H-reflex and M-wave responses after voluntary and electrically evoked muscle cramping

Despite the widespread occurrence of muscle cramps, their underlying neurophysiological mechanisms remain unknown. To better understand the etiology of muscle cramps, this study investigated acute effects of muscle cramping induced by maximal voluntary isometric contractions (MVIC) and neuromuscular electrical stimulation (NMES) on the amplitude of Hoffmann reflexes (H-reflex) and compound muscle action potentials (M-wave).

Healthy men (n = 14) and women (n = 3) participated in two identical sessions separated by 7 days. Calf muscle cramping was induced by performing MVIC of the plantar flexors in a prone position followed by 2.5-s NMES over the plantar flexors with increasing frequency and intensity. H-reflexes and M-waves evoked by tibial nerve stimulation in gastrocnemius medialis (GM) and soleus were recorded at baseline, and after MVIC-induced cramps and the NMES protocol.

Six participants cramped after MVIC, and H-reflex amplitude decreased in GM and soleus in Session 1 (- 33 ± 32%, - 34 ± 33%, p = 0.031) with a similar trend in Session 2 (5 cramped, p = 0.063), whereas the maximum M-wave was unchanged. After NMES, 11 (Session 1) and 9 (Session 2) participants cramped. H-reflex and M-wave recruitment curves shifted to the left in both sessions and muscles after NMES independent of cramping (p ≤ 0.001).

Changes in H-reflexes after a muscle cramp induced by MVIC and NMES were inconsistent. While MVIC-induced muscle cramps reduced H-reflex amplitude, muscle stretch to end cramping was a potential contributing factor. By contrast, NMES may potentiate H-reflexes and obscure cramp-related changes. Thus, the challenge for future studies is to separate the neural consequences of cramping from methodology-based effects.