Relationship between muscle sympathetic nerve activity and rapid increases in circulating leukocytes during experimental muscle pain

Although pain is usually caused by an unpleasant noxious stimulus, it is an essential process that helps protect the body as well as serving as an indicator of injury and illness. We have used intramuscular infusions of hypertonic saline (5%)—a noxious stimulus that depolarises unmyelinated muscle nociceptors without causing overt tissue damage [6]—as a model of long-lasting muscle pain and shown that this noxious stimulus evokes an increase in muscle sympathetic nerve activity (MSNA), blood pressure (BP) and heart rate (HR) in some individuals but not in others [4]. Whether MSNA increased or not was consistent in a given individual when the painful stimulus was delivered weeks to months apart [5]. Importantly, there were no differences in the reported quality, extent or intensity of the pain, indicating that the noxious inputs to the central nervous system were identical in the two groups. These divergent sympathetic responses to long-lasting muscle pain were not determined by an individual’s baseline MSNA, BP, heart rate (HR), heart rate variability (HRV), age, sex or body mass index (BMI) [8]. Moreover, there were no differences in baseline anxiety ratings or attitudes to pain across participants that could explain these divergent responses [9]. Nevertheless, brain imaging indicated differences in cortical and subcortical responses in the two groups, suggesting that they were “hard-wired” in the brain [10]. …