Eur J Appl Physiol (2010) 110:1135–1141 DOI 10.1007/s00421-010-1605-5 123 ORIGINAL ARTICLE EVects of eccentric exercise-induced muscle damage on intramyocellular lipid concentration and high energy phosphates Jonathan D. Hughes · Nathan A. Johnson · Stephen J. Brown · Toos Sachinwalla · David W. Walton · Stephen R. Stannard Accepted: 30 July 2010 / Published online: 13 August 2010  Springer-Verlag 2010 Abstract Eccentric exercise is known to cause changes to the ultrastructure of skeletal muscle and, in turn, may alter the ability of the muscle to store and utilise intracellular substrates such as intramyocellular lipid (IMCL). The purpose of this study was to test the hypothesis that exer- cise-induced muscle damage (EIMD) results in IMCL accumulation. Six males (31 § 6 years; mean § SD, and 72.3 § 9.7 kg body mass) performed 300 unilateral, maxi- mal, isokinetic, eccentric contractions (Ecc) (30° s ¡1 ) of the quadriceps on an isokinetic dynamometer, followed imme- diately by an equal amount of work by the contralateral leg but with concentric action (Con). Phosphate compounds and IMCL content of the vastus lateralis of both legs were measured using 31 P and 1 H magnetic resonance spectros- copy. IMCL content was higher in Ecc than Con 24 h post but the reverse was evident 48 h post-exercise (P = 0.046). A signiWcant time £ trial interaction for resting [P i ] (P = 0.045), showed increases in Ecc across time but no change in Con. A signiWcant main eVect of trial (P = 0.002) was apparent indicating the Ecc leg had marked metabolic dysfunction. The P i /PCr ratio showed a signiWcant eVect of trial (P = 0.001) with an increase evident in Ecc leg, pri- marily due to increases in [P i ]. The present study highlights changes in IMCL content of skeletal muscle following EIMD. Keywords Eccentric exercise · Intramyocellular lipid · Inorganic phosphate · Muscle damage · Magnetic resonance spectroscopy Introduction Exercise-induced muscle damage (EIMD) occurs following eccentric work to which the muscle is unaccustomed. The symptoms of EIMD are well deWned and characterised by disruption to normal sarcomere arrangement of a muscle Wbre (Newham et al. 1983) cytoskeletal and membrane dis- ruption (Feasson et al. 2002; Hamer et al. 2002; Lovering and De Deyne 2004), loss of calcium homeostasis (Balnave et al. 1997), excitation–contraction coupling impairment (Warren et al. 1993), and loss of force production (Byrne et al. 2004). Although muscle contraction improves sensitivity of skeletal muscle to insulin-mediated glucose uptake in the short and longer term (Holloszy et al. 1998), paradoxically, strenuous eccentric muscular work has been shown to reduce resting muscle insulin sensitivity (Del Aguila et al. 2000). Although there is no deWnitive explanation for this impairment, it has been proposed that the reduced insulin sensitivity results from a systemic inXammatory response to EIMD (Costill et al. 1990). Whole body insulin resistance in obesity, lipid infusion and starvation is closely associated with accumulation and Communicated by Jean-René Lacour. J. D. Hughes (&) · S. J. Brown · S. R. Stannard Institute of Food, Nutrition, and Human Health, Massey University, Palmerston North, New Zealand e-mail: J.D.Hughes@massey.ac.nz N. A. Johnson Discipline of Exercise and Sport Science, University of Sydney, Sydney, Australia T. Sachinwalla Northside Medical Imaging, Hornsby, Sydney, Australia D. W. Walton Sydney Hills Imaging, Norwest Private Hospital, Sydney, Australia