Ca2+ regulatory systems in rat myocardium are altered by 24 weeks treadmill training

Morán, María; Saborido, Ana; Megías, Alicia

doi:10.1007/s00424-003-1019-x

Cited by 20 publications

(27 citation statements)

References 31 publications

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“…In accordance, they also exhibited increased CS activity of cardiac muscle (Fig. 2B), which is consistent with several previous studies (1,20), although most of previous studies have demonstrated that CS activity is not increased or little increased by endurance exercise in rodent hearts (4,19). In ET-SARKO mice, on the other hand, CS activity was not increased in either soleus or cardiac muscle (Fig.…”

Section: Resultssupporting

confidence: 92%

“…One observation that may be relevant to this question is the significant decrease in the expression and activity of SERCA2a in ET-SARKO mice. A number of previous studies have reported that endurance exercise training increased the expression and/or activity of SERCA2a in healthy (9,10,20,22,30,35) or diseased rodents (6,21,24,34,39); similarly, we found that the expression and activity of SERCA2a increased after endurance exercise training in control mice. Yet other studies have demonstrated that endurance exercise training does not change the expression and/or activity of SERCA2a (3,4) or Ca 2ϩ transients (12) in rodents.…”

Section: Discussionsupporting

confidence: 73%

“…Therefore, it is extremely important for us to understand the effect of endurance exercise training on SERCA2a function and thus on the Ca 2ϩ storage system in the heart. In this regard, a considerable number of previous studies on animals have demonstrated that endurance exercise training increases the expression and/or activity of SERCA2a in the heart, resulting in enhanced cardiac function of the healthy (9,10,20,22,30,35) or pathological heart (6,15,21,24,34,39). Sarcalumenin (SAR) is an SR luminal glycoprotein responsible for Ca 2ϩ buffering in skeletal and cardiac muscles (13,16).…”

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confidence: 99%

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Sarcalumenin is essential for maintaining cardiac function during endurance exercise training

Jiao

Bai²,

Akaike³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Sarcalumenin (SAR), a Ca(2+)-binding protein located in the longitudinal sarcoplasmic reticulum (SR), regulates Ca(2+) reuptake into the SR by interacting with cardiac sarco(endo)plasmic reticulum Ca(2+)-ATPase 2a (SERCA2a). We have previously demonstrated that SAR deficiency induced progressive heart failure in response to pressure overload, despite mild cardiac dysfunction in sham-operated SAR knockout (SARKO) mice (26). Since responses to physiological stresses often differ from those to pathological stresses, we examined the effects of endurance exercise on cardiac function in SARKO mice. Wild-type (WT) and SARKO mice were subjected to endurance treadmill exercise training ( approximately 65% of maximal exercise ability for 60 min/day) for 12 wk. After exercise training, maximal exercise ability was significantly increased by 5% in WT mice (n = 6), whereas it was significantly decreased by 37% in SARKO mice (n = 5). Cardiac function assessed by echocardiographic examination was significantly decreased in accordance with upregulation of biomarkers of cardiac stress in SARKO mice after training. After training, expression levels of SERCA2a protein were significantly downregulated by 30% in SARKO hearts, whereas they were significantly upregulated by 59% in WT hearts. Consequently, SERCA2 activity was significantly decreased in SARKO hearts after training. Furthermore, the expression levels of other Ca(2+)-handling proteins, including phospholamban, ryanodine receptor 2, calsequestrin 2, and sodium/calcium exchanger 1, were significantly decreased in SARKO hearts after training. These results indicate that SAR plays a critical role in maintaining cardiac function under physiological stresses, such as endurance exercise, by regulating Ca(2+) transport activity into the SR. SAR may be a primary target for exercise-related adaptation of the Ca(2+) storage system in the SR to preserve cardiac function.

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Section: Resultssupporting

confidence: 92%

Section: Discussionsupporting

confidence: 73%

mentioning

confidence: 99%

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Sarcalumenin is essential for maintaining cardiac function during endurance exercise training

Jiao

Bai²,

Akaike³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…No change in expression of SERCA2a or PLB but an increase in pS 16 -PLB was detected after swim training of adult male C57bl/6 mice (35). In adult male Wistar rats, high SERCA2a expression was correlated with high treadmill performance (52) but treadmill training has also led to no increase in SERCA2a (38). In contrast to all the above studies, we found no change in SERCA2a or its regulators, PLB or pS 16 -PLB, with swim training in PBS-treated rats.…”

Section: Dox Toxicity In Intact Rats Is Not Alleviated By Dex Coinjeccontrasting

confidence: 55%

Cardiac response to doxorubicin and dexrazoxane in intact and ovariectomized young female rats at rest and after swim training

Calvé¹,

Haddad²,

Barama³

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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Calvé A, Haddad R, Barama SN, Meilleur M, Sebag IA, Chalifour LE. Cardiac response to doxorubicin and dexrazoxane in intact and ovariectomized young female rats at rest and after swim training. Am J Physiol Heart Circ Physiol 302: H2048 -H2057, 2012. First published March 23, 2012; doi:10.1152/ajpheart.01069.2011The impact of cancer therapies on adult cardiac function is becoming a concern as more children survive their initial cancer. Cardiovascular disease is now a significant problem to adult survivors of childhood cancer. Specifically, doxorubicin (DOX) may be particularly harmful in young girls. The objective of this study was to characterize DOX damage and determine the ability of dexrazoxane (DEX) to reduce DOX-mediated cardiac damage in sedentary and swim-trained female rats. Female Sprague-Dawley rats were left intact or ovariectomized (OVX) at weaning then injected with DEX (60 mg/kg) before DOX (3 mg/kg), DOX alone, or PBS. Rats were separated into sedentary and swim cohorts. Body weight was reduced in DOX:DEX-but not PBSor DOX-treated rats. Echocardiographic parameters were similar in sedentary rats. Swim training revealed greater concentric remodeling in DOX-treated rats and reduced fractional shortening in DOX:DEXtreated rats. Calsequestrin 2 was reduced with DOX and increased with DOX:DEX postswim. Sarco(endo)plasmic reticulum Ca 2ϩ -ATPase 2a was reduced and calsequestrin 2 reduced further by swim training only in intact rats. OVX rats were heavier and developed eccentric remodeling post-swim with DOX and eccentric hypertrophy with DOX:DEX. Changes in SERCA2a and calsequestrin 2 expression were not observed. Ovariectomized DOX-and DOX:DEXtreated rats stopped growing during swim training. DEX coinjection did not relieve DOX-mediated cardiotoxicity in intact or hormonedeficient rats. DOX-mediated reductions in growth, cardiac function, and expression of calcium homeostasis proteins were exacerbated by swim. DEX coadministration did not substantially relieve DOXmediated cardiotoxicity in young female rats. Ovarian hormones reduce DOX-induced cardiotoxicity.echocardiography; Sprague-Dawley rat; ovariectomy; sarco(endo) plasmic reticulum Ca 2ϩ -ATPase 2a; calsequestrin 2IT IS WELL RECOGNIZED THAT increasing numbers of children now survive childhood cancer because of treatment improvements. However, almost two-thirds of childhood cancer survivors have at least one chronic illness and close to one-third had severe or life-threatening conditions when only in their midtwenties (9, 44, 61). In addition, exercise testing of childhood cancer survivors has demonstrated a below-predicted exercise capacity (22, 63). The risk for cardiovascular disease was found to be high and was attributed to anthracycline treatment years earlier (2,27,49,54,65). Anthracycline use, mostly doxorubicin (DOX), daunorubicin, and epirubicin, remains common, and it is estimated that about one-half of childhood cancer survivors will have received anthracyclines. Evidence suggests that young females may have a greater incidence of DOX...

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“…SERCA2 removes the main bulk of Ca 2+ from the cytosol (Ca 2+ decay), and restores sarcoplasmatic reticulum Ca 2+ load before the next contraction cycle. During long-term exercise training, RYR receptor is also upregulated, which may increase the Ca 2+ uptake to the SR and trigger more CICR (Morán et al 2003).…”

Section: Evects Of Swimming Training On Calcium Current Characteristicsmentioning

confidence: 99%

Swimming training can affect intrinsic calcium current characteristics in rat myocardium

et al. 2008

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Endurance exercise is widely assumed to improve cardiac function in humans, but the mechanisms involved in such changes are not clearly understood. The purpose of this study is to determine whether training elicits adaptations at the level of the L-type Ca(2+) channel. Sprague-Dawley rats performed swimming training at either moderate intensity (MOD) or high intensity (HIGH) during 8 weeks. The trained rats were studied by echocardiography and the whole-cell L-type Ca(2+) currents (I (Ca,L)) characteristics in a single cell were measured by standard whole-cell patch-clamp recording technique. Echocardiography showed that septal and posterior wall thickness in MOD and HIGH increased with the increased LV mass by 43 and 41%, respectively (P < 0.05). Training (P < 0.05) increased mean myocyte capacitance (approximately 38% in MOD and HIGH) and myocyte length (approximately 20% longer in MOD and 26% longer in HIGH), thus providing electrophysiological and morphological evidence that the training elicited LV cardiocyte hypertrophy. Mean peak I (Ca,L) was not different in three groups. However, whole-cell I (Ca,L) density was decreased in MOD and HIGH versus sedentary (P < 0.05), but there was no significant difference between MOD and HIGH. The present study provides the evidence of a training adaptation in intrinsic I (Ca,L) characteristics in ventricular myocardium, which demonstrates a remarkable adaptive plasticity of L-type channel characteristics in training rat heart.

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Ca2+ regulatory systems in rat myocardium are altered by 24 weeks treadmill training

Cited by 20 publications

References 31 publications

Sarcalumenin is essential for maintaining cardiac function during endurance exercise training

Sarcalumenin is essential for maintaining cardiac function during endurance exercise training

Cardiac response to doxorubicin and dexrazoxane in intact and ovariectomized young female rats at rest and after swim training

Swimming training can affect intrinsic calcium current characteristics in rat myocardium

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