|Cancer||Cell death||Cell cycle||Cytoskeleton||Exo/endocytosis||Differentiation||Division||Organelles||Signalling||Stem cells||Trafficking|
Cell Biology International (2000) 24, 263272 (Printed in Great Britain)
SATELLITE CELL REGULATION FOLLOWING MYOTRAUMA CAUSED BY RESISTANCE EXERCISE
Janet Viercka, Becky O'Reillya, Kim Hossnerb, Jose Antonioc, Katherine Byrnead, Luke Buccie and Michael Dodsona,f1
aMuscle Biology Laboratory, Department of Animal Sciences, Washington State University, Pullman, WA, 99164-6351, U.S.A.
bDepartment of Animal Sciences, Colorado State University, Fort Collins, CO, 80523, U.S.A.
cDepartment of HPERLS – Human Performance Laboratory, University of Nebraska, Kearney, NE, 68849, U.S.A.
dMolecular Immunology Laboratory, Department of Animal Science, Washington State University, Pullman, WA, 99164-6351, U.S.A.
eWeider Nutrition International, 2002 South 5070 West, Salt Lake City, UT, 84104-4726, U.S.A.
It is generally accepted that the primary mechanisms governing skeletal muscle hypertrophy are satellite cell activation, proliferation, and differentiation. Specific growth factors and hormones modulate satellite cell activity during normal muscle growth, but as a consequence of resistance exercise additional regulators may stimulate satellite cells to contribute to gains in myofiber size and number. Present knowledge of the regulation of the cellular, biochemical and molecular events accompanying skeletal muscle hypertrophy after resistance exercise is incomplete. We propose that resistance exercise may induce satellite cells to become responsive to cytokines from the immune system and to circulating hormones and growth factors. The purpose of this paper is to review the role of satellite cells and growth factors in skeletal muscle hypertrophy that follows resistance exercise.
Key words: satellite cells, hormones, growth factors, steroids, cytokines, resistance exercise.
f1To whom correspondence should be addressed: M. V. Dodson, Ph.D., 139 Clark Hall, Muscle Biology Laboratory, Department of Animal Sciences, Washington State University, Pullman, WA 99164-6310, U.S.A. E-mail:email@example.com
Received 18 August 1999; accepted 10 January 2000doi:10.1006/cbir.2000.0499