Aims: 

In vitro studies of skeletal muscle fatigue have often used long-duration tetani (350 600ms) produced at room temperature to assess the role of myoplasmic free Ca2+ ([Ca2+]i) in fatigue. These conditions differ from those experienced by the muscle during locomotion in vivo. The purpose here was to investigate fatigue-induced alterations in [Ca2+]i and force following repetitive brief tetani at high temperatures that more closely mimic locomoti on in vivo.

Methods: 

Fifteen mechanically dissected intact single fibers from flexor digitorum brevis (FDB) muscles of C57 mice were perfused with Tyrode solution (32–34°C) and injected with indo-1 to assess [Ca2+]i. Before fatigue and up to 30min after fatigue, FDB fibers were electrically stimulated at various frequencies to determine force-[Ca2+]i relations hips. Fatigue was induced with brief 150ms, 70Hz tetani given every 1s for a total of 60 contractions. Data are reported as means ± SD.

Results: 

Immediately after fatigue, 30Hz force was decreased to 48± 38% of the initial and this decrease was greater than that at 120H z (70±23%); [Ca2+]i was not significantly (P>0.05) changed at either frequency (110±36% and 85±34%). During the 30min recovery period, prolonged low-frequency force depression was evident with greater relative reductions in force at 30Hz compared with 120Hz, whereas [Ca2+ ]i remained unchanged.

Conclusion: 

After fatigue induced under conditions similar to those prevailing during locomotion in vivo, the prolonged low frequency force depression during the 30min recovery period was not explained by decreased SR Ca2+ release, but rather by decreased myofibrillar Ca2+ sensitivity.