PAIN DUE TO TISSUE ACIDOSIS - A MECHANISM FOR INFLAMMATORY AND ISCHEMIC MYALGIA

To study the role of protons in ischemic muscle pain we employed the ' submaximal effort tourniquet technique' and, in a second attempt, an i ntramuscular pressure infusion of acid phosphate buffer. The pH measur ed in the forearm skin covering the muscles at work during the tourniq uet test continuously dropped to a mean value of pH 7.00 +/- 0.26, sta rting 1 min after the contractions, while the pain increased in direct correlation with the hydrogen ion concentration (r = 0.96). After res toring the blood supply, the intradermal proton concentration decrease d more slowly than the muscular pain. The same subjective quality of d eep muscular pain was achieved with pressure infusion of acid phosphat e buffer (pH 5.2) into the forearm muscles. Constant flow rates evoked constant, apparently non-adapting magnitudes of pain with a log-linea r stimulus-response relationship (r = 0.93). Changes in flow rate were followed by changes in pain ratings with a certain phase lag. We conc lude that muscular pain induced by infusion of acidic phosphate buffer and pain from ischemic contractions are generated through the same me chanisms based on the algogenic action of protons.