Place 2022 Abstract Bioblast

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3.4. «5 min»
Place Nicolas
Zanou N, Donnelly C, Kayser B, Place Nicolas (2022) Ca2+-induced mitochondrial adaptations in response to a single session of sprint interval training. Bioblast 2022: BEC Inaugural Conference. In: https://doi.org/10.26124/bec:2022-0001

Link: Bioblast 2022: BEC Inaugural Conference

Zanou Nadège, Donnelly Chris, Kayser Bengt, Place Nicolas (2022)

Event: Bioblast 2022

Sprint interval training (SIT) has been shown to induce similar or greater mitochondrial adaptions as compared to moderate intensity continuous training (MICT) despite a much lower training volume. Previous data suggests that intramuscular Ca2+ handling is altered in response to a single session of SIT, as ryanodine receptors (RyR1, the intracellular Ca2+ release channels) can be markedly affected [1]. Ca2+ leak through RyR1 has previously been associated with pathological conditions such as skeletal muscle weakness [2], although it was recently suggested that an acute transient SR Ca2+ leak via RyR1 channels paradoxically might have a beneficial role [3]. We therefore assessed whether a single session of SIT resulted in leaky RyR1 and whether this leak of Ca2+ could contribute to mitochondrial remodeling. Muscle biopsies collected after a single session of SIT or MICT in recreationally-trained participants revealed dissociation of calstabin1 from RyR1, a signature of leaky RyR1, in response to SIT only. To assess the underlying mechanisms, cellular models based on SIT- and MICT-mimicking stimulation were developed and they also revealed a leaky RyR1 signature after the SIT stimulation pattern only. Using various pharmacological interventions, we could establish that the Ca2+ leaking through RyR1 entered the mitochondria and enhanced mitochondrial content / function, as attested by increased levels of mitochondrial oxidative phosphorylation proteins and enhanced NADH-linked mitochondrial respiratory capacity [4]. Our data thus show that acute Ca2+ leak through RyR1 can induce beneficial mitochondrial adaptations and thus contributes to the multiple health promoting benefits of exercise.

  1. Place N et al (2015) Ryanodine receptor fragmentation and sarcoplasmic reticulum Ca2+ leak after one session of high-intensity interval exercise. https://doi.org/10.1073/pnas.1507176112
  2. Andersson DC, Betzenhauser MJ, Reiken S, Meli AC, Umanskaya A, Xie W, Shiomi T, Zalk R, Lacampagne A, Marks AR (2011) Ryanodine receptor oxidation causes intracellular calcium leak and muscle weakness in aging. https://doi.org/10.1016/j.cmet.2011.05.014
  3. Ivarsson N, Mattsson CM, Cheng AJ, Bruton JD, Ekblom B, Lanner JT, Westerblad H (2019) SR Ca2+ leak in skeletal muscle fibers acts as an intracellular signal to increase fatigue resistance. https://doi.org/10.1085/jgp.201812152
  4. Zanou N, Dridi H, Reiken S, Imamura de Lima T, Donnelly C, De Marchi U, Ferrini M, Vidal J, Sittenfeld L, Feige JN, Garcia-Roves PM, Lopez-Mejia IC, Marks AR, Auwerx J, Kayser B, Place N (2021) Acute RyR1 Ca 2+ leak enhances NADH-linked mitochondrial respiratory capacity. https://doi.org/10.1038/s41467-021-27422-1

Keywords: ryanodine receptor, mitochondria, sprint interval training, human, calcium

O2k-Network Lab: CH Lausanne Place N


Affiliation

Institute of Sport Sciences, Univ. Lausanne, Switzerland - nicolas.place@unil.ch

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Event: A3