Tibialis anterior muscle
About: Tibialis anterior muscle is a research topic. Over the lifetime, 1108 publications have been published within this topic receiving 31021 citations.
Papers published on a yearly basis
TL;DR: Architectural parameters of several human muscles were measured during isometric contractions of from 0 to 100% maximal voluntary contraction to investigate the ability of ultrasonography to estimate muscle activity.
Abstract: To investigate the ability of ultrasonography to estimate muscle activity, we measured architectural parameters (pennation angles, fascicle lengths, and muscle thickness) of several human muscles (tibialis anterior, biceps brachii, brachialis, transversus abdominis, obliquus internus abdominis, and obliquus externus abdominis) during isometric contractions of from 0 to 100% maximal voluntary contraction (MVC). Concurrently, electromyographic (EMG) activity was measured with surface (tibialis anterior only) or fine-wire electrodes. Most architectural parameters changed markedly with contractions up to 30% MVC but changed little at higher levels of contraction. Thus, ultrasound imaging can be used to detect low levels of muscle activity but cannot discriminate between moderate and strong contractions. Ultrasound measures could reliably detect changes in EMG of as little as 4% MVC (biceps muscle thickness), 5% MVC (brachialis muscle thickness), or 9% MVC (tibialis anterior pennation angle). They were generally less sensitive to changes in abdominal muscle activity, but it was possible to reliably detect contractions of 12% MVC in transversus abdominis (muscle length) and 22% MVC in obliquus internus (muscle thickness). Obliquus externus abdominis thickness did not change consistently with muscle contraction, so ultrasound measures of thickness cannot be used to detect activity of this muscle. Ultrasound imaging can thus provide a noninvasive method of detecting isometric muscle contractions of certain individual muscles.
TL;DR: The primary cause of the poor recovery after long-term denervation is a profound reduction in the number of axons that successfully regenerate through the deteriorating intramuscular nerve sheaths, which contributes to the progressive decline in muscle force.
Abstract: The effects of prolonged denervation, independent from those of prolonged axotomy, on the recovery of muscle function were examined in a nerve cross-anastomosis paradigm. The tibialis anterior muscle was denervated for various durations by cutting the common peroneal nerve before a freshly cut tibial nerve was cross-sutured to its distal stump. Nerve regeneration and muscle reinnervation were quantified by means of electrophysiological and histochemical methods. Progressively fewer axons reinnervated the muscle with prolonged denervation; for example, beyond 6 months the mean (+/- SE) motor unit number was 15 +/- 4, which was far fewer than that after immediate nerve suture (137 +/- 21). The poor regeneration after prolonged denervation is not due to inability of the long-term denervated muscle to accept reinnervation because each regenerated axon reinnervated three- to fivefold more muscle fibers than normal. Rather, it is due to progressive deterioration of the intramuscular nerve sheaths because the effects of prolonged denervation were simulated by forcing regenerating axons to grow outside the sheaths. Fewer regenerated axons account for reinnervation of less than 50% of the muscle fibers in each muscle and contribute to the progressive decline in muscle force. Reinnervated muscle fibers failed to fully recover from denervation atrophy: muscle fiber cross-sectional area being 1171 +/- 84 microns2 as compared to 2700 +/- 47 microns2 after immediate nerve suture. Thus, the primary cause of the poor recovery after long-term denervation is a profound reduction in the number of axons that successfully regenerate through the deteriorating intramuscular nerve sheaths. Muscle force capacity is further compromised by the incomplete recovery of muscle fibers from denervation atrophy.
TL;DR: Although prolonged axotomy does not compromise the number of muscle fibers innervated by each axon, it does reduce the capacity of motor axons to regenerate and thus is an important contributing factor to the poor functional recovery in delayed nerve repair.
Abstract: The contribution of prolonged motoneuron axotomy to the poor functional recovery after delayed nerve repair was determined by means of a nerve cross-anastomosis paradigm in the rat. The tibial nerve was axotomized up to 12 months before it was cross-sutured to the distal stump of the freshly cut common peroneal nerve to innervate the freshly denervated tibialis anterior muscle. Three to 17 months later, muscle and motor unit (MU) forces were measured to quantify the number of axons that had successfully regenerated and reinnervated the muscle. The extent of axonal branching was estimated by the innervation ratio (IR) (i.e., the number of muscle fibers innervated by each axon), which was obtained directly by counting muscle fibers in a single glycogen-depleted MU in each muscle and indirectly by calculation. The total number of MUs in each muscle significantly decreased with progression of axotomy and was only 35% of the control when axotomy was prolonged more than 3 months. Concurrently, MU force and IR increased exponentially, with a mean increase of threefold when axotomy was more than 3 months, which largely compensated for the reduction in the number of axons that reinnervated the muscle. Consequently, muscles reinnervated by tibial motor axons that had been axotomized up to 12 months produced as much force as those reinnervated by freshly axotomized tibial motor axons. Muscle weight, size, and muscle fiber size were similar to those after immediate nerve suture. Although prolonged axotomy does not compromise the number of muscle fibers innervated by each axon, it does reduce the capacity of motor axons to regenerate and thus is an important contributing factor to the poor functional recovery in delayed nerve repair.
TL;DR: It is concluded that a surface myoelectric signal detected on the skin above a leg muscle and having a peak-to-peak amplitude of up to 16.6% of a signal detected above a neighboring muscle may be due to cross-talk rather than to activation of the muscle below the electrode.
Abstract: Surface myoelectric signals were detected from the skin surface above the tibialis anterior muscle, the peroneus brevis muscle, the soleus muscle and the tibial bone during selective maximal electrical stimulation of the tibialis anterior muscle in 12 normal subjects. The double differential technique developed by Broman et al. (1985) was used to determine if the detected signal was due to volume conduction from the tibialis anterior fibers. The peak-to-peak (PP), average rectified (ARV) and root mean square (RMS) amplitudes of the M waves were computed for each detection location. The values detected on the tibial bone, on the peroneus and on the soleus muscles were normalized with respect to those detected on the tibialis anterior and ranged from 4.8% to 33.0% (PP), 4.7% to 36.0% (ARV), and 7.7% to 37.4% (RMS) for the tibial bone area; from 4.0% to 20.0% (PP), 3.5% to 10.0% (ARV), and 3.0% to 10.0% (RMS) for the peroneus brevis muscle area; and from 3.0% to 8.0% (PP), 3.4% to 9.1% (ARV), and 2.0% to 9.8% (RMS) for the soleus muscle area. Neither peak-to-peak values, average rectified values nor root mean square values appeared to be correlated with leg size. It is concluded that a surface myoelectric signal detected on the skin above a leg muscle and having a peak-to-peak amplitude of up to 16.6% of a signal detected above a neighboring muscle may be due to cross-talk rather than to activation of the muscle below the electrode.
TL;DR: There were no vestibular‐evoked responses when seated subjects made voluntary contractions of the leg muscles or when they stood upright with the trunk supported, using the ankles to balance a body‐like load.
Abstract: 1. To identify the vestibular contribution to human standing, responses in leg muscles evoked by galvanic vestibular stimulation were studied. Step impulses of current were applied between the mastoid processes of normal subjects and the effects on the soleus and tibialis anterior electromyograms (EMGs), ankle torque, and body sway were identified by post-stimulus averaging. The responses were measured when subjects stood on a stable platform or on an unstable platform and the effects of eye closure were also assessed. Responses were also recorded during voluntary contraction of the leg muscles and when subjects balanced a load equivalent to their own body in a situation where vestibular postural reflexes would not be useful. 2. At a mean post-stimulus latency of 56 ms, there were reciprocal changes in soleus and tibialis anterior muscle activity followed, at 105 ms, by larger responses of opposite sign. These were termed the short- and middle-latency responses, respectively. Both responses increased with stimulus intensity, but the short-latency response had a higher threshold. The early response had a similar latency to EMG responses evoked by rapid postural perturbations. Both responses were larger when the eyes were closed, but eye closure was associated with increased sway and EMG activity, and the responses were of similar magnitude when scaled to background EMG level. 3. Both short- and middle-latency EMG responses in soleus and tibialis anterior muscles produced small transient postural sways. The transient changes in EMG activity were followed by a larger prolonged sway which was not attributable to the activity in these muscles but rather to reflex or volitional adjustments to movements at other body segments. When subjects were prevented from swaying, the galvanic stimulus produced illusory movements in the opposite direction to the sway evoked when standing, and it is possible that the prolonged sway is a reaction to the illusion of sway. 4. The short- and middle-latency responses were modified during different postural tasks according to the dependence on vestibular reflexes. When the support platform was unstable, the EMG responses to galvanic stimulation were larger. There were no vestibular-evoked responses when seated subjects made voluntary contractions of the leg muscles or when they stood upright with the trunk supported, using the ankles to balance a body-like load.(ABSTRACT TRUNCATED AT 400 WORDS)
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