Endurance Trained Athletes Do Not per se Have Higher Hoffmann Reflexes Than Recreationally Active Controls

The impact of endurance training on spinal neural circuitries remains largely unknown. Some studies have reported higher H-reflexes in endurance trained athletes and therefore, adaptations within the Ia afferent pathways after long term endurance training have been suggested. In the present study we tested the hypothesis that cyclists (n = 12) demonstrate higher Hoffmann reflexes (H-reflexes) compared to recreationally active controls (n = 10). Notwithstanding, highly significant differences in endurance performance (VO2peak: 60.6 for cyclists vs. 46.3 ml/min/kg for controls (p < 0.001) there was no difference in the size of the SOL H-reflex between cyclists and controls (Hmax/Mmax ratio 61.3 vs. 60.0%, respectively (p = 0.840). Further analyses of the H and M recruitment curves for SOL revealed a significant steeper slope of the M recruitment curve in the group of cyclists (76.2 ± 3.8° vs. 72.0 ± 4.4°, p = 0.046) without a difference in the H-recruitment curve (84.6 ± 3.0° vs. 85.0 ± 2.8°, p = 0.784) compared to the control group. Cycling is classified as an endurance sport and thus the findings of the present study do not further support the assumption that long-term aerobic training leads to a general increase of the H-reflex. Amongst methodological differences in assessing the H-reflex, the training-specific sensorimotor control of the endurance sport itself might differently affect the responsiveness of spinal motoneurons on Ia-afferent inputs.

Facilitation of sensory axon conduction to motoneurons during cortical or sensory evoked primary afferent depolarization (PAD) in humans

Sensory and cortical pathways activate GABAergic interneurons with axo-axonic connections onto proprioceptive (Ia) afferents that depolarize these afferents (termed primary afferent depolarization, PAD). In rodents sensory-evoked PAD is produced by GABAA receptors at nodes of Ranvier in Ia-afferents, rather than at presynaptic terminals, and facilitates action potential propagation to motoneurons by preventing branch point failures, rather than causing presynaptic inhibition. Here we examined if PAD likewise facilitates the Ia-afferent mediated H-reflex in humans by evoking PAD with both sensory and corticospinal tract (CST) stimulation. H-reflexes in several lower limb muscles were facilitated by prior conditioning from low-threshold proprioceptive, cutaneous or CST pathways, with a similar time course (~200 ms) to the PAD measured in rodent Ia-afferents. Long trains of repeated cutaneous or proprioceptive afferent stimulation produced long-lasting facilitation of the H-reflex for up to 2 minutes, consistent with the tonic depolarization of rodent Ia-afferents mediated by nodal α5-GABAA receptors for similar stimulation trains. Facilitation of the conditioned H-reflexes was not mediated by direct facilitation of the motoneurons because isolated stimulation of sensory or CST pathways did not modulate the firing rate of tonically activated motor units in tested muscles. Furthermore, cutaneous conditioning increased the firing probability of a single motor unit during the H-reflex without increasing its firing rate at this time, indicating that the underlying excitatory postsynaptic potential (EPSP) was more probable, but not larger. These results are consistent with sensory and CST pathways activating nodal GABAA receptors that reduce intermittent failure of action potentials propagating into Ia-afferent branches.

RUNNING-INDUCED CHANGES IN H-REFLEX AMPLITUDES IN NON-TRAINED MEN

Effect of 5-weeks running training on modulation of the H-reflex amplitude on soleus muscle in non-trained men was studied. It was established that modulation of the H-reflex amplitude occurs in two phases. In the course of the first 3 weeks of running training (first phase) statistically significant (p < 0.05) increase in H-reflex amplitudes and the maximum H-reflex to the maximum M-response amplitudes ratio (10%) were registered. In contrast to the first phase, decrease in investigated parameters up to initial values were observed during the next 2 weeks of the training (second phase). An increase in the of the soleus H-reflex amplitude, is probably due to the enhanced drive in descending pathways, increased motoneuron excitability and changes in presynaptic Ia afferent inhibition, whereas decrease in the amplitude of the H-reflex might occurs presumably due to motor learning. Apparently, that the repetitive task, which automatically performed and controlled on a spinal or brainstem level can be reflected in the normalization and stabilization of the H-reflexes registered after running training in later period.

Lack of cortical or Ia-afferent spinal pathway involvement in muscle force loss after passive static stretching

This study is the first to specifically examine potential sites underlying the decreases in neural activation of muscle and force production after a bout of muscle stretching. However, no changes were found in either the H-reflex or motor-evoked potential amplitude during submaximal contractions.

Cortical and Subcortical Contributions to Neuroplasticity after Repetitive Transspinal Stimulation in Humans

The objectives of this study were to establish cortical and subcortical contributions to neuroplasticity induced by noninvasive repetitive transspinal stimulation in human subjects free of any neurological disorder. To meet our objectives, before and after 40 minutes of transspinal stimulation we established changes in tibialis anterior (TA) motor-evoked potentials (MEPs) in response to paired transcranial magnetic stimulation (TMS) pulses at interstimulus intervals (ISIs) consistent with I-wave periodicity. In order to establish to what extent similar actions are exerted at the spinal cord and motor axons, changes in soleus H-reflex and transspinal evoked potential (TEP) amplitude following transspinal and group Ia afferent conditioning stimulation, respectively, were established. After 40 min of transspinal stimulation, the TA MEP consecutive peaks of facilitation produced by paired TMS pulses were significantly decreased supporting for depression of I-waves. Additionally, the soleus H-reflex and ankle TEP depression following transspinal and group Ia afferent conditioning stimulation was potentiated at intervals when both responses interacted at the spinal cord and nerve axons. These findings support the notion that repetitive transspinal stimulation decreases corticocortical inputs onto corticospinal neurons and promotes a surround inhibition in the spinal cord and nerve axons. This novel method may be a suitable neuromodulation tool to alter excitability at cortical and subcortical levels in neurological disorders.

Noncontractile tissue forces mask muscle fiber forces underlying muscle spindle Ia afferent firing rates in stretch of relaxed rat muscle

Stretches of relaxed cat and rat muscle elicit similar history-dependent muscle spindle Ia firing rates that resemble history-dependent forces seen in single activated muscle fibers (Nichols and Cope, 2004). During stretch of relaxed cat muscle, whole musculotendon forces exhibit history-dependence that mirror history-dependent muscle spindle firing rates, where both muscle force and muscle spindle firing rates are elevated in the first stretch in a series of stretch-shorten cycles (Blum et al., 2017). By contrast, rat musculotendon are only mildly history-dependent and do not mirror history-dependent muscle spindle firing rates in the same way (Haftel et al., 2004). We hypothesized that history-dependent muscle spindle firing rates elicited in stretch of relaxed rat muscle would mirror history-dependent muscle fiber forces, which are masked by noncontractile tissue at the level of whole musculotendon force. We removed noncontractile tissue force contributions from the recorded musculotendon force using an exponentially-elastic tissue model. We then show that the remaining estimated muscle fiber force resembles history-dependent muscle spindle firing rates recorded simultaneously. These forces also resemble history-dependent forces recorded in stretch of single activated fibers and attributed to muscle cross-bridge mechanisms (Campbell and Moss, 2000). Our results suggest that history-dependent muscle spindle firing in both rats and cats arise from stretch of cross-bridges in muscle fibers.