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Low‐frequency fatigue: an in situ skeletal muscle model
Author(s) -
Fitts Robert H,
Peters James R,
Nix Michele L,
Ford Amy R,
Bain James L,
Riley Danny A
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a939-a
Low frequency muscle fatigue (LFF) characterized as a loss of force at low (10–40 Hz) but not high (>80 Hz) frequencies has been observed in humans in vivo and in single fibers. The etiology is thought to involve a disruption in Ca 2+ release from the SR. To study the SR Ca 2+ release channel, it is important to develop an in situ model. We modified the protocol of Westerblad et al. ( J Appl Physiol 75 :–388, 1993) to produce LFF in the in situ soleus (Sol). A force‐frequency (f‐f) curve was determined, and fatigue elicited with .35 s 120 Hz tetani at an interval of 4 s for 2 min with the interval reduced every 2 min (3, 2.5, 2, 2.75, 1.5, 1.25, 1 s) until force fell by 70%. After 10 min, LFF was assessed by the low/high frequency ratio (20/120 Hz), and fatigue test repeated until LFF was detected. Low/high ratio and f‐f curve were determined at 3 hr post‐stimulation (Fig.) The low/high Hz ratio declined from 0.50±0.02 (pre) to 0.23±0.03∗ (P<0.05). EM analysis determined that LFF was not caused by tissue damage as >95% of the myofibrils were intact.

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