Article

[No influence of increased frequency on fatigability of tetanic contraction in rat atrophic soleus].

Department of Aerospace Physiology, the Fouth Military Medical University, Xi'an 710032, China.
Sheng li xue bao: [Acta physiologica Sinica] 11/2005; 57(5):653-8.
Source: PubMed

ABSTRACT The present study was performed to observe the time course and features of intermittent tetanic contractile function changes in soleus and extensor digitorum longus (EDL) muscles of tail-suspended rats. The optimal stimulating frequency, fatigability and time-dependent recovery after fatigue were measured in isolated muscle strips. The optimal stimulating frequency of soleus and EDL was 60 Hz and 120 Hz in control rats, respectively. It was not changed in 1-week unloaded soleus, but shifted to 80 Hz and 100 Hz in 2- and 4-week unloaded soleus, respectively. The maximal isometric tension (P(o)) of tetanic contraction at optimal stimulating frequency did not alter in 1- and 2-week unloaded soleus, but significantly decreased in 4-week unloaded soleus. After 5 min of fatigue, tetanic contractile tension of control soleus was decreased to 22.8% P(o), but significantly decreased to 10.4%, 10.0% and 11.6% P(o) in 1-, 2- and 4-week unloaded soleus, respectively. The tetanic contractile tension recovered to 98% P(o) in control soleus at the twentieth minute after fatigue, but only recovered to 79.0%, 83.6% and 78.5% P(o) in 1-, 2- and 4-week unloaded soleus. The optimal stimulating frequency, P(o), fatigability and time-dependent recovery of intermittent tetanic contraction were not altered in unloaded EDL compared with control. These results indicate that higher stimulating frequency can compensate the P(o) reduction in 1- and 2-week unloaded soleus, but not in 4-week unloaded soleus. The unloaded soleus, but not EDL, is more susceptible to fatigue than the synchronous controls. The unloaded soleus not only fatigues to a greater extent but also recovers significantly less than the control.

0 0
 · 
0 Bookmarks
 · 
51 Views
  • Source
    [show abstract] [hide abstract]
    ABSTRACT: Spaceflight (SF) has been shown to cause skeletal muscle atrophy; a loss in force and power; and, in the first few weeks, a preferential atrophy of extensors over flexors. The atrophy primarily results from a reduced protein synthesis that is likely triggered by the removal of the antigravity load. Contractile proteins are lost out of proportion to other cellular proteins, and the actin thin filament is lost disproportionately to the myosin thick filament. The decline in contractile protein explains the decrease in force per cross-sectional area, whereas the thin-filament loss may explain the observed postflight increase in the maximal velocity of shortening in the type I and IIa fiber types. Importantly, the microgravity-induced decline in peak power is partially offset by the increased fiber velocity. Muscle velocity is further increased by the microgravity-induced expression of fast-type myosin isozymes in slow fibers (hybrid I/II fibers) and by the increased expression of fast type II fiber types. SF increases the susceptibility of skeletal muscle to damage, with the actual damage elicited during postflight reloading. Evidence in rats indicates that SF increases fatigability and reduces the capacity for fat oxidation in skeletal muscles. Future studies will be required to establish the cellular and molecular mechanisms of the SF-induced muscle atrophy and functional loss and to develop effective exercise countermeasures.
    Journal of Applied Physiology 09/2000; 89(2):823-39. · 3.48 Impact Factor

Full-text (2 Sources)

View
3 Downloads
Available from
Jan 30, 2014