Author(s): CHETOUANI, A., RUGGIERO, L., CASOLO, A., GONCALVES, B., GRUBER, M., AVELA, J., BACA, A., Institution: UNIVERSITY OF VIENNA & UNIVERSITY OF JYVÄSKYLÄ, Country: AUSTRIA, Abstract-ID: 2628

INTRODUCTION:
Sensory feedback transmitted through afferent nerve fibers is essential for accurate motor control. Ischemic nerve blocks of Ia-afferents have been widely used as a model to investigate human motor control in a deafferented state. However, besides the Ia-afferent block, the neuromuscular effects induced by ischemia, and their subsequent effect on motor unit discharge rates (MUDR), are still unclear. Therefore, we investigated the effects of an ischemic Ia-afferent block on MUDR during submaximal isometric plantar flexions.
METHODS:
In this preliminary analysis, four participants (3 males) performed trapezoidal contractions at 20% of maximal voluntary isometric torque (MVT) before (PRE) and after (POST) an ischemic Ia-afferent block, both at the same absolute (ABS) and relative (REL) torque levels. Contractions were performed at 5% MVT/s with a 16-s plateau at the target torque. Ischemia was induced through an inflatable cuff strapped over the proximal thigh at pressures of 191mmHg (SD 34). Soleus MUDR were analyzed from high-density surface electromyography. Trapezoidal contractions under ischemia were performed with complete Ia-afferent block, which was verified by the disappearance of H-reflexes. Motor axon transmission was assessed through maximal M-waves. H-reflexes and M-waves were elicited before and every minute during ischemia via posterior tibial nerve stimulation. To define the REL torque level with ischemia, a maximal isometric contraction after ABS with Ia-afferent block was performed.
RESULTS:
Complete Ia-afferent block was achieved after 17.5min (SD 5.0) of ischemia. M-wave peak-to-peak amplitude did not change from PRE (2.9mV SD 1.7) to the end of ischemia (2.6mV SD 1.5). MVT was significantly reduced following Ia-afferent block (PRE: 69.3Nm SD 28.3; POST: 59.0Nm SD 30.1; p=0.03). A total of 52 motor units were tracked across the three measurements (PRE, POST ABS and POST REL). When pooling all motor units within each trial, MUDR was higher during POST ABS (9.3pps SD 1.4) compared to PRE (8.0pps SD 1.4, p=0.001) and POST REL (8.7pps SD 1.0, p=0.009), with no differences between PRE and POST REL.
CONCLUSION:
In this study, an ischemic block of Ia-afferents increased MUDR when contractions were performed at the same absolute torque, but not at the same relative torque-level compared to baseline. Given that previous pilot studies have shown a reduction in twitch torque to supramaximal stimulation at the time of Ia-afferent block, it is plausible that the increase in MUDR at ABS likely reflects a neural strategy compensating for peripheral changes to maintain the same absolute torque target. Further, motor unit discharge is regulated through an interplay of supraspinal drive, neuromodulatory input, and afferent feedback to motoneurons. The loss of afferent feedback during the ischemic Ia-afferent block induced in the present study, might therefore have increased the relative contribution of central and neuromodulatory mechanisms to sustain MUDR.