| Full text | |
| Author(s): Show less - |
Zanou, Nadege
[1, 2]
;
Dridi, Haikel
[3]
;
Reiken, Steven
[3]
;
de Lima, Tanes Imamura
[4]
;
Donnelly, Chris
[1, 2]
;
De Marchi, Umberto
[5]
;
Ferrini, Manuele
[1, 2]
;
Vidal, Jeremy
[1, 2]
;
Sittenfeld, Leah
[3]
;
Feige, Jerome N.
[5, 6]
;
Garcia-Roves, Pablo M.
[7, 8]
;
Lopez-Mejia, Isabel C.
[9]
;
Marks, Andrew R.
[3, 10]
;
Auwerx, Johan
[4]
;
Kayser, Bengt
[1, 2]
;
Place, Nicolas
[1, 2]
Total Authors: 16
|
| Affiliation: | [1] Univ Lausanne, Inst Sport Sci, Lausanne - Switzerland
[2] Univ Lausanne, Dept Biomed Sci, Lausanne - Switzerland
[3] Columbia Univ, Clyde & Helen Wu Ctr Mol Cardiol, Dept Physiol & Cellular Biophys, Vagelos Coll Phys & Surg, New York, NY - USA
[4] Ecole Polytech Fed Lausanne EPFL, Lab Integrat Syst Physiol LISP, Lausanne - Switzerland
[5] Ecole Polytech Fed Lausanne EPFL, Nestle Res, Innovat Pk, Lausanne - Switzerland
[6] Ecole Polytech Fed Lausanne EPFL, Sch Life Sci, Lausanne - Switzerland
[7] Univ Barcelona, Sch Med & Hlth Sci, Dept Physiol Sci, Barcelona - Spain
[8] Bellvitge Biomed Res Inst IDIBELL, Barcelona - Spain
[9] Univ Lausanne, Ctr Integrat Genom, Lausanne - Switzerland
[10] Columbia Univ, Dept Med, Med Ctr, Div Cardiol, New York, NY - USA
Total Affiliations: 10
|
| Document type: | Journal article |
| Source: | NATURE COMMUNICATIONS; v. 12, n. 1 DEC 10 2021. |
| Web of Science Citations: | 0 |
| Abstract | |
Sustained ryanodine receptor (RyR) Ca2+ leak is associated with pathological conditions such as heart failure or skeletal muscle weakness. We report that a single session of sprint interval training (SIT), but not of moderate intensity continuous training (MICT), triggers RyR1 protein oxidation and nitrosylation leading to calstabin1 dissociation in healthy human muscle and in in vitro SIT models (simulated SIT or S-SIT). This is accompanied by decreased sarcoplasmic reticulum Ca2+ content, increased levels of mitochondrial oxidative phosphorylation proteins, supercomplex formation and enhanced NADH-linked mitochondrial respiratory capacity. Mechanistically, (S-)SIT increases mitochondrial Ca2+ uptake in mouse myotubes and muscle fibres, and decreases pyruvate dehydrogenase phosphorylation in human muscle and mouse myotubes. Countering Ca2+ leak or preventing mitochondrial Ca2+ uptake blunts S-SIT-induced adaptations, a result supported by proteomic analyses. Here we show that triggering acute transient Ca2+ leak through RyR1 in healthy muscle may contribute to the multiple health promoting benefits of exercise. Ryanodine receptor type 1 (RyR1) are involved in skeletal muscle contraction. Here, the authors show that a transient calcium leak in response to exercise-induced post translational modifications of RyR1 causes mitochondrial remodeling to improve respiration. (AU) | |
| FAPESP's process: | 19/11171-7 - Screening platform for the identification of molecular targets involved in mitochondrial homeostasis |
| Grantee: | Tanes Imamura de Lima |
| Support Opportunities: | Scholarships abroad - Research Internship - Post-doctor |