Peripheral Mechanisms of Muscle Pain: Response Behavior of Muscle Nociceptors and Factors Eliciting Local Muscle Pain

Potential Nociceptive Role of the Thoracolumbar Fascia: A Scope Review Involving in Vivo and Ex Vivo Studies

“…In humans, the pain evoked by ultrasound-guided bolus injection of hypertonic saline [35] or stimulation electrical [36] in TLF tissue exceeded those of muscle. Furthermore, the pain after chemical stimulation of TLF, was described by the patients in rather extreme terms like cutting, tearing and stinging, which suggests innervation by both A-and C-fiber nociceptors [35,59,60]. In contrast, musclederived pain was predominantly attributed to sensory qualities like throbbing and pounding [37].…”

Regular physical activity prevents development of chronic pain and activation of central neurons

“…These models involve assessing pain sensitivity at 1) the site of injury (muscle), termed primary hyperalgesia, which is thought to be mediated by hypersensitivity in the peripheral nervous system; and 2) outside the site of injury (paw), termed secondary hyperalgesia, and is thought to be mediated by hypersensitivity in the central nervous system. The acute inflammatory pain model, induced by 3% carrageenan, is associated with both primary and secondary hyperalgesia that is maintained primarily by acute inflammation and nociceptor activation (41). The chronic noninflammatory pain model is associated with secondary hyperalgesia and is maintained by central nervous system sensitization (54,60).…”

Sensory nerve fibers containing calcitonin gene-related peptide in gastrocnemius, latissimus dorsi and erector spinae muscles and thoracolumbar fascia in mice

“…While C and Ao cutaneous afferents correlate with group IV and III muscle afferents (Mense, 2010b), differences in pain associated with muscle compared to skin suggest the underlying mechanisms may not be identical (Mense, 2008). For example electrical stimulation of cutaneous nerves induces a first and second pain, but in muscle only a single pain is induced.…”

“…Neurons with CGRP-IR but not SP-IR have previously been reported in mouse DRG, and nerve fibers with this IR have been identified in human skin (Gibbins et al, 1987;Morris et al, 2005;Clarke et al, 2011) but it remains unclear how this subpopulation contributes to nociception. Within skeletal muscle there is more than one class of potential nociceptor and despite recent advances, details of their physiological and anatomical characteristics, including the distribution of their central and peripheral projections and their contribution to chronic pain mechanisms are not yet fully understood (Mense, 2010b;Jankowski et al, 2013). It is understood nociception is mediated mainly by small-and medium-sized neurons, being unmyelinated or lightly myelinated and classified by their conduction velocity as C (slowing conducting, small soma size) or Ao (intermediate conduction velocity, various soma size) (Harper and Lawson, 1985;Lawson and Waddell, 1991;Fang et al, 2005).…”

“…The first stage in the development of muscle pain is activation of nociceptive afferent fibers in muscles, described as thin, unmyelinated or lightly myelinated fibers with medium (group III) or slow (group IV) conduction velocity and free nerve endings, some of which contain peptides such as calcitonin generelated peptide (CGRP) and substance P (SP) (Stacey, 1969;Mense and Meyer, 1985;Reinert et al, 1998;Hoheisel et al, 2005;Mense, 2010b;Jankowski et al, 2013). Neurons containing one or both peptides have been identified in trigeminal and dorsal root ganglia (DRG) (Lee et al, 1985;Morris et al, 2005).…”