Introduction: Delayed-onset muscle soreness (DOMS), a condition triggered by eccentric exercise, affects muscle cells at a biochemical level in a poorly understood fashion. The objective of the present study was to examine human muscle proteome modifications induced by strenuous eccentric exercises after a specific training aimed to prevent DOMS.
Methods: Biopsy samples of the rectus femoris were obtained from healthy human volunteers in three successive conditions: 1) at rest, 2) 24 h after an injuring exercise protocol consisting of three series of 30 maximal contractions of the quadriceps on an isokinetic dynamometer, and 3) 24 h after a similar exercise bout preceded either by five eccentric training sessions or by no training.
Results: Muscle damage was assessed before and 1 d after each maximal eccentric test by comparing three indirect markers: plasma activity of creatine kinase, muscle stiffness, and subjective pain intensity. Compared with the first eccentric test, those markers were reduced after the second test and further reduced if this second test followed the eccentric training, thus confirming the protective effect of such training. Muscle protein extracts were subjected to a two-dimensional difference gel electrophoresis proteomic analysis coupled with matrix-assisted laser desorption/ionization–time-of-flight mass spectrometry protein identification. Surprisingly, we observed that myosin heavy chains decreased after the first eccentric test and were reduced further with other contractile proteins after the second test. Furthermore, the expression of several glycolytic enzymes decreased only after the second test, which was preceded by a specific training.
Conclusions: These findings suggest that the eccentric training resulted in a switch to oxidative metabolism, which may be associated with protection from DOMS.
1GIGA – Neuroscience, University of Liège, BELGIUM; 2CRP – Gabriel Lippmann, Belvaux, LUXEMBOURG; 3Department of Motricity Sciences, University of Liège, BELGIUM; 4Department of Physical Medicine, CHU of Liège, BELGIUM; 5Department of Neurology, CHU and University of Liège, BELGIUM; and 6GIGA – Development, Stem Cells and Regenerative Medicine, University of Liège, BELGIUM
Address for correspondence: Bernard Rogister, M.D., Ph.D., GIGA – Neuroscience, University of Liège, Avenue de l’Hôpital, 1 - Batiment B36 +1, 4000 Liège, Belgium; E-mail: Bernard.Rogister@ulg.ac.be.
Submitted for publication March 2011.
Accepted for publication April 2011.
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