Abstract
We previously demonstrated that the loss of female hormones induces cardiac and mitochondrial dysfunction in the female heart. Here, we show the impact of endurance training for twelve weeks, a nonpharmacological therapy against cardiovascular disease caused by ovariectomy and its contribution to cardiac contractility, mitochondrial quality control, bioenergetics and oxidative damage. We found that ovariectomy induced cardiac hypertrophy and dysfunction by decreasing SERCA2 and increasing phospholamban protein expression. Endurance training restored myocardial contractility, SERCA2 levels, increased calcium transient in ovariectomized rats but did not change phospholamban protein expression or cardiac hypertrophy. Additionally, ovariectomy decreased the amount of intermyofibrillar mitochondria and induced mitochondrial fragmentation that were accompanied by decreased levels of mitofusin 1, PGC-1α, NRF-1, total AMPK-α and mitochondrial Tfam. Endurance training prevented all these features except for mitofusin 1. Ovariectomy reduced O2 consumption, elevated O2 .- release and increased Ca2+-induced mitochondrial permeability transition pore opening in both mitochondrial subpopulations. Ovariectomy also increased NOX-4 protein expression in the heart, reduced mitochondrial Mn-SOD, catalase protein expression and increased protein carbonylation in both mitochondrial subpopulations, which were prevented by endurance training. Taken together, our findings show that endurance training prevented cardiac contractile dysfunction and mitochondrial quality control in ovariectomized rats.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 174-188 |
| Number of pages | 15 |
| Journal | Free Radical Biology and Medicine |
| Volume | 130 |
| DOIs | |
| State | Published - Jan 1 2019 |
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Keywords
- Bioenergetics
- Cardiac dysfunction
- Endurance training
- Female hormone deprivation
- Intermyofibrillar and subsarcolemmal mitochondria
- Mitochondrial quality control
ASJC Scopus subject areas
- Biochemistry
- Physiology (medical)
Cite this
Endurance training restores spatially distinct cardiac mitochondrial function and myocardial contractility in ovariectomized rats. / Morra, Elis Aguiar; Rodrigues, Paula Lopes; Jesus, Itamar Couto Guedes de; Do Val Lima, Patrícia Ribeiro; Ávila, Renata Andrade; Zanardo, Tadeu Ériton Caliman; Nogueira, Breno Valentim; Bers, Donald M; Guatimosim, Silvia; Stefanon, Ivanita; Ribeiro Júnior, Rogério Faustino.
In: Free Radical Biology and Medicine, Vol. 130, 01.01.2019, p. 174-188.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Endurance training restores spatially distinct cardiac mitochondrial function and myocardial contractility in ovariectomized rats
AU - Morra, Elis Aguiar
AU - Rodrigues, Paula Lopes
AU - Jesus, Itamar Couto Guedes de
AU - Do Val Lima, Patrícia Ribeiro
AU - Ávila, Renata Andrade
AU - Zanardo, Tadeu Ériton Caliman
AU - Nogueira, Breno Valentim
AU - Bers, Donald M
AU - Guatimosim, Silvia
AU - Stefanon, Ivanita
AU - Ribeiro Júnior, Rogério Faustino
PY - 2019/1/1
Y1 - 2019/1/1
N2 - We previously demonstrated that the loss of female hormones induces cardiac and mitochondrial dysfunction in the female heart. Here, we show the impact of endurance training for twelve weeks, a nonpharmacological therapy against cardiovascular disease caused by ovariectomy and its contribution to cardiac contractility, mitochondrial quality control, bioenergetics and oxidative damage. We found that ovariectomy induced cardiac hypertrophy and dysfunction by decreasing SERCA2 and increasing phospholamban protein expression. Endurance training restored myocardial contractility, SERCA2 levels, increased calcium transient in ovariectomized rats but did not change phospholamban protein expression or cardiac hypertrophy. Additionally, ovariectomy decreased the amount of intermyofibrillar mitochondria and induced mitochondrial fragmentation that were accompanied by decreased levels of mitofusin 1, PGC-1α, NRF-1, total AMPK-α and mitochondrial Tfam. Endurance training prevented all these features except for mitofusin 1. Ovariectomy reduced O2 consumption, elevated O2 .- release and increased Ca2+-induced mitochondrial permeability transition pore opening in both mitochondrial subpopulations. Ovariectomy also increased NOX-4 protein expression in the heart, reduced mitochondrial Mn-SOD, catalase protein expression and increased protein carbonylation in both mitochondrial subpopulations, which were prevented by endurance training. Taken together, our findings show that endurance training prevented cardiac contractile dysfunction and mitochondrial quality control in ovariectomized rats.
AB - We previously demonstrated that the loss of female hormones induces cardiac and mitochondrial dysfunction in the female heart. Here, we show the impact of endurance training for twelve weeks, a nonpharmacological therapy against cardiovascular disease caused by ovariectomy and its contribution to cardiac contractility, mitochondrial quality control, bioenergetics and oxidative damage. We found that ovariectomy induced cardiac hypertrophy and dysfunction by decreasing SERCA2 and increasing phospholamban protein expression. Endurance training restored myocardial contractility, SERCA2 levels, increased calcium transient in ovariectomized rats but did not change phospholamban protein expression or cardiac hypertrophy. Additionally, ovariectomy decreased the amount of intermyofibrillar mitochondria and induced mitochondrial fragmentation that were accompanied by decreased levels of mitofusin 1, PGC-1α, NRF-1, total AMPK-α and mitochondrial Tfam. Endurance training prevented all these features except for mitofusin 1. Ovariectomy reduced O2 consumption, elevated O2 .- release and increased Ca2+-induced mitochondrial permeability transition pore opening in both mitochondrial subpopulations. Ovariectomy also increased NOX-4 protein expression in the heart, reduced mitochondrial Mn-SOD, catalase protein expression and increased protein carbonylation in both mitochondrial subpopulations, which were prevented by endurance training. Taken together, our findings show that endurance training prevented cardiac contractile dysfunction and mitochondrial quality control in ovariectomized rats.
KW - Bioenergetics
KW - Cardiac dysfunction
KW - Endurance training
KW - Female hormone deprivation
KW - Intermyofibrillar and subsarcolemmal mitochondria
KW - Mitochondrial quality control
UR - http://www.scopus.com/inward/record.url?scp=85056200636&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85056200636&partnerID=8YFLogxK
U2 - 10.1016/j.freeradbiomed.2018.10.406
DO - 10.1016/j.freeradbiomed.2018.10.406
M3 - Article
VL - 130
SP - 174
EP - 188
JO - Free Radical Biology and Medicine
JF - Free Radical Biology and Medicine
SN - 0891-5849
ER -