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Skeletal muscle 1 H MRSI before and after prolonged exercise. II. visibility of free carnitine
Author(s) -
Boss Andreas,
Kreis Roland,
Saillen Pierre,
Zehnder Monica,
Boesch Chris,
Vermathen Peter
Publication year - 2012
Publication title -
magnetic resonance in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.696
H-Index - 225
eISSN - 1522-2594
pISSN - 0740-3194
DOI - 10.1002/mrm.24167
Subject(s) - chemistry , carnitine , magnetic resonance imaging , skeletal muscle , echo time , medicine , nuclear magnetic resonance , endocrinology , biochemistry , physics , radiology
Abstract Carnitine (Car) buffers excess acetyl‐CoA through the formation of acetylCar (AcCar). AcCar's acetyl group (AG‐AcCar) gives rise to a peak at 2.13 ppm in 1 H MR spectra of skeletal muscle, whereas the trimethylammonium (TMA) groups of both, AcCar and Car, are thought to contribute to the TMA peak at 3.23 ppm. Surprisingly, in previous studies both resonances, AG‐AcCar and TMA, increased after exercise. The aim of this study was to assess if the exercise‐related TMA increase correlated with AcCar production. Magnetic resonance spectroscopic imaging (pulse repetition time/echo time = 1200/35 ms) was performed before and after prolonged exercise in the lower leg and thigh of eight runners and eight cyclists, respectively. TMA and AG‐AcCar increased after exercise ( P < 0.001). TMA's increase correlated with the AG‐AcCar increase ( R 2 = 0.73, P < 0.001, lower leg; R 2 = 0.28, P < 0.001, thigh). The correlation of ΔTMA with ΔAG‐AcCar suggests that the TMA increase is due to AcCar formation. As total Car (Car + AcCar) remains unchanged with exercise, these findings suggest that the contribution of free Car to the TMA peak is limited and, therefore, is partly invisible in muscle 1 H MR spectra. This indicates that the biochemically relevant cytosolic content of free Car is considerably lower than the overall concentration determined by radioisotopic assays, a potentially important result with respect to regulation of substrate oxidation. Magn Reson Med, 2012. © 2012 Wiley Periodicals, Inc.