Hypertonic saline-evoked muscle pain in the quadriceps reduces neuromuscular performance and alters corticospinal excitability.

Muscle pain can alter corticospinal function, but the specific excitatory/inhibitory effects on the quadriceps across different levels of corticospinal neuron recruitment remain unclear. Furthermore, maximal force production is reduced with muscle pain, but how the rate of force development, a key component of neuromuscular function, remains less known. To investigate this, healthy participants completed an isometric maximal voluntary contraction (MVC) followed by submaximal, intermittent contractions after receiving a hypertonic saline injection into the vastus lateralis to cause quadriceps pain (HYP), or isotonic saline, a nonpainful control (ISO). Peripheral nerve stimulation was delivered during and after MVCs to determine neuromuscular function. Transcranial magnetic stimulation (TMS) was delivered at 120% and 150% of active motor threshold during submaximal contractions to determine corticospinal excitability/inhibition, along with paired-pulse TMS to determine short-interval intracortical inhibition (SICI). Results revealed a moderate effect size (ES) reduction in MVC force (ES = -0.68, P = 0.020), early-phase rate of force development (ES = -0.57, P = 0.029), and voluntary activation (ES = -0.66, P = 0.008) in HYP compared with ISO. Corticospinal excitability increased in HYP compared with ISO (ES = 0.60, P = 0.023), whereas corticospinal inhibition decreased in HYP at higher stimulation intensities only (ES = 0.63, P = 0.017). Conversely, SICI increased in HYP compared with ISO (ES = 0.58, P = 0.035). Our findings indicate that muscle pain induced by a hypertonic saline injection reduced quadriceps neuromuscular function due to centrally mediated mechanisms, potentially involving both excitatory and inhibitory effects on the corticospinal tract.NEW & NOTEWORTHY Hypertonic saline-induced quadriceps muscle pain reduced knee-extensor maximal voluntary force, rate of force development, and voluntary activation, without altering peripheral muscle function, suggesting a centrally mediated impairment of neuromuscular performance in healthy individuals. Alongside these changes was an increase in corticospinal excitability at both low and high stimulation intensities, whereas pain decreased corticospinal inhibition at high stimulation intensities only. Furthermore, hypertonic saline-induced pain increased intracortical inhibition, suggesting nonuniform effects of pain on the corticospinal tract.