effect on the motoneuron pool, and presynaptic inhibition of Ia afferents. In contrast, percutaneous muscle stimulation facilitated both MEPs and the H-reflex. However, muscle contraction produced by a combination of voluntary effort and electrical stimulation also reduced the contralateral H-reflex. After voluntary contractions, the H-reflex remained depressed for 35 s, but after stimulationevoked contractions, it rapidly returned to baseline. Under both conditions, MEPs recovered rapidly. After voluntary contractions, CMEPs were also depressed for approximately 10 s despite their lack of change during contractions. Wrist tendon vibration (100 Hz) did not affect, and 20-Hz median nerve stimulation or forearm medial cutaneous nerve stimulation mildly facilitated, the H-reflex without affecting MEPs. Voluntary wrist extension, similarly to wrist flexion, increased MEPs and depressed H-reflexes. However, ankle dorsiflexion facilitated the H-reflex akin to the Jendrassik maneuver. These data suggest that a unilateral voluntary muscle contraction has contralateral effects at both cortical and segmental levels and that the segmental effects are not replicated by stimulated muscle contraction or by input from muscle spindles or non-nociceptive cutaneous afferents.
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