Controlling instabilities with the legs (as per the Lower Extremity Strength-Dexterity (LED) paradigm) is likely a product of a hierarchical organization of neural control, in agreement with current thinking. A pilot study showed that LED performance deteriorates with 20 minutes of downhill walking in the absence of fatigue. This suggests that the control of leg dexterity might degrade with eccentric contractions—and may be a plausible mechanism for non-contact sports injuries. However, this effect remains ambiguous because concentric and eccentric phases coexist in the stance phase of downhill walking. Hierarchical control of instabilities involves “low level” sub-cortical or spinal mechanisms. Such short-latency responses are often mediated by tunable spindle afferents. The ability to perform short-latency corrections should, therefore, be dependent on the gain and gaiting of spindle afferent signals. Therefore, we hypothesized that purely eccentric contractions of the soleus muscle would affect spindle afferent gains; and therefore preferentially affect a subjects’ ability to stabilize the leg. Hoffman’s reflex (H-reflex) is a measure of spinally modulated gating of afferent signals onto alpha-motoneurone excitability that is independent of fusimotor gain. We further hypothesized that effect of eccentric contractions on spindle gating would be manifested in changes in H-reflex. We compared resting H-reflex excitability and LED performance bilaterally in nine young adult male subjects (25.4±3.8 yrs) before and after exposure to unilateral eccentric contractions at 15% maximal voluntary contraction (MVC) vs. level treadmill walking. There was no measurable fatigue as per objective MVC measurements (mean relative increase of 18.8±23.6%) and the subjective Borg scale (mean value of 2.0±0.7 out of 10).
Despite an increase in MVC and no measurable fatigue, we found that eccentric contractions had an adverse effect on the LED compression force (i.e., a reduction in the maximal level of controllable instability) when compared with contralateral control and walking condition. Thus, exposure to non-fatiguing, purely eccentric contractions disrupted the ability to dynamically stabilize the leg. It did not, however, affect resting H-reflex. These results, alongside with retained neural drive to the involved muscles measured by EMG signals, suggest the decreased LED performance did not stem from deficit of the central neural drive or spinally modulated gating of afferent signals. We speculate eccentric contractions lead to possible fusimotor reprogramming of spindle sensitivity and therefore afferent signals. Our results compel further studies to test these different levels in hierarchical organization of neural control of instabilities. Moreover, such an adverse effect of eccentric contraction on the ability to control instabilities may provide new insights into sensorimotor processing of proprioceptive signals in the context of neuromuscular performance and injury mechanisms.