Epidemiological research provides strong evidence for a link between repetitive work (RW) and the development of chronic trapezius myalgia (TM). The aims were to further elucidate if an accumulation of sensitising substances or impaired oxygenation is evident in painful muscles during RW. Females with TM (n=14) were studied during rest, 30 min RW and 60 min recovery. Microdialysate samples were obtained to determine changes in [glutamate], [PGE2], [lactate], and [pyruvate] relative to work. Muscle oxygenation (%StO2) was assessed using near-infrared spectroscopy. During work all investigated substances, except PGE2, increased significantly: [glutamate] (54%, P<0.0001), [lactate] (26%, P<0.005), [pyruvate] (19%, P<0.0001), while the %StO2 decreased (P<0.05). During recovery [PGE2] decreased (P<0.005), [lactate] remained increased (P<0.001), [pyruvate] increased progressively (P<0.0001), and %StO2 had returned to baseline. Changes in substance concentrations and oxygenation in response to work indicate normal increase in metabolism but no ongoing inflammation in subjects withTM.

The aim of this study was to investigate the effects of duration of low-load repetitive work on intramuscular lactate, pyruvate, glutamate and prostaglandin E2 (PGE2), and oxygen saturation in the trapezius muscle. Twenty healthy females were studied during baseline rest, during low-load repetitive work for either 30 (REP 30) or 60 (REP 60) minutes, and 60 minutes recovery. Intramuscular microdialysate (IMMD) samples were obtained, and local muscle tissue oxygenation (StO2 %) assessed with near infrared spectroscopy (NIRS). Subjects rated their perceived exertion (Borg CR-10 scale) and capillary blood was sampled for lactate analysis. The results showed a significant increase in IMMD lactate in response to both REP 30 and REP 60 (P<0.05 and P<0.01 respectively) and glutamate (P<0.0001), but no progressive increase with increasing work duration. Both IMMD pyruvate and lactate tended to be significantly increased during the recovery period. No corresponding increase in blood-lactate was found. Local muscle StO2 % did not change significantly in response to work and was not correlated to the IMMD lactate concentration. The ratings of perceived exertion increased in response to work, and remained increased after recovery for REP 60.

In conclusion, the results of this study show significantly increased IMMD lactate and, glutamate concentrations in the trapezius muscle of healthy females in response to low-load work, but no progressive increase with increased work duration. Further, they do not indicate that the increased IMMD lactate concentration was caused by a locally decreased or insufficient muscle tissue oxygenation.

Much is still unknown concerning the mechanisms underlying the development of chronic muscle pain. The presence and magnitude of inflammatory substances and neurotransmitters in chronic painful conditions is not clear. The aims of the present study were to determine, with the use of microdialysis, the interstitial concentrations and the equilibration times for PGE(2) and glutamate in the trapezius muscles of nine female subjects with chronic muscle pain, and nine pain-free age-matched controls. A microdialysis probe was implanted in the upper part of the trapezius muscle and perfused with Ringer-acetate solution at a flow rate of 0.3 muL/min. Samples were obtained every 30 min, during a 4-h rest period. At equilibration, the mean concentrations (+/-SE) of PGE(2) were 0.71 (+/-0.11) ng/mL for the pain-group and 0.97 (+/-0.35) ng/mL for the controls. For glutamate the mean concentrations for the pain-group were 66.3 (+/-13.3) mumol/L and 60.6 (+/-22.9) mumol/L for the controls. For the pain group and the control group, respectively, equilibration for PGE(2) was reached at 180 and 150 min, and for glutamate at 150 and 120 min. The present study showed no differences between groups in the concentrations of PGE(2) and glutamate in the trapezius muscle. Further, it revealed that when using the slow-flow method, a period of at least 2.0-2.5 h is needed, after probe insertion, to reach steady state for glutamate and PGE(2).