Augmented mechanical response of muscle thin-fiber sensory receptors recorded from rat muscle-nerve preparations in vitro after eccentric contraction.
Unaccustomed strenuous exercise, especially that from eccentric muscular work, often causes muscle tenderness, which is a kind of mechanical hyperalgesia. We developed an animal model of delayed-onset muscle soreness (DOMS) from eccentric muscular contraction (ECC) in rats and demonstrated the existence of muscle tenderness by means of behavioral pain tests and c-Fos protein expression in the spinal dorsal horn. The purpose of the present study was to examine whether the sensitivities of muscle thin-fiber sensory receptors to mechanical, chemical, and thermal stimuli were altered after repetitive ECC in a rat model of DOMS. ECC was caused in the animals by electrical stimulation of the common peroneal nerve innervating the extensor digitorum longus muscle (EDL) while the muscle was being stretched. Activities of single thin-fiber receptors (sensitive to pressure but insensitive to stretch, with conduction velocity slower than 2.0 m/s) were recorded from muscle (EDL)-nerve preparations in vitro 2 days after ECC when mechanical hyperalgesia was at its peak. The mechanical threshold of thin-fiber receptors was found to be very much lower in the ECC preparations than in the nontreated control (CTR) [median 65.4 mN (interquartile range [IQR]; 46.6-122.0 mN) in the CTR preparation vs. 38.2 mN (IQR; 26.8-55.8 mN) in the ECC, P < 0.001]. In addition, the total number of evoked discharges during a ramp mechanical stimulus, taken as an index of the magnitude of the mechanical response, nearly doubled in the ECC preparations compared with the CTR [24.7 spikes (IQR; 14.2-37.1 spikes) in the CTR preparation vs. 54.2 spikes (IQR; 24.3-89.0 spikes) in the ECC, P < 0.001]. In contrast, the numbers of discharges induced by chemical (pH 5.5, lactic acid, adenosine triphosphate, and bradykinin) and thermal (cold and heat) stimuli were not different between the two preparations. These results suggest that augmentation of the mechanical response in muscle thin-fiber sensory receptors might be related to the muscle tenderness in DOMS after ECC.
Taguchi
Toru
T
Department of Neural Regulation, Division of Regulation of Organ Function, Research Institute of Environmental Medicine, Nagoya, Japan.
Sato
Jun
J
Mizumura
Kazue
K
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D000255:Adenosine Triphosphate / Q000494:pharmacology; D000818:Animals; D001920:Bradykinin / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D006358:Hot Temperature; D006863:Hydrogen-Ion Concentration; D006930:Hyperalgesia / Q000503:physiopathology; D066298:In Vitro Techniques; D019344:Lactic Acid / Q000494:pharmacology; D008297:Male; D009119:Muscle Contraction / Q000502:physiology / Q000528:radiation effects*; D018485:Muscle Fibers, Skeletal / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects*; D018482:Muscle, Skeletal / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects*; D009431:Neural Conduction / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D010812:Physical Stimulation / Q000379:methods*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011984:Sensory Receptor Cells / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D012684:Sensory Thresholds / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D013268:Stimulation, Chemical
D019344:Lactic Acid; D000255:Adenosine Triphosphate; D001920:Bradykinin