Depression of the Hoffman reflex (H-reflex) is used to examine spinal control mechanisms during exercise, fatigue, and vibration and in response to training. H-reflex depression protocols frequently use trains of stimuli; this is time-consuming and prevents instantaneous assessment of motor neuronal excitability. The purpose of this study was to determine if paired-pulse H-reflex depression is reproducible and whether paired-pulse stimulation adequately estimates the depression induced by the more traditional ten-pulse train. H-reflexes were elicited via ten-pulse trains at 0.1, 0.2, 1, 2, and 5 Hz in ten neurologically intact individuals on two separate days. We measured the depression elicited by the second pulse (H2) and the mean depression elicited by pulses 2–10 (Hmean). H2 was consistent at all frequencies on both days (r2 = 0.97, p < 0.05, and ICC(3,1) = 0.81). H2 did not differ from Hmean (p > 0.05). The results indicate that paired-pulse H-reflex depression has high between-day reliability and yields depression estimates that are comparable to those obtained via ten-pulse trains. Paired-pulse H-reflex depression may be especially useful for studies that require rapid assessment of motor neuronal excitability, such as during exercise, fatigue, and vibration, or to establish recovery curves following inhibition.
After spinal cord injury (SCI), widespread reorganization occurs within spinal reflex systems. Regular muscle activity may influence reorganization of spinal circuitry after SCI. The purpose of this study is to investigate the effects of long-term soleus training on H-reflex depression in humans after SCI. Seven subjects with acute (<7 weeks) SCI (AC group) underwent testing of H-reflex depression at several frequencies of repetitive stimulation. Eight subjects (including 3 from AC) stimulated one soleus muscle daily, leaving the other leg as an untrained within-subject control. Trained limb H-reflexes were assessed during year 1 (TR1) and year 2 (TR2) of training. Untrained limbs were tested during year 2 (UN). H-reflex amplitude was lower at 1, 2 and 5 Hz than at 0.1 or 0.2 Hz (p < 0.05). The pattern of depression differed between AC and UN (p < 0.05), but not between TR2 and UN (p > 0.05) despite significant adaptations in torque and fatigue resistance (p < 0.05). Three subjects who began training very early after SCI retained H-reflex post activation depression, suggesting that early intervention of daily muscular activity may be important.
H-reflex depression (diminution of amplitude after a conditioning stimulus) is mediated presynaptically and therefore can help distinguish central versus peripheral mechanisms of fatigue. We examined the effects of a dynamic exercise protocol on H-reflex depression using two conditioning methods: homonymous conditioning (paired-pulse tibial nerve stimulation); and heteronymous conditioning (common peroneal nerve stimulation). Ten subjects performed dynamic contractions of the soleus muscle through 30° ankle range of motion. The concentric phase required a target force of 10% of maximum voluntary isometric contraction (MVIC) and the eccentric phase force target was 80% MVIC. Fatigue persisted for >20 min after cessation of the exercise. Compared with prefatigue values, the dynamic fatigue protocol did not increase presynaptic inhibition after either homonymous or heteronymous conditioning. Peak to peak amplitude of unconditioned H-reflexes was likewise unchanged despite a long term depression of muscle force (long duration fatigue). These results suggest that persistent fatigue after dynamic exercise is attributed to muscle changes and not altered spinal mechanisms.
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.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.