Abstract
In this study, we compared muscle fatigue induced by high-intensity interval exercise (HIIE) and moderate-intensity continuous exercise (MICE), with a focus on changes in the function of sarcoplasmic reticulum (SR) and myofibril. To achieve the aim of this study with mechanically skinned fibers with sealed transverse tubules and intact SR membrane, myofibrillar Ca2+ sensitivity, depolarization-induced force, and action potential-induced force were evaluated. Rat gastrocnemius muscles were subjected to HIIE-mimicking or MICE-mimicking stimulation in situ. The number of contractions was the same for MICE- and HIIE-mimicking stimulation (total of 360 contractions). Three hours after cessation of stimulation, the superficial regions of gastrocnemius muscles were dissected and used for biochemical and skinned fiber analyses. At 3 h of recovery, forces at 20 and 100 Hz in whole muscles had returned to resting levels in MICE but not HIIE muscles. The reduced glutathione content was decreased only in HIIE muscles. Both MICE- and HIIE-mimicking stimulation resulted in an increase in myofibrillar Ca2+ sensitivity in skinned fibers. Only HIIE-mimicking stimulation led to a decrease in the ratio of force at 1 Hz to that at 50 Hz and the ratio of depolarization-induced force to the maximum Ca2+-activated force. These results reflect the properties of type IIX and IIB fibers (the latter is not expressed in human skeletal muscles) and suggest that HIIE requires longer recovery periods than those normally used with MICE, which is ascribable to long-lasting depressions in SR Ca2+ release.NEW & NOTEWORTHY Over the past decade, high-intensity interval exercise (HIIE) training has received attention as a more efficient training to improve endurance capacity. It is unclear, however, whether the extent of acute exercise-related muscle fatigue differs between HIIE and moderate-intensity continuous exercise, traditional endurance training. Here we provide evidence that restoration of force production takes a longer time after HIIE, which is ascribable to long-lasting depressions in Ca2+ release of the sarcoplasmic reticulum.
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