Introduction: The molecular adaptations specifically induced by different muscle contraction types have only been partially elucidated. We previously demonstrated that eccentric contractions in human quadriceps elicited proteome modifications that suggest a muscle fiber typology adaptation. We address this question in a more systematic way by examining here the effects of different running modes on the mouse muscle proteome and the muscle fiber typology.
Methods: Male adult mice (C57BL6) were randomly divided into downhill running (DHR) (quadricipital eccentrically biased contractions), uphill running (UHR) (quadricipital concentrically biased contractions), and untrained control (CONT) groups. Running groups performed five training sessions on an inclined treadmill for 75 to 135 min·d−1, and the quadriceps muscles were dissected 96 h after the last session. Muscle protein extracts of DHR and UHR groups (n = 4/group) were subjected to a two-dimensional difference in gel electrophoresis (2D-DIGE) analysis coupled with mass spectrometry. The assessment of fiber type, size, and number was performed on the rectus femoris of the three groups (n = 6/group) using myosin heavy chain immunohistochemistry.
Results: In the proteomic analysis, eight spots identified as the fast myosin heavy chain isoforms exhibited a lower abundance in DHR compared with UHR (P < 0.05, t-test). In contrast, adenosine triphosphate (ATP) synthase subunit α and tubulin β were more expressed in DHR (P < 0.05). A significant higher proportion of Type I and IIa fibers was found for DHR compared with UHR or CONT groups (P < 0.05, one-way ANOVA).
Conclusions: Our data suggest that the eccentrically biased contractions in mice induced specific adaptations in protein expression and muscle fiber composition, which may reflect a more oxidative muscle phenotype. The differences in stress placed on the muscle between both trainings may be responsible for some unique adaptations resulting from the eccentrically biased training.
1GIGA-Neurosciences, University of Liège, Liège, BELGIUM; 2Laboratory of Histology–Cytology, GIGA-R and CART, University of Liège, Liège, BELGIUM; 3Department of Motricity Sciences, University of Liège, Liège, BELGIUM; 4Department of Physical Medicine, CHU of Liège, Liège, BELGIUM; 5Department of Neurology, CHU, University of Liège, Liège, BELGIUM; and 6GIGA-Development, Stem Cells and Regenerative Medicine, University of Liège, 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 November 2012.
Accepted for publication January 2013.