We tested the hypothesis that low-intensity vibration training in mice improves contractile function of hindlimb skeletal muscles and promotes exercise-related cellular adaptations.
We subjected C57BL/6J mice to 6 wk, 5 d·wk−1, 15 min·d−1 of sham or low-intensity vibration (45 Hz, 1.0g) while housed in traditional cages (Sham-Active, n = 8; Vibrated-Active, n = 10) or in small cages to restrict physical activity (Sham-Restricted, n = 8; Vibrated-Restricted, n = 8). Contractile function and resistance to fatigue were tested in vivo (anterior and posterior crural muscles) and ex vivo on the soleus muscle. Tibialis anterior and soleus muscles were evaluated histologically for alterations in oxidative metabolism, capillarity, and fiber types. Epididymal fat pad and hindlimb muscle masses were measured. Two-way ANOVAs were used to determine the effects of vibration and physical inactivity.
Vibration training resulted in a 10% increase in maximal isometric torque (P = 0.038) and 16% faster maximal rate of relaxation (P = 0.030) of the anterior crural muscles. Posterior crural muscles were unaffected by vibration, except greater rates of contraction in Vibrated-Restricted mice compared with Vibrated-Active and Sham-Restricted mice (P = 0.022). Soleus muscle maximal isometric tetanic force tended to be greater (P = 0.057), and maximal relaxation was 20% faster (P = 0.005) in vibrated compared with sham mice. The restriction of physical activity induced muscle weakness but was not required for vibration to be effective in improving strength or relaxation. Vibration training did not affect muscle fatigability or any indicator of cellular adaptation investigated (P ≥ 0.431). Fat pad but not hindlimb muscle masses were affected by vibration training.
Vibration training in mice improved muscle contractility, specifically strength and relaxation rates, with no indication of adverse effects to muscle function or cellular adaptations.
1Rehabilitation Science and Program in Physical Therapy, University of Minnesota, Minneapolis, MN; 2Department of Kinesiology, University of Minnesota, Minneapolis, MN; and 3Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, MN
Address for correspondence: Dawn A. Lowe, Ph.D., FACSM, 420 Delaware St. SE, MMC 388, University of Minnesota, Minneapolis, MN 55455; E-mail: firstname.lastname@example.org.
Submitted for publication September 2012.
Accepted for publication November 2012.