Experimental pain by ischaemic contractions compared with pain by intramuscular infusions of adenosine and hypertonic saline

Abstract

Deep tissue pain can be related to reduced muscle blood flow, which comprises the metabolic demand under muscle work. The tissues and receptors involved in nociception after ischaemic muscle contractions are not known. The concentration of adenosine is increased after ischaemic contractions and might act as an algesic substance. In 15 subjects, adenosine, hypertonic saline (algesic), and isotonic mannitol (placebo) were infused into the tibialis anterior muscle and compared with the pain caused by ischaemic contractions. The muscle pain intensity (visual analogue scale; VAS), distribution, and quality were assessed. Pressure pain thresholds were recorded to assess the deep tissue sensitivity. Adenosine did not induce more pain than the placebo. The maximal VAS score after hypertonic saline and ischaemic contractions was higher compared with adenosine/placebo infusions. The duration and area of pain were significantly increased after hypertonic saline infusions compared with ischaemic contractions. Higher scores on the McGill pain questionnaire were given to the "stabbing", "burning", "heavy", and "exhausting" word categories after ischaemic contractions, and "cramping" was rated higher during hypertonic saline-induced muscle pain compared with ischaemic contractions. During hypertonic saline infusions, the pressure pain threshold was decreased compared with before and immediately after the pain had vanished. The present study shows that pharmacological levels of adenosine in skeletal muscle did not induce pain. Excitation of muscle nociceptors by hypertonic saline evoked hyperalgesia, larger areas of pain, and a different quality of pain compared with ischaemic contractions, suggesting that the pain after ischaemic contractions is mediated by other populations of nociceptors in muscle and/or other tissues than excited by hypertonic saline.

Different types of variant muscle nociception after intermittent and continuous neuromuscular stimulation in rats

“…Our result is consistent with the human study of muscle pain conducted by Graven-Nielsen et al [14] who have suggested that dull pain after ischaemic contractions is mediated by a specific population of muscle nociceptors, which differs from those mediating the cramping variant generated by the administration of hypertonic saline. Whether prolonged contraction against low loads results in ischemia and/or it plays a significant role in the development of chronic muscle pain requires further investigation.…”

“…Additionally, muscle nociceptors are distributed in the muscle fascia and blood vessels [11], and conducted by distinct afferents [12,13]. Corresponding to the location of muscle nocicepors, the sensation of muscle pain has two different characteristics, distention and ischemic pain [14]. Therefore, clarification of the basic features of nociceptive transmission resulting from different modes of muscular contraction may contribute to delineation of the central mechanisms of peripheral nociceptive stimulation from muscle nociceptors.…”

An expansion of Simons’ integrated hypothesis of trigger point formation

“…Exercise under ischemic conditions [14] and eccentric muscle exercise result in muscle pain. Delayed-onset muscle soreness occurs after ischemic exercise [15] and after eccentric exercise.…”

Association Between Regional Idiopathic Neuropathy and Salivary Involvement as the Possible Mechanism for Oral Sensory Complaints

“…15,41,44 In any case, the hypotheses as to whether the observed alteration in the salivary composition in OSC subjects is the cause or the result of the regional neuropathy and why the salivary flow is not simultaneously affected remain open. Thus, these findings may be attributed to a regional smallfiber idiopathic neuropathy that affects salivary secretion and oral sensation in patients with OSC.…”