2014
DOI: 10.1590/1414-431x20144063
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Effect of exercise training on Ca2+ release units of left ventricular myocytes of spontaneously hypertensive rats

Abstract: In cardiomyocytes, calcium (Ca2+) release units comprise clusters of intracellular Ca2+ release channels located on the sarcoplasmic reticulum, and hypertension is well established as a cause of defects in calcium release unit function. Our objective was to determine whether endurance exercise training could attenuate the deleterious effects of hypertension on calcium release unit components and Ca2+ sparks in left ventricular myocytes of spontaneously hypertensive rats. Male Wistar and spontaneously hypertens… Show more

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Cited by 17 publications
(14 citation statements)
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“…Our results indicate that training reduced the deleterious effects of hypertension by decreasing calcium leakage through ryanodine receptor (decrease in spark site density for HIIE) and by improving calcium uptake, resulting in temporal and spatial shortening of sparks (FDHM and FWHM were decreased). To our knowledge, only one study on the effect of training on spontaneous calcium release during hypertension has been published (12). For the four parameters studied previously, however, the reported results of this study are contradictory with ours: an increase in amplitude, FDHM, FWHM, and peak time after 8 wk of training was observed.…”
Section: Discussioncontrasting
confidence: 99%
“…Our results indicate that training reduced the deleterious effects of hypertension by decreasing calcium leakage through ryanodine receptor (decrease in spark site density for HIIE) and by improving calcium uptake, resulting in temporal and spatial shortening of sparks (FDHM and FWHM were decreased). To our knowledge, only one study on the effect of training on spontaneous calcium release during hypertension has been published (12). For the four parameters studied previously, however, the reported results of this study are contradictory with ours: an increase in amplitude, FDHM, FWHM, and peak time after 8 wk of training was observed.…”
Section: Discussioncontrasting
confidence: 99%
“…Such increase in physical capacity in response to aerobic training has been previously demonstrated. 10 , 17 , 18 More importantly, physical training reduced SAP in hypertensive animals, and such effect is well established in the literature. 11 , 19 …”
Section: Discussionmentioning
confidence: 58%
“…The impact of exercise and physical activity on the progression of cardiac aging is also an active area of research. There is evidence in both healthy animal models and models of other cardiac disease phenotypes that exercise can induce alterations in cardiac Ca 2+ cycling [175,176,177]. Endurance exercise attenuated increased Ca 2+ spark frequency, CaMKII-mediated RyR2 phosphorylation at Serine-2814, and Ca 2+ alternans in a dog model of sudden cardiac death, which reduced ischemically-induced VF [175].…”
Section: Perspectivementioning
confidence: 99%
“…Long-term interval training also reduced CaMKII-dependent phosphorylation of RyR2 and the incidence of VT in a mouse model of CPVT [176]. In spontaneously hypertensive rats, endurance exercise training reversed increased RyR2 expression and attenuated the proarrhythmic increase in Ca 2+ spark activity in left ventricular myocytes [177]. In the context of the aging heart, research on the effects of exercise on intracellular Ca 2+ homeostasis remains limited.…”
Section: Perspectivementioning
confidence: 99%