Ryanodine receptor fragmentation and sarcoplasmic reticulum Ca2+ leak after one session of high-intensity interval exercise.

Details

Serval ID
serval:BIB_9A29E4A594FA
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Ryanodine receptor fragmentation and sarcoplasmic reticulum Ca2+ leak after one session of high-intensity interval exercise.
Journal
Proceedings of the National Academy of Sciences of the United States of America
Author(s)
Place N., Ivarsson N., Venckunas T., Neyroud D., Brazaitis M., Cheng A.J., Ochala J., Kamandulis S., Girard S., Volungevičius G., Paužas H., Mekideche A., Kayser B., Martinez-Redondo V., Ruas J.L., Bruton J., Truffert A., Lanner J.T., Skurvydas A., Westerblad H.
ISSN
1091-6490 (Electronic)
ISSN-L
0027-8424
Publication state
Published
Issued date
12/2015
Peer-reviewed
Oui
Volume
112
Number
50
Pages
15492-15497
Language
english
Notes
Publication types: Clinical Trial ; Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Abstract
High-intensity interval training (HIIT) is a time-efficient way of improving physical performance in healthy subjects and in patients with common chronic diseases, but less so in elite endurance athletes. The mechanisms underlying the effectiveness of HIIT are uncertain. Here, recreationally active human subjects performed highly demanding HIIT consisting of 30-s bouts of all-out cycling with 4-min rest in between bouts (≤3 min total exercise time). Skeletal muscle biopsies taken 24 h after the HIIT exercise showed an extensive fragmentation of the sarcoplasmic reticulum (SR) Ca(2+) release channel, the ryanodine receptor type 1 (RyR1). The HIIT exercise also caused a prolonged force depression and triggered major changes in the expression of genes related to endurance exercise. Subsequent experiments on elite endurance athletes performing the same HIIT exercise showed no RyR1 fragmentation or prolonged changes in the expression of endurance-related genes. Finally, mechanistic experiments performed on isolated mouse muscles exposed to HIIT-mimicking stimulation showed reactive oxygen/nitrogen species (ROS)-dependent RyR1 fragmentation, calpain activation, increased SR Ca(2+) leak at rest, and depressed force production due to impaired SR Ca(2+) release upon stimulation. In conclusion, HIIT exercise induces a ROS-dependent RyR1 fragmentation in muscles of recreationally active subjects, and the resulting changes in muscle fiber Ca(2+)-handling trigger muscular adaptations. However, the same HIIT exercise does not cause RyR1 fragmentation in muscles of elite endurance athletes, which may explain why HIIT is less effective in this group.
Keywords
Adult, Animals, Athletes, Calcium/metabolism, Exercise/physiology, Humans, Male, Mice, Mice, Inbred C57BL, Muscle Fibers, Skeletal/physiology, Physical Endurance, Reactive Oxygen Species/metabolism, Recreation, Ryanodine Receptor Calcium Release Channel/metabolism, Sarcoplasmic Reticulum/metabolism
Pubmed
Web of science
Open Access
Yes
Create date
05/01/2016 9:54
Last modification date
21/08/2019 5:36
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