Acute exercise is not cardioprotective and may induce apoptotic signalling in heart surgery: a randomized controlled trial†

Smenes, Benedikte Therese; Bækkerud, Fredrik Hjulstad; Slagsvold, Katrine Hordnes; Hassel, Erlend; Wohlwend, Martin; Pinho, Maria João; Høydal, Morten A.; Wisløff, Ulrik; Rognmo, Øivind; Wahba, Alexander

doi:10.1093/icvts/ivx439

Cited by 5 publications

(4 citation statements)

References 28 publications

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“…In previous studies, regular exercise reduced ROS and elevated antioxidant enzymes in isolated heart mitochondria [10] and skeletal muscle [7]. However, several previous studies reported that acute exercise, unlike chronic exercise, augments mitochondrial oxidative stress [18]. In the current study, we observed that a single bout of exercise showed tissue-specific differences in mitochondrial H 2 O 2 emission (Fig.…”

Section: Discussionsupporting

confidence: 58%

Effects of Acute Exercise on Mitochondrial Function, Dynamics, and Mitophagy in Rat Cardiac and Skeletal Muscles

Yoo

Heo

et al. 2019

Int Neurourol J

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This study aimed to investigate the effects of single-bout exercise on mitochondrial function, dynamics (fusion, fission), and mitophagy in cardiac and skeletal muscles. Methods: Fischer 344 rats (4 months old) were randomly divided into the control (CON) or acute exercise (EX) group (n = 10 each). The rats performed a single bout of treadmill exercise for 60 minutes. Mitochondrial function (e.g., O2 respiration, H2O2 emission, Ca 2+ retention capacity), mitochondrial fusion (e.g., Mfn1, Mfn2, Opa1), mitochondrial fission (e.g., Drp1, Fis1), and mitophagy (e.g., Parkin, Pink1, LC3II, Bnip3) were measured in permeabilized cardiac (e.g., left ventricle) and skeletal (e.g., soleus, white gastrocnemius) muscles. Results: Mitochondrial O2 respiration and Ca 2+ retention capacity were significantly increased in all tissues of the EX group compared with the CON group. Mitochondrial H2O2 emissions showed tissue-specific results; the emissions showed no significant differences in the left ventricle or soleus (type I fibers) but was significantly increased in the white gastrocnemius (type II fibers) after acute exercise. Mitochondrial fusion and fission were not altered in any tissues of the EX group. Mitophagy showed tissue-specific differences: It was not changed in the left ventricle or white gastrocnemius, whereas Parkin and LC3II were significantly elevated in the soleus muscle. Conclusions: A single bout of aerobic exercise may improve mitochondrial function (e.g., O2 respiration and Ca 2+ retention capacity) in the heart and skeletal muscles without changes in mitochondrial dynamics or mitophagy.

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Section: Discussionsupporting

confidence: 58%

Effects of Acute Exercise on Mitochondrial Function, Dynamics, and Mitophagy in Rat Cardiac and Skeletal Muscles

Yoo

Heo

et al. 2019

Int Neurourol J

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“…* P < 0.05, compared with the CON group; # P < 0.05, compared with the EE group; Δ P < 0.05, compared with the LEP + EE group. [33]. Feriani et al found significant improvement in inflammatory parameters and cardiac function indicators in exhausted rats after aerobic exercise training.…”

Section: Discussionmentioning

confidence: 98%

Different Intensity Exercise Preconditions Affect Cardiac Function of Exhausted Rats through Regulating TXNIP/TRX/NF‐ĸB_p65/NLRP3 Inflammatory Pathways

Li¹,

Xu²,

Wang³

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Objective. To investigate whether exercise preconditioning (EP) improves the rat cardiac dysfunction induced by exhaustive exercise (EE) through regulating NOD-like receptor protein 3 (NLRP3) inflammatory pathways and to confirm which intensity of EP is better. Method. Ninety healthy male Sprague Dawley rats were randomly divided into five groups: a control group (CON), exhaustive exercise group (EE), low-, middle-, and high-intensity exercise precondition and exhaustive exercise group (LEP + EE, MEP + EE, HEP + EE group). We established the experimental model by referring to Bedford’s motion load standard to complete the experiment. Then, the pathological changes of the myocardium were observed under a light microscope. Biomarker of myocardial injury in serum and oxidative stress factor in myocardial tissue were evaluated by ELISAs. The cardiac function parameters were detected using a Millar pressure and volume catheter. The levels of thioredoxin-interacting protein (TXNIP), thioredoxin protein (TRX), nuclear transcription factor kappa Bp65 (NF-ĸBp65), NLRP3, and cysteinaspartate specific proteinase 1 (Caspase-1) protein in rats’ myocardium were detected by western blotting. Results. 1. The myocardial structures of three EP + EE groups were all improved compared with EE groups. 2. The levels of the creatine phosphating-enzyme MB (CK-MB), reactive oxygen species (ROS), interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor alpha (TNF-α) in three EP + EE groups were all increased compared with CON but decreased compared with the EE group (P<0.05). 3. Compared with the CON group, slope of end-systolic pressure volume relationship (ESPVR), ejection fraction (EF), and peak rate of the increase in pressure (dP/dtmax) all dropped to the lowest level in the EE group (P<0.05), while the values of cardiac output (CO), stroke volume (SV), end-systolic volume (Ves), end-diastolic volume (Ved), and relaxation time constant (Tau) increased in the EE group (P<0.05). 4. Compared with the CON group, the expression levels of TXNIP, NF-ĸBp65, NLRP3, and Caspase-1 all increased obviously in the other groups (P<0.05); meanwhile, they were all decreased in three EP + EE groups compared with the EE group (P<0.05). 5. NLRP3 was positively correlated with heart rate, IL-6, and ROS, but negatively correlated with EF (P<0.01). Conclusion. EP protects the heart from EE-induced injury through downregulating TXNIP/TRX/NF-ĸBp65/NLRP3 inflammatory signaling pathways. Moderate intensity EP has the best protective effect.

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“…In dogs, sympathetic stimulation of the renal nerves for 3 hours increased the neuronal activity of the left stellate ganglion, facilitating the occurrence of ventricular arrhythmias in the course of acute myocardial ischemia 66 . Other risk was reported in a different study in which the results indicate that exercise did not precondition the heart against damage related to surgery 67 . Exercise can make the myocardium and mitochondria more vulnerable to perioperative damage.…”

Section: Possible Adverse Effectsmentioning

confidence: 89%

Efeitos do exercício físico na prevenção e tratamento de lesões por isquemia: uma revisão de literatura

Costa

Silva

Macedo

et al. 2020

Rev. Med. (São Paulo)

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Introdução: Em 2013 mais de 17,3 milhões de mortes/ano foram causadas por doenças cardiovasculares, acompanhado de uma estimativa de mais de 23,6 milhões de mortes para 2030, representando a maior causa global de morte. Objetivo: Esta revisão de literatura tem como objetivo a sistematização do conhecimento acerca dos efeitos do exercício físico como medida de prevenção e/ou tratamento em lesões causadas por isquemia, a fim de instigar novas pesquisas e contribuir para a disseminação de informação atual. Metodologia: Este estudo constitui uma revisão bibliográfica de caráter analítico dos estudos a respeito dos efeitos do exercício físico como medida de prevenção e tratamento de lesões causados por isquemia nos tecidos de animais submetidos a experimentação científica, em que foram coletados 99 artigos a partir de uma busca nas bases de dados Pubmed, SciELO e Lilacs com os descritores: “ischemia”, “exercise”, “rats” e “muscle”. Resultados e Conclusão: A atual literatura aponta para um consenso acerca dos efeitos cardioprotetores e neuroprotetores do atividade física, com ênfase no aumento da resistência contra agentes oxidantes, melhoria no processo de angiogênese, maior resistência contra acidificação do meio, melhoria no processo de cardiomiogênese, e apresenta as vias de sinalização moleculares que possivelmente explicam os efeitos advindos do exercício físico nas suas mais diferentes intensidades.

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Acute exercise is not cardioprotective and may induce apoptotic signalling in heart surgery: a randomized controlled trial†

Abstract: NCT00218985 (https://clinicaltrials.gov/ct2/show/NCT00218985).

Cited by 5 publications

References 28 publications

Effects of Acute Exercise on Mitochondrial Function, Dynamics, and Mitophagy in Rat Cardiac and Skeletal Muscles

Effects of Acute Exercise on Mitochondrial Function, Dynamics, and Mitophagy in Rat Cardiac and Skeletal Muscles

Different Intensity Exercise Preconditions Affect Cardiac Function of Exhausted Rats through Regulating TXNIP/TRX/NF‐ĸB_p65/NLRP3 Inflammatory Pathways

Efeitos do exercício físico na prevenção e tratamento de lesões por isquemia: uma revisão de literatura

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Acute exercise is not cardioprotective and may induce apoptotic signalling in heart surgery: a randomized controlled trial†

Abstract: NCT00218985 (https://clinicaltrials.gov/ct2/show/NCT00218985).

Cited by 5 publications

References 28 publications

Effects of Acute Exercise on Mitochondrial Function, Dynamics, and Mitophagy in Rat Cardiac and Skeletal Muscles

Effects of Acute Exercise on Mitochondrial Function, Dynamics, and Mitophagy in Rat Cardiac and Skeletal Muscles

Different Intensity Exercise Preconditions Affect Cardiac Function of Exhausted Rats through Regulating TXNIP/TRX/NF‐ĸBp65/NLRP3 Inflammatory Pathways

Efeitos do exercício físico na prevenção e tratamento de lesões por isquemia: uma revisão de literatura

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Different Intensity Exercise Preconditions Affect Cardiac Function of Exhausted Rats through Regulating TXNIP/TRX/NF‐ĸB_p65/NLRP3 Inflammatory Pathways