Moderate intensity of regular exercise improves cardiac SR Ca2+ uptake activity in ovariectomized rats

2009 ◽  
Vol 107 (4) ◽  
pp. 1105-1112 ◽  
Author(s):  
Tepmanas Bupha-Intr ◽  
Jitanan Laosiripisan ◽  
Jonggonnee Wattanapermpool

The impact of regular exercise in protecting cardiac deteriorating results of female sex hormone deprivation was evaluated by measuring changes in intracellular Ca2+ removal activity of sarcoplasmic reticulum (SR) in ovariectomized rats following 9-wk treadmill running exercise at moderate intensity. Despite induction of cardiac hypertrophy in exercised groups of both sham-operated and ovariectomized rats, exercise training had no effect on SR Ca2+ uptake and SR Ca2+-ATPase (SERCA) in hormone intact rat heart. However, exercise training normalized the suppressed maximum SR Ca2+ uptake and SERCA activity in ovariectomized rat heart. While exercise training normalized the leftward shift in pCa (−log[Ca2+])-SR Ca2+ uptake relation in ovariectomized rats, no effect was detected in exercised sham-operated rats. Similar phenomena were also observed on SERCA and on phospholamban (PLB) phosphorylation levels; exercise training in ovariectomized rats enhanced SERCA expression to reach the level as that in sham-operated rats, in which there were no differences in SERCA and phospho-PLB levels between sedentary and exercised groups. In addition, the reduction in phospho-Thr17 PLB in myocardium of ovariectomized rats was abolished by exercise training. These results showed that regular exercise maintains the molecular activation of cardiac SR Ca2+ uptake under normal physiological conditions and is able to induce a protective impact on cardiac SR Ca2+ uptake in ovarian sex hormone-deprived status.

2020 ◽  
Vol 318 (5) ◽  
pp. R829-R842
Author(s):  
Sukanya Phungphong ◽  
Anusak Kijtawornrat ◽  
Theerachat Kampaengsri ◽  
Jonggonnee Wattanapermpool ◽  
Tepmanas Bupha-Intr

Cardiac inflammation has been proposed as one of the primary mechanisms of anthracycline-induced acute cardiotoxicity. A reduction in cardiac inflammation might also reduce cardiotoxicity. This study aimed to evaluate the potential of estrogen therapy and regular exercise on attenuating cardiac inflammation in the context of doxorubicin-induced cardiomyopathy. Ovariectomized rats were randomly allocated into estrogen supplementation, exercise training, and mast cell stabilizer treatment groups. Eight weeks after ovariectomy, rats received six cumulative doses of doxorubicin for two weeks. Echocardiography demonstrated a progressive decrease in ejection fraction in doxorubicin-treated rats without hypertrophic effect. This systolic defect was completely prevented by either estrogen supplementation or mast cell stabilizer treatment but not by regular exercise. As a heart disease indicator, increased β-myosin heavy chain expression induced by doxorubicin could only be prevented by estrogen supplementation. Decrease in shortening and intracellular Ca2+ transients of cardiomyocytes were due to absence of female sex hormones without further effects of doxorubicin. Again, estrogen supplementation and mast cell stabilizer treatment prevented these changes but exercise training did not. Histological analysis indicated that the hyperactivation of cardiac mast cells in ovariectomized rats was augmented by doxorubicin. Estrogen supplementation and mast cell stabilizer treatment completely prevented both increases in mast cell density and degranulation, whereas exercise training partially attenuated the hyperactivation. Our results, therefore, suggest that estrogen supplementation acts similarly to mast cell stabilizers in attenuating the effects of doxorubicin. Ineffectiveness of regular exercise in preventing the acute cardiotoxicity of doxorubicin might be due to a lesser effect on preventing cardiac inflammation.


2018 ◽  
Vol 315 (4) ◽  
pp. H885-H896 ◽  
Author(s):  
Xinrui Wang ◽  
Robert H. Fitts

Exercise training is known to protect the heart from ischemia and improve function during exercise by reducing cardiomyocyte action potential duration (APD) and increasing contractility. The cellular mechanisms involve β-adrenergic regulation and the ATP-sensitive K+ (KATP) channel, but how each alters function of the left ventricle and sex specificity is unknown. To address this, female and male Sprague-Dawley rats were randomly assigned to wheel-running (TRN) or sedentary (SED) groups. After 6–8 wk of training, myocytes were isolated from the left ventricle and field stimulated at 1, 2, and 5 Hz. TRN significantly increased cardiomyocyte contractility, the kinetics of the Ca2+ transient, and responsiveness to the adrenergic receptor agonist isoproterenol (ISO), as reflected by an increased sarcomere shortening. Importantly, we demonstrated a TRN-induced upregulation of KATP channels, which was reflected by elevated content, current density, and the channel’s contribution to APD shortening at high activation rates and in the presence of the activator pinacidil. TRN induced increase in KATP current occurred throughout the left ventricle, but channel subunit content showed regional specificity with increases in Kir6.2 in the apex and SUR2A in base regions. In summary, TRN elevated cardiomyocyte cross-bridge kinetics, Ca2+ sensitivity, and the responsiveness of contractile function to β-adrenergic receptor stimulation in both sexes. Importantly, upregulation of the KATP channel accelerates repolarization and shortens APD during stress and exercise. These adaptations have clinical importance, as increased contractility and reduced APD would help protect cardiac output and reduce intracellular Ca2+ overload during stresses such as regional ischemia. NEW & NOTEWORTHY Our results demonstrate that regular exercise significantly increased ventricular myocyte shortening and relaxation velocity and the rate of rise in intracellular Ca2+ transient and enhanced the response of biomechanics and Ca2+ reuptake to β-adrenergic stimulation. Importantly, exercise training upregulated the cardiomyocyte sarcolemma ATP-sensitive K+ channel across the left ventricle in both sexes, as reflected by elevated channel subunit content, current density, and the channel’s contribution to reduced action potential duration at high activation rates.


Author(s):  
Rachel J. Skow ◽  
Lawrence Labrecque ◽  
Jade A. Rosenberger ◽  
Patrice Brassard ◽  
Craig D. Steinback ◽  
...  

We performed a randomised controlled trial measuring dynamic cerebral autoregulation (dCA) using a sit-to-stand maneuver before (SS1) and following (SS2) an acute exercise test at 16-20 weeks gestation (trimester 2; TM2) and then again at 34-37 weeks gestation (third trimester; TM3). Following the first assessment, women were randomised into exercise training or control (standard care) groups; women in the exercise training group were prescribed moderate intensity aerobic exercise for 25-40 minutes on 3-4 days per week for 14±1weeks. Resting seated mean blood velocity in the middle cerebral artery (MCAvmean) was lower in TM3 compared to TM2 but not impacted by exercise training intervention. dCA was not impacted by gestational age, or exercise training during SS1. During SS2, dCA was altered such that there were greater absolute and relative decreases in mean arterial blood pressure (MAP) and MCAvmean, but this was not impacted by the intervention. There was also no difference in the relationship between the decrease in MCAvmean compared to the decrease in MAP (%/%), or the onset of the regulatory response with respect to acute exercise, gestational age, or intervention; however, rate of regulation was faster in women in the exercise group following acute exercise (interaction effect, p=0.048). These data highlight the resilience of the cerebral circulation in that dCA was well maintained or improved in healthy pregnant women between TM2 and TM3. However, future work addressing the impact of acute and chronic exercise on dCA in women who are at risk for cardiovascular complications during pregnancy is needed.


2020 ◽  
Vol 21 (20) ◽  
pp. 7724
Author(s):  
Nancy Vargas-Mendoza ◽  
Marcelo Ángeles-Valencia ◽  
Eduardo Osiris Madrigal-Santillán ◽  
Mauricio Morales-Martínez ◽  
Judith Margarita Tirado-Lule ◽  
...  

(1) Background: Regular exercise induces physiological and morphological changes in the organisms, but excessive training loads may induce damage and impair recovery or muscle growth. The purpose of the study was to evaluate the impact of Silymarin (SM) consumption on endurance capacity, muscle/cardiac histological changes, bodyweight, and food intake in rats subjected to 60 min of regular exercise training (RET) five days per week. (2) Methods: Male Wistar rats were subjected to an eight-week RET treadmill program and were previously administered SM and vitamin C. Bodyweight and food consumption were measured and registered. The maximal endurance capacity (MEC) test was performed at weeks one and eight. After the last training session, the animals were sacrificed, and samples of quadriceps/gastrocnemius and cardiac tissue were obtained and process for histological analyzes. (3) Results: SM consumption improved muscle recovery, inflammation, and damaged tissue, and promoted hypertrophy, vascularization, and muscle fiber shape/appearance. MEC increased after eight weeks of RET in all trained groups; moreover, the SM-treated group was enhanced more than the group with vitamin C. There were no significant changes in bodyweight and in food and nutrient consumption along the study. (5) Conclusion: SM supplementation may enhance physical performance, recovery, and muscle hypertrophy during the eight-week RET program.


2015 ◽  
Vol 119 (7) ◽  
pp. 831-839 ◽  
Author(s):  
Pavarana Vutthasathien ◽  
Jonggonnee Wattanapermpool

Data from the trial known as Testosterone in Older Men with Mobility Limitations (TOM) has indicated an association between testosterone administration and a greater risk for adverse cardiovascular events. We therefore propose that regular exercise is a cardioprotective alternative that prevents detrimental changes in contractile activation when a deficiency in male sex hormones exists. Ten-week-old orchidectomized (ORX) rats were subjected to a 9-wk treadmill running program at moderate intensity starting 1 wk after surgery. Although exercise-induced cardiac hypertrophy was observed both in rats that underwent ORX and sham surgery, regular exercise enhanced cardiac myofilament Ca2+ sensitivity and myosin light-chain 2 phosphorylation only in rats that underwent a sham operation. Although the rats that had sham surgery and and given exercise exhibited no change in maximum developed tension, regular running prevented the suppression of maximum active tension in the hearts of ORX rats. Regular exercise also prevented a shift in myosin heavy chain (MHC) isoforms toward β-MHC, a reduction in sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) activity, and an increase in SERCA sensitivity in the hearts of ORX rats. Neither SERCA content nor its modulating component, phospholamban (PLB), was altered by exercise in either sham-operated or ORX rats. However, decreases in the phosphorylated Thr17 form of PLB and the phosphorylated Thr287 form of Ca2+/calmodulin-dependent kinase II in the hearts of ORX rats were abolished after regular exercise. These results thus support the use of regular running as a cardioprotective alternative to testosterone replacement in hypogonadal conditions.


2012 ◽  
Vol 303 (2) ◽  
pp. R127-R134 ◽  
Author(s):  
Erika Koltai ◽  
Nikolett Hart ◽  
Albert W. Taylor ◽  
Sataro Goto ◽  
Jenny K. Ngo ◽  
...  

A decline in mitochondrial biogenesis and mitochondrial protein quality control in skeletal muscle is a common finding in aging, but exercise training has been suggested as a possible cure. In this report, we tested the hypothesis that moderate-intensity exercise training could prevent the age-associated deterioration in mitochondrial biogenesis in the gastrocnemius muscle of Wistar rats. Exercise training, consisting of treadmill running at 60% of the initial V̇o2max, reversed or attenuated significant age-associated (detrimental) declines in mitochondrial mass (succinate dehydrogenase, citrate synthase, cytochrome- c oxidase-4, mtDNA), SIRT1 activity, AMPK, pAMPK, and peroxisome proliferator-activated receptor gamma coactivator 1-α, UCP3, and the Lon protease. Exercise training also decreased the gap between young and old animals in other measured parameters, including nuclear respiratory factor 1, mitochondrial transcription factor A, fission-1, mitofusin-1, and polynucleotide phosphorylase levels. We conclude that exercise training can help minimize detrimental skeletal muscle aging deficits by improving mitochondrial protein quality control and biogenesis.


2016 ◽  
Vol 86 (1-2) ◽  
Author(s):  
Francesco Giallauria ◽  
Neil Andrew Smart ◽  
Antonio Cittadini ◽  
Carlo Vigorito

Exercise training (ET) is strongly recommended in patients with chronic heart failure (CHF). Moderate-intensity aerobic continuous ET is the best established training modality in CHF patients. In the last decade, however, high-intensity interval exercise training (HIIT) has aroused considerable interest in cardiac rehabilitation community. Basically, HIIT consists of repeated bouts of high-intensity exercise alternated with recovery periods. In CHF patients, HIIT exerts larger improvements in exercise capacity compared to moderate-continuous ET. These results are intriguing, mostly considering that better functional capacity translates into an improvement of symptoms and quality of life. Notably, HIIT did not reveal major safety issues; although CHF patients should be clinically stable, have had recent exposure to at least regular moderate-intensity exercise, and appropriate supervision and monitoring during and after the exercise session are mandatory. The impact of HIIT on cardiac dimensions and function and on endothelial function remains uncertain. HIIT should not replace other training modalities in heart failure but should rather complement them. Combining and tailoring different ET modalities according to each patient’s baseline clinical characteristics (i.e. exercise capacity, personal needs, preferences and goals) seem the most astute approach to exercise prescription.


2017 ◽  
Vol 49 (5S) ◽  
pp. 157
Author(s):  
Amanda Q.x. Nio ◽  
Eric J. Stöhr ◽  
Samantha Rogers ◽  
Rachel Mynors-Wallis ◽  
Jane M. Black ◽  
...  

2021 ◽  
Vol 34 ◽  
Author(s):  
Frederico Souzalima Caldoncelli FRANCO ◽  
Antônio José NATALI ◽  
Neuza Maria Brunoro COSTA

ABSTRACT Objective To evaluate the impact of low to moderate aerobic exercise and ovariectomy on body composition and food consumption in female rats. Methods Forty adult Wistar female rats (age: 23 weeks; body weight: 275.2±3.6g; mean±SEM) were divided into 4 groups (n=10): laparotomy-sedentary; laparotomy-exercised; ovariectomy-sedentary; and ovariectomy-exercised. The exercised groups were submitted to a treadmill running program (16m/min; 30min/day, 5 days/week), for 8 weeks. Body weight and food consumption were monitored during the experiment. Visceral fat and carcass water, protein, ash, fat and carbohydrate fractions were analyzed. Two-way ANOVA plus the Tukey’s post hoc test was used for comparisons and p<0.05 was considered significant. Results The ovariectomized (ovariectomy-sedentary+ovariectomy-exercised) and sedentary (laparotomy-sedentary+ovariectomy-sedentary) animals showed higher (p<0.05) weight gain, food consumption, food efficiency ratio and weight gain/body weight ratio than laparotomy animals (laparotomy-sedentary+laparotomy-exercised) and exercised (exercised laparotomy+exercised ovariectomy), respectively. The ovariectomized and sedentary animals showed higher (p<0.05) carcass weight, fat percentage and visceral fat than laparotomy and exercised rats, respectively. Conclusion Ovariectomy and physical inactivity increase obesogenic indicators, whereas regular aerobic exercise of low to moderate intensity attenuates these unfavorable effects in female rats.


2018 ◽  
Vol 125 (2) ◽  
pp. 401-408 ◽  
Author(s):  
Andrew Haynes ◽  
Matthew D. Linden ◽  
Elisa Robey ◽  
Louise H. Naylor ◽  
Philip N. Ainslie ◽  
...  

Platelet activation, including the formation of monocyte platelet aggregates (MPAs), contributes to atherosclerosis, thrombus formation, and acute coronary syndromes. Regular participation in exercise can lower cardiovascular risk, but little is known regarding the impact of exercise training on platelet function. We investigated the effect of 6 mo of walking exercise on platelet function in sedentary older adults without significant cardiovascular disease. Twenty-seven participants were randomly allocated to 6 mo of either: no-exercise ( n = 13) or 3 × 50 min/wk of supervised center-based walking ( n = 14). Circulating and agonist-induced MPAs were assessed using flow cytometry before [ month 0 (0M)] and after [ month 6 (6M)] the intervention. Circulating MPAs increased from 0M (3.7 ± 1.0%) to 6M (4.7 ± 1.6%) in the no-exercise group ( P = 0.009), whereas a nonsignificant decrease was observed in the walking group (0M 4.3 ± 1.7 vs. 6M 3.7 ± 1.2 %, P = 0.052). The change in MPAs between groups was significant ( P = 0.001). There were no differences between groups in platelet responses to agonists across the interventions (all P > 0.05). Collectively, these data suggest that the absence of regular exercise may increase MPAs, which are cellular mediators involved in atherosclerosis, while regular walking inhibits such increases. The thrombotic function of platelets appears to be relatively unaltered by exercise training. This study provides novel data related to the cardioprotective effects associated with participation in exercise.NEW & NOTEWORTHY Monocyte-platelet aggregates contribute to atherosclerosis and exercise can lower cardiovascular risk. This is the first study to discover that a lack of regular physical activity is associated with increased monocyte-platelet aggregates over a 6-mo intervention period. In contrast, walking exercise inhibits increased monocyte-platelet aggregates in the circulation. This study highlights a novel pathway by which regular participation in exercise exerts its cardioprotective effects.


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