Effect of Long-Term Classical Ballet Dance Training on Postactivation Depression of the Soleus Hoffmann-Reflex

Classical ballet dancing is a good model for studying the long-term activity-dependent plasticity of the central nervous system in humans, as it requires unique ankle movements to maintain ballet postures. The purpose of this study was to investigate whether postactivation depression is changed through long-term specific motor training. Eight ballet dancers and eight sedentary subjects participated in this study. The soleus Hoffmann reflexes were elicited at after the completion of a slow, passive dorsiflexion of the ankle. The results demonstrated that the depression of the soleus Hoffmann reflex (i.e., postactivation depression) was larger in classical ballet dancers than in sedentary subjects at two poststretch intervals. This suggests that the plastic change through long-term specific motor training is also expressed in postactivation depression of the soleus Hoffmann reflex. Increased postactivation depression would strengthen the supraspinal control of the plantarflexors and may contribute to fine ankle movements in classical ballet dancers.

Fatigue-induced modulation of human soleus H-reflex in conditions of pair tibial nerve stimulation in untrained and trained people

Monosynaptic reflex indices peculiarities, concerned with adaptative reactions to the long-term physical exercise, might add new data about mechanisms of human nervous system plasticity. The objective of the research was to investigate the influence of fatigue on human soleus H (Hoffmann) reflex in conditions of pair stimulation of tibial nerve with inter stimulus interval 500 m sin tenun trained people (age: M = 25,3, SE = 1,6 years) and ten trained athletes (age: M = 20,5, SE = 0,5 years). H-reflex study was performed using neurodiagnostic complex Nicolet Biomedical Viking Select (Viasys Health care, USA) at rest: before and after long-lasting isometric voluntary contraction of calf muscle, which caused the soleus muscle fatigue; the muscle force was equal to 75 % of maximal voluntary contraction. Test and conditioned responses (by means of stimulation with first and second impulses from pair) were registered. Homosynaptic postactivation depression (HPAD), associated with pair stimulation of tibial nerve, led to 56 % and 51 % inhibition of H-reflex in untrained and trained people at rest, respectively (p < 0,05). After fatiguing voluntary contraction the amplitudes of test and conditioned soleus H-reflex were both reduced approximately in half. Then both H-reflex amplitudes subsequently recovered, more rapidly in trained people. Soleus H-reflex inhibition might be due to the activation of the groups III and IV afferent nerves under the influence of mechanical and metabolic changes in the muscle. It was also found that HPAD H-reflex inhibition intensity increased by 20 % in untrained people and by 15 % in trained ones at 90 s after fatiguing voluntary contraction (p < 0,05). It is assumed that complex influence of fatigue and homosynaptic postactivation depression was more pronounced in untrained people in comparison with trained ones. It can be ascribed to athletes adaptation to the long-term physical exercise.

Fatigue-incduced modulation of human soleus Hoffmann reflex under conditions of homosynaptic postactivation depression due to pair tibial nerve stimulation

The purpose of our work was to investigate in detail the influence of pair stimulation of tibial nerve (n.tibialis) on human soleus H-reflex amplitude at rest and after long-lasting voluntary contraction of calf muscle (m.m. gastrocnemius-soleus), which caused the fatigue of soleus muscle. The method of H-reflex of soleus muscle was used. Test and conditioned responses (by pair stimulation of n. tibialis) were registered. Homosynaptic postactivation depression led to inhibition of H-reflex at rest. After fatiguing voluntary static contraction the amplitudes of test and conditioned soleus H-reflex were significantly reduced. Then both H-reflex amplitudes subsequently recovered. Soleus H-reflex inhibition might be due to the activation of the groups III and IV afferent nerves under the influence of mechanical and metabolic changes in the muscle.

Transspinal constant-current long-lasting stimulation: a new method to induce cortical and corticospinal plasticity

Functional neuroplasticity in response to stimulation and motor training is a well-established phenomenon. Transcutaneous stimulation of the spine is used mostly to alleviate pain, but it may also induce functional neuroplasticity, because the spinal cord serves as an integration center for descending and ascending neuronal signals. In this work, we examined whether long-lasting noninvasive cathodal (c-tsCCS) and anodal (a-tsCCS) transspinal constant-current stimulation over the thoracolumbar enlargement can induce cortical, corticospinal, and spinal neuroplasticity. Twelve healthy human subjects, blind to the stimulation protocol, were randomly assigned to 40 min of c-tsCCS or a-tsCCS. Before and after transspinal stimulation, we established the afferent-mediated motor evoked potential (MEP) facilitation and the subthreshold transcranial magnetic stimulation (TMS)-mediated flexor reflex facilitation. Recruitment input-output curves of MEPs and transspinal evoked potentials (TEPs) and postactivation depression of the soleus H reflex and TEPs was also established. We demonstrate that both c-tsCCS and a-tsCCS decrease the afferent-mediated MEP facilitation and alter the subthreshold TMS-mediated flexor reflex facilitation in a polarity-dependent manner. Both c-tsCCS and a-tsCCS increased the tibialis anterior MEPs recorded at 1.2 MEP resting threshold, intermediate, and maximal intensities and altered the recruitment input-output curve of TEPs in a muscle- and polarity-dependent manner. Soleus H-reflex postactivation depression was reduced after a-tsCCS and remained unaltered after c-tsCCS. No changes were found in the postactivation depression of TEPs after c-tsCCS or a-tsCCS. Our findings reveal that c-tsCCS and a-tsCCS have distinct effects on cortical and corticospinal excitability. This method can be utilized to induce targeted neuroplasticity in humans.

Postactivation depression of the Ia EPSP in motoneurons is reduced in both the G127X SOD1 model of amyotrophic lateral sclerosis and in aged mice

Postactivation depression (PActD) of Ia afferent excitatory postsynaptic potentials (EPSPs) in spinal motoneurons results in a long-lasting depression of the stretch reflex. This phenomenon (PActD) is of clinical interest as it has been shown to be reduced in a number of spastic disorders. Using in vivo intracellular recordings of Ia EPSPs in adult mice, we demonstrate that PActD in adult (100–220 days old) C57BL/6J mice is both qualitatively and quantitatively similar to that which has been observed in larger animals with respect to both the magnitude (with ∼20% depression of EPSPs at 0.5 ms after a train of stimuli) and the time course (returning to almost normal amplitudes by 5 ms after the train). This validates the use of mouse models to study PActD. Changes in such excitatory inputs to spinal motoneurons may have important implications for hyperreflexia and/or glutamate-induced excitotoxicity in the neurodegenerative disease amyotrophic lateral sclerosis (ALS). With the use of the G127X SOD1 mutant mouse, an ALS model with a prolonged asymptomatic phase and fulminant symptom onset, we observed that PActD is significantly reduced at both presymptomatic (16% depression) and symptomatic (17.3% depression) time points compared with aged-matched controls (22.4% depression). The PActD reduction was not markedly altered by symptom onset. Comparing these PActD changes at the EPSP with the known effect of the depression on the monosynaptic reflex, we conclude that this is likely to have a much larger effect on the reflex itself (a 20–40% difference). Nevertheless, it should also be accounted that in aged (580 day old) C57BL/6J mice there was also a reduction in PActD although, aging is not usually associated with spasticity.

Reduced postactivation depression of soleus H reflex and root evoked potential after transcranial magnetic stimulation

Postactivation depression of the Hoffmann (H) reflex is associated with a transient period of suppression following activation of the reflex pathway. In soleus, the depression lasts for 100–200 ms during voluntary contraction and up to 10 s at rest. A reflex root evoked potential (REP), elicited after a single pulse of transcutaneous stimulation to the thoracolumbar spine, has been shown to exhibit similar suppression. The present study systematically characterized the effect of transcranial magnetic stimulation (TMS) on postactivation depression using double-pulse H reflexes and REPs. A TMS pulse reduced the period of depression to 10–15 ms for both reflexes. TMS could even produce postactivation facilitation of the H reflex, as the second reflex response was increased to 243 ± 51% of control values at the 75-ms interval. The time course was qualitatively similar for the REP, yet the overall increase was less. While recovery of the H reflex was slower in the relaxed muscle, the profile exhibited a distinct bimodal shape characterized by an early peak at the 25-ms interval, reaching 72 ± 23% of control values, followed by a trough at 50 ms, and then a gradual recovery at intervals > 50 ms. The rapid recovery of two successively depressed H reflexes, ∼25 ms apart, was also possible with double-pulse TMS. The effect of the TMS-induced corticospinal excitation on postactivation depression may be explained by a combination of pre- and postsynaptic mechanisms, although further investigation is required to distinguish between them.

Characteristics of preceding Ia activity on postactivation depression in health and disease

Previous activation of the soleus Ia afferents causes a depression in the amplitude of the H-reflex. This mechanism is referred to as postactivation depression (PAD) and is suggested to be presynaptically mediated. With the use of a paired reflex depression paradigm (eliciting two H-reflexes with conditioning-test intervals from 80 ms to 300 ms), PAD was examined in a group of healthy individuals and a group of hemiplegic patients. Healthy individuals showed substantial depression of the test H-reflex at all intervals. Although the patient group showed substantially less depression at all intervals, increasing the interval between the two reflexes sharply reduced the depression. In a separate experiment, we varied the size of the conditioning H-reflex against a constant test H-reflex. In healthy individuals, by increasing the size of the conditioning H-reflex, the amplitude of the test H-reflex exponentially decreased. In the patient group, however, this pattern was dependent on the conditioning-test interval; increasing the size of the conditioning H-reflex caused an exponential decrease in the size of the test reflex at intervals shorter than 150 ms. This pattern was similar to that of healthy individuals. However, conducting the same protocol at a longer interval (300 ms) in these patients resulted in an abnormal pattern (instead of an exponential decrease in the size of the test reflex, exaggerated responses were observed). Fisher discriminant analysis suggested that these two patterns (which differed only in the timing between the two stimuli) were substantially different from each other. Therefore, it is suggested that the abnormal pattern of PAD in hemiplegic stroke patients could be a contributing factor for the pathophysiology of spasticity.