Exercising calf muscle T2* changes correlate with pH, PCr recovery and maximum oxidative phosphorylation

Abstract

Skeletal muscle metabolism is impaired in disorders like diabetes mellitus or peripheral vascular disease. The skeletal muscle echo planar imaging (EPI) signal (SEPI) and its relation to energy metabolism are still debated. Localised 31P MRS and SEPI data from gastrocnemius medialis of 19 healthy subjects were combined in one scanning session to study direct relationships between phosphocreatine (PCr), pH kinetics and parameters of T2* time courses. Dynamic spectroscopy (semi-LASER) and EPI were performed immediately before, during and after 5min of plantar flexions. Data were acquired in a 7T MR scanner equipped with a custom-built ergometer and a dedicated 31P/1H radio frequency (RF) coil array. Using a form-fitted multi-channel 31P/1H coil array resulted in high signal-to-noise ratio (SNR). PCr and pH in the gastrocnemius medialis muscle were quantified from each 31P spectrum, acquired every 6s. During exercise, SEPI(t) was found to be a linear function of tissue pH(t) (cross-correlation r=-0.85±0.07). Strong Pearson's correlations were observed between post exercise time-to-peak (TTP) of SEPI and (a) the time constant of PCr recovery τPCrrecovery (r=0.89, p<10-6), (b) maximum oxidative phosphorylation using the linear model, Qmax,lin (r=0.65, p=0.002), the adenosine-diphosphate-driven model, Qmax,ADP (r=0.73, p=0.0002) and (c) end exercise pH (r=0.60, p=0.005). Based on combined accurately localised 31P MRS and T2* weighted MRI, both with high temporal resolution, strong correlations of the skeletal muscle SEPI during exercise and tissue pH time courses and of post exercise SEPI and parameters of energy metabolism were observed. In conclusion, a tight coupling between skeletal muscle metabolic activity and tissue T2* signal weighting, probably induced by osmotically driven water shift, exists and can be measured non-invasively, using NMR at 7T. © 2014 The Authors. NMR in Biomedicine published by John Wiley & Sons, Ltd.