Submitted on July 18, 2008
Revised on December 2, 2008
Accepted on December 17, 2008
Muscle metabolism and acid-base status during exercise in forearm work-related myalgia measured with 31P-MRS
Graydon Raymer1*, Howard J. Green2, Don Ranney2, Gregory D. Marsh, and R Terry Thompson3
1 Nipissing University
2 University of Waterloo
3 The University of Western Ontario
* To whom correspondence should be addressed. E-mail: graydonr{at}nipissingu.ca.
In this study, we examined muscle metabolic and acid-base status during incremental wrist extension exercise in the forearm of individuals with work-related myalgia (WRM). Eighteen females employed in full-time occupations involving repetitive forearm labour were recruited in this cross-sectional study. Nine of these females were diagnosed with WRM, while the other nine had no previous WRM history and were used as age-matched controls (CON). Phosphorus-31 magnetic resonance spectroscopy (31P-MRS) was used to non-invasively monitor the intracellular concentrations of phosphocreatine ([PCr]), inorganic phosphate ([Pi]), as well as intracellular pH status (pHi) during exercise in WRM and CON. We observed a 38 % decreased work capacity in WRM compared to CON (0.18 W (SD 0.03) vs. 0.28 W (SD 0.10) respectively, P=0.007). Piecewise linear regression of the incremental exercise data revealed that the onset of a faster decrease in pHi (i.e. the pH threshold, pHT) and the onset of a faster increase in log([Pi]/[PCr]) (i.e. the phosphorylation threshold, PT) occurred at a 14% relatively lower power output in WRM (pHT: 45.2 % (SD 5.3) vs. 59.0 % (SD 4.6), P<0.001; PT: 44.8 % (SD 4.3) vs. 57.8 % (SD 3.1), P<0.001; % of peak power output, CON vs. WRM respectively). Mono-exponential modelling of the kinetics of [PCr] and pHi recovery following exercise demonstrated a slower (P=0.005) time constant (
) for [PCr] in WRM (113 s (SD 25)) compared to CON (77 s (SD 23)), and a slower (P=0.007) for pHi in WRM (370 s (SD 178)) compared to CON (179 s (SD 52)). In conclusion, our results suggest WRM is associated with an increased reliance on non-oxidative metabolism. Possible mechanisms include a reduction in local muscle blood flow and perfusion, an increased ATP-cost of force production, or both.
