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. 2019 Jul;29(7):944-951.
doi: 10.1111/sms.13421. Epub 2019 Apr 4.

Sustained submaximal contraction yields biphasic modulation of soleus Post-activation depression in healthy humans

Preeti D Oza  1 , Shauna Dudley-Javoroski  2 , Richard K Shields  2
Affiliations

Sustained submaximal contraction yields biphasic modulation of soleus Post-activation depression in healthy humans

Preeti D Oza et al. Scand J Med Sci Sports. 2019 Jul.

Abstract

The amplitude of the H-reflex during the development and progression of fatigue reflects a complex interplay between central and peripheral factors. The purpose of this study is to characterize H-reflex homosynaptic post-activation depression (PAD) in an online fashion during a sustained submaximal fatigue task. The task required a high motor output in order to increase the likelihood of creating partial muscle ischemia with accumulation of fatigue metabolites, an important potential inhibitory influence upon the H-reflex during the progression of fatigue. Eleven subjects without neurologic impairment maintained volitional, isometric plantar flexion at 60% of maximal voluntary contraction until exhaustion. A paired-pulse stimulus (2 Hz) was delivered to the tibial nerve to elicit paired H-reflexes before, during, and after the fatigue protocol. The normalized amplitude of the second H-reflex (depression ratio) served as an estimate of PAD. Depression ratio increased during the first half of the fatigue protocol (P < 0.001), indicating a diminution of PAD, and then returned as exhaustion approached. The biphasic behavior of homosynaptic H-reflex depression during fatigue to exhaustion suggests a role for metabolic mediators of post-activation depression during fatigue.

Keywords: H-reflex; fatigue; homosynaptic depression; ischemia.

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Figures

FIGURE 1
FIGURE 1
Representative example of H-reflex depression before, during, and after fatigue. Note the consistency of the small m-wave associated with the H-reflex for both H1 and H2 in all conditions
FIGURE 2
FIGURE 2
Force, EMG, and H-reflexes measured during the fatigue task. Note that there is more fluctuation in force toward the end of the fatigue task, when peak-to-peak EMG is maximal
FIGURE 3
FIGURE 3
H-reflex amplitude before, during (F1, F2, and F3), and after the fatigue task. *Significantly different from PRE (P < 0.05). #Significantly different from POST (P < 0.05)
FIGURE 4
FIGURE 4
Stimulus consistency before, during (F1, F2, and F3), and after the fatigue task
See this image and copyright information in PMC

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References

    1. Calancie B, Broton JG, Klose KJ, Traad M, Difini J, Ayyar DR. Evidence that alterations in presynaptic inhibition contribute to segmental hypo- and hyperexcitability after spinal cord injury in man. Electroencephalogr Clin Neurophysiol. 1993;89:177–186. - PubMed
    1. Grey MJ, Klinge K, Crone C, et al. Post-activation depression of soleus stretch reflexes in healthy and spastic humans. Exp Brain Res. 2008;185:189–197. - PubMed
    1. Yen CL, McHenry CL, Petrie MA, Dudley-Javoroski S, Shields RK. Vibration training after chronic spinal cord injury: Evidence for persistent segmental plasticity. Neurosci Lett. 2017;647:129–132. - PMC - PubMed
    1. Shields RK, Dudley-Javoroski S, Oza PD. Low-frequency H-reflex depression in trained human soleus after spinal cord injury. Neurosci Lett. 2011;499:88–92. - PMC - PubMed
    1. Butler AJ, Yue G, Darling WG. Variations in soleus H-reflexes as a function of plantarflexion torque in man. Brain Res. 1993;632:95–104. - PubMed