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

  • Place N Institute of Sport Sciences and Department of Physiology, Faculty of Biology and Medicine, University of Lausanne, 1015 Lausanne, Switzerland;
  • Ivarsson N Department of Physiology and Pharmacology, Karolinska Institutet, SE 171 77 Stockholm, Sweden;
  • Venckunas T Sports Science and Innovation Institute, Lithuanian Sports University, LT-44221 Kaunas, Lithuania;
  • Neyroud D Institute of Sport Sciences and Department of Physiology, Faculty of Biology and Medicine, University of Lausanne, 1015 Lausanne, Switzerland; Institute of Movement Sciences and Sports Medicine, University of Geneva, 1205 Geneva, Switzerland;
  • Brazaitis M Sports Science and Innovation Institute, Lithuanian Sports University, LT-44221 Kaunas, Lithuania;
  • Cheng AJ Department of Physiology and Pharmacology, Karolinska Institutet, SE 171 77 Stockholm, Sweden;
  • Ochala J Centre of Human and Aerospace Physiological Sciences, King's College London, London SE1 1UL, United Kingdom;
  • Kamandulis S Sports Science and Innovation Institute, Lithuanian Sports University, LT-44221 Kaunas, Lithuania;
  • Girard S Institute of Movement Sciences and Sports Medicine, University of Geneva, 1205 Geneva, Switzerland;
  • Volungevičius G Sports Science and Innovation Institute, Lithuanian Sports University, LT-44221 Kaunas, Lithuania;
  • Paužas H Surgery Department, Lithuanian University of Health Sciences, LT-50009 Kaunas, Lithuania;
  • Mekideche A Electroneuromyography and Neuromuscular Disorders Unit, Department of Clinical Neurosciences, Geneva University Hospital, 1211 Geneva, Switzerland.
  • Kayser B Institute of Sport Sciences and Department of Physiology, Faculty of Biology and Medicine, University of Lausanne, 1015 Lausanne, Switzerland;
  • Martinez-Redondo V Department of Physiology and Pharmacology, Karolinska Institutet, SE 171 77 Stockholm, Sweden;
  • Ruas JL Department of Physiology and Pharmacology, Karolinska Institutet, SE 171 77 Stockholm, Sweden;
  • Bruton J Department of Physiology and Pharmacology, Karolinska Institutet, SE 171 77 Stockholm, Sweden;
  • Truffert A Electroneuromyography and Neuromuscular Disorders Unit, Department of Clinical Neurosciences, Geneva University Hospital, 1211 Geneva, Switzerland.
  • Lanner JT Department of Physiology and Pharmacology, Karolinska Institutet, SE 171 77 Stockholm, Sweden;
  • Skurvydas A Sports Science and Innovation Institute, Lithuanian Sports University, LT-44221 Kaunas, Lithuania;
  • Westerblad H Department of Physiology and Pharmacology, Karolinska Institutet, SE 171 77 Stockholm, Sweden; Sports Science and Innovation Institute, Lithuanian Sports University, LT-44221 Kaunas, Lithuania; hakan.westerblad@ki.se.
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  • 2015-11-18
Published in:
  • Proceedings of the National Academy of Sciences of the United States of America. - 2015
Ca2+
high-intensity exercise
reactive oxygen species
ryanodine receptor 1
skeletal muscle
Adult
Animals
Athletes
Calcium
Exercise
Humans
Male
Mice
Mice, Inbred C57BL
Muscle Fibers, Skeletal
Physical Endurance
Reactive Oxygen Species
Recreation
Ryanodine Receptor Calcium Release Channel
Sarcoplasmic Reticulum
English 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.
Language
  • English
Open access status
bronze
Identifiers
Persistent URL
https://sonar.ch/global/documents/192620
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