Cortical Somatosensory Excitability Is Modulated in Response to Several Days of Muscle Soreness

Abstract

Changes in excitability of the sensorimotor cortex have been demonstrated in clinical musculoskeletal pain, although the timing is unknown. Eccentric exercise provokes delayed-onset muscle soreness providing a model to study the temporal profile of sensorimotor cortical plasticity during progressively developing muscle soreness. Twelve healthy participants performed eccentric exercise of the wrist extensors. Likert pain scores, pressure pain thresholds at the extensor carpi radialis (ECR) muscle, somatosensory evoked potentials from electrical stimulation of the radial nerve, maximal wrist extension force, and ECR motor evoked potentials to transcranial magnetic stimulation were recorded before (baseline) and at 2 hours (2-h post), 2 days (day 2), and 6 days (day 6) after exercise. Compared with baseline, 1) the Likert pain score was increased at 2-h post and increased further at day 2 (P < .01); 2) the ECR pressure pain thresholds were decreased at day 2 (P < .001); 3) the P45 amplitude of the somatosensory evoked potential from central-parietal recording sites was increased at day 2 (P < .001); 4) maximal wrist extension force was reduced 2-h post and at day 2 (P < .002); and 5) the cortical area from which ECR motor evoked potentials could be elicited was reduced at 2-h post and at day 2 (P < .03). A decrease in the ECR pressure pain thresholds was correlated (P < .027) with an increase in the P45 amplitude at a centroparietal recording site. PERSPECTIVE: These novel data demonstrate that the somatosensory cortical excitability may be affected by muscle soreness developing over days in parallel with a deficit in the motor system. Cortical neuroplasticity may thus develop in the subacute phase and be relevant for understanding neural adaptation in the transition from acute to persistent pain.

Masseter corticomotor excitability is decreased after intramuscular administration of nerve growth factor

“…Interestingly, when eccentric exercises were applied in NGF‐sensitized ECRB, such combined effect results in decreased cortical excitability that is most probably driven by neural protective mechanisms (De Martino, Zandalasini, et al, ). In addition, tonic infusion of hypertonic saline or muscle soreness induced by eccentric exercises in the upper limbs is also related with reduced corticomotor output (De Martino, Petrini, Schabrun, & Graven‐Nielsen, ; Le Pera et al, ; Schabrun, Burns, & Hodges, ). Therefore, it has been suggested that the inhibitory motor effects associated with prolonged nociceptive inputs can override the proclivity to short‐term increase in corticomotor excitability in already NGF‐sensitized muscles (De Martino, Zandalasini, et al, ).…”

Ischemic preconditioning of the muscle reduces the metaboreflex response of the knee extensors

“…Any change in pain threshold reflects, albeit indirectly and with some limitations, the change in sensitivity of group III/IV muscle afferents. Therefore, any change in pain pressure threshold can be used an indirect marker of change in sensitivity of group III/IV muscle afferents (Graven-Nielsen et al 2004 ; Schabrun et al 2016 ; De Martino et al 2018 ). Sensitivity of group III/IV muscle afferents was quantified by means of pain pressure threshold (PPT was assessed alternatively in both thighs (exercising vs non-exercising leg) after each cycle of occlusion during IP and SHAM treatment by a pressure algometer (Force Ten FDX 50, Wagner Instruments, Greenwich, CT).…”

Assessment of conditioned pain modulation in healthy participants and patients with chronic pain: manifestations and implications for pain progression

“…Recent studies have indicated that transcranial direct current stimulation (tDCS) and other transcranial stimulation methods, such as repetitive transcranial magnetic stimulation, can modulate musculoskeletal pain development in experimental settings [32,33] and yield pain relief in patients with fibromyalgia [34,35]. As patients with knee osteoarthritis often display impaired CPM compared with healthy participants [36], a recent study by Ahn et al [37 & ] assessed the modulatory effect of tDCS on CPM in patients with osteoarthritis.…”