ATP concentrations and muscle tension increase linearly with muscle contraction

Abstract

Previous studies have suggested that activation of ATP-sensitive P2X receptors in skeletal muscle play a role in mediating the exercise pressor reflex (Li J and Sinoway LI. Am J Physiol Heart Circ Physiol 283: H2636-H2643, 2002). To determine the role ATP plays in this reflex, it is necessary to examine whether muscle interstitial ATP (ATPi) concentrations rise with muscle contraction. Accordingly, in this study, muscle contraction was evoked by electrical stimulation of the L7 and S1 ventral roots of the spinal cord in 12 decerebrate cats. Muscle ATPi was collected from microdialysis probes inserted in the muscle. ATP concentrations were determined by the HPLC method. Electrical stimulation of the ventral roots at 3 and 5 Hz increased mean arterial pressure by 13 +/- 2 and 16 +/- 3 mmHg (P < 0.05), respectively, and it increased ATP concentration in contracting muscle by 150% (P < 0.05) and 200% (P < 0.05), respectively. ATP measured in the opposite control limb did not rise with ventral root stimulation. Section of the L7 and S1 dorsal roots did not affect the ATPi seen with 5-Hz ventral root stimulation. Finally, ventral roots stimulation sufficient to drive motor nerve fibers did not increase ATP in previously paralyzed cats. Thus ATPi is not largely released from sympathetic or motor nerves and does not require an intact afferent reflex pathway. We conclude that ATPi is due to the release of ATP from contracting skeletal muscle cells.

Augmented Mechanical Response of Muscle Thin-Fiber Sensory Receptors Recorded from Rat Muscle–Nerve Preparations In Vitro After Eccentric Contraction

“…This result might suggest that the above substances are unlikely to be responsible for the sensitization to mechanical stimulus in the ECC group because the heat sensitivities were not altered in the present experiment. In addi-tion, elevation of ATP (Li et al 2003) and BK (Blais et al 1999) concentrations after exercise reaches a peak within a half day; therefore the possibility would seem to be low that these substances are sensitizers involved in DOMS. There might be another or yet unknown substance(s) that sensitize(s) nociceptors specifically to mechanical stimulus.…”

“…Eccentric exercise has been widely used in human and animal studies of DOMS, many of which have found histological Friden and Lieber 1998;McCurry and Faulkner 1985), ultrastructural (Newham et al 1983;Ogilvie et al 1988), biochemical Blais et al 1999;Ostrowski et al 1998), and physical (see Proske and Morgan 2001 for review) changes. Lactic acid was long considered to be responsible for DOMS, but this belief has been largely rejected because of the failure of higher levels of lactate to induce soreness in concentric exercise (Armstrong 1984;Schwane et al 1983) or in McArdle's disease (Kazemi-Esfarjani et al 2002), a different time course for soreness and the blood lactate increase after exercise , and other findings.…”

“…Although there has been dispute as to whether an inflammatory process is involved in the underlying mechanisms of DOMS (see Smith 1991 for review), the possibility cannot be excluded that some inflammatory mediators or cytoplasmic components, released from muscle cells as a result of the micro-injury after eccentric contraction, may sensitize the nociceptors to mechanical stimulation. There have been reports of elevated muscle interstitial adenosine 5Ј-triphosphate (ATP) (Li et al 2003) and venous bradykinin (BK) (Blais et al 1999;Stebbins et al 1990) during contraction, but these elevated ATP/BK levels did not last long after cessation of the exercise and thus are unlikely to have been sensitizing agents in DOMS. Higher local temperature was found in muscle exercised eccentrically than in muscle undergoing concentric contractions (Nadel et al 1972).…”

Bradykinin and Nerve Growth Factor Play Pivotal Roles in Muscular Mechanical Hyperalgesia after Exercise (Delayed-Onset Muscle Soreness)

“…Many substances are released from exercising muscle: lactate (Tegeder et al, 2002); bradykinin (including kallidin-like pep-tide) (Blais et al, 1999;Boix et al, 2002); ATP (Li et al, 2003); and other substances (Tegeder et al, 2002). Among these substances, bradykinin, glutamate, and ATP are able to induce not only excitation/sensitization of nociceptors, but also changes in expression of neuropeptides and channels in several types of cell (Ferreira et al, 1993;Baker, 2005;Inoue et al, 2006).…”

Exercise pressor reflex in health and diseases: Animal studies

“…ATP rises in skeletal muscle interstitium with contraction 73) , and stimulates P2X receptors on thin fiber muscle afferents 10) , thereby not only stimulating chemically sensitive afferents, but also sensitizing mechanically sensitive afferents 74) . Li and colleagues 70) found that α,β-methylene ATP infused intra-arterially into hindlimb circulation of the decerebrate rats enhanced the pressor response to passive stretch to a larger degree in rats with HF than in healthy controls.…”