scholarly journals Early Moderate Intensity Aerobic Exercise Intervention Prevents Doxorubicin-caused Cardiac Dysfunction through Inhibition of Cardiac Fibrosis and Inflammation

Cancers ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1102
Author(s):  
Hsin-Lun Yang ◽  
Pei-Ling Hsieh ◽  
Ching-Hsia Hung ◽  
Hui-Ching Cheng ◽  
Wan-Ching Chou ◽  
...  
Keyword(s):  
Cardiac Dysfunction ◽  
Cardiac Fibrosis ◽  
Exercise Intervention ◽  
Treadmill Exercise ◽  
Cardiac Injury ◽  
Treated Group ◽  
Exercise Group ◽  
Moderate Intensity ◽  
Cardiac Damage ◽  
Creatine Kinase Mb

Doxorubicin (DOX) is known as an effective drug in the fight against various cancers. However, one of the greatest impediments is DOX-induced cardiomyopathy, which may potentially lead to heart failure. Accumulating evidence has shed light on the pathological mechanism of DOX-induced cardiotoxicity, but treatments to mitigate the cardiac damage are still required. In an attempt to address this issue, we evaluated whether exercise provides cardioprotective effects on the DOX-induced cardiotoxicity. We showed that treadmill exercise (3 times/week; 1-week of exercise acclimatization and 4-weeks of endurance exercise) during the DOX treatment successfully prevented the cardiac dysfunction. The DOX-stimulated expression of IκBα, NF-κB, COX-2, and IL-8 were all downregulated by exercise as well as the fibrosis factors (TGF-β1, phosphorylated ERK, Sp1, and CTGF). Moreover, we showed that treadmill exercise diminished the expression of several cardiac remodeling-associated factors, such as FGF2, uPA, MMP2, and MMP9. These results were in line with the finding that exercise intervention reduced cardiac fibrosis and restored cardiac function, with higher values of ejection fraction and fractional shortening compared to the DOX-treated group. Two commonly used indicators of cardiac injury, lactate dehydrogenase, and creatine kinase-MB, were also decreased in the exercise group. Collectively, our results suggested that it may be beneficial to prescribe treadmill exercise as an adjunct therapy to limit cardiac damage caused by DOX.

scholarly journals The effects of an individualized exercise intervention on body composition in breast cancer patients undergoing treatment

2007 ◽  
Vol 125 (1) ◽  
pp. 22-28 ◽  
Author(s):  
Claudio Battaglini ◽  
Martim Bottaro ◽  
Carolyn Dennehy ◽  
Logan Rae ◽  
Edgar Shields ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Body Composition ◽  
Resistance Training ◽  
Cancer Treatment ◽  
Cancer Patients ◽  
Exercise Intervention ◽  
Exercise Group ◽  
Moderate Intensity ◽  
Control Group ◽  
Breast Cancer Patients

CONTEXT AND OBJECTIVE: Changes in metabolism have been reported in the majority of patients undergoing cancer treatment, and these are usually characterized by progressive change in body composition. The effects of aerobic exercise programs to combat the cancer and cancer treatment-related side effects, which include the negative changes in body composition, have been extensively reported in the literature. However, few resistance exercise intervention studies have hypothesized that breast cancer patients might benefit from this type of exercise. The purpose of this study was to determine whether exercise protocols that emphasize resistance training would change body composition and strength in breast cancer patients undergoing treatment. DESIGN AND SETTING: Randomized controlled trial, at the Campus Recreation Center and Rocky Mountain Cancer Rehabilitation Institute of the University of Northern Colorado, and the North Colorado Medical Center. METHODS: Twenty inactive breast cancer patients were randomly assigned to a 21-week exercise group (n = 10) or a control group (n = 10). The exercise group trained at low to moderate intensity for 60 minutes on two days/week. The primary outcome measurements included body composition (skinfold method) and muscle strength (one repetition maximum). RESULTS: Significant differences in lean body mass, body fat and strength (p = 0.004, p = 0.004, p = 0.025, respectively) were observed between the groups at the end of the study. CONCLUSION: The results suggest that exercise emphasizing resistance training promotes positive changes in body composition and strength in breast cancer patients undergoing treatment.

scholarly journals Renovascular hypertension induces myocardial mitochondrial damage, contributing to cardiac injury and dysfunction in pigs with metabolic syndrome

2020 ◽  
Author(s):  
Arash Aghajani Nargesi ◽  
Mohamed C Farah ◽  
Xiang-Yang Zhu ◽  
Lei Zhang ◽  
Hui Tang ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Renovascular Hypertension ◽  
Cardiac Fibrosis ◽  
Cardiac Injury ◽  
Left Ventricular ◽  
Mitochondrial Damage ◽  
Mitochondrial Morphology ◽  
H2o2 Production ◽  
Cardiac Damage ◽  
Cardiovascular Morbidity And Mortality

Abstract Background Subjects with renovascular hypertension (RVH) often manifest with metabolic syndrome (MetS) as well. Coexisting MetS and hypertension increases cardiovascular morbidity and mortality, but the mechanisms underlying cardiac injury remain unknown. We hypothesized that superimposition of MetS induces myocardial mitochondrial damage, leading to cardiac injury and dysfunction in swine RVH. Methods Pigs were studied after 16 weeks of diet-induced MetS with or without RVH (unilateral renal artery stenosis), and Lean controls (n=6 each). Systolic and diastolic cardiac function were assessed by multi-detector CT, and cardiac mitochondrial morphology (transmission electron microscopy) and myocardial function in tissue and isolated mitochondria. Results Body weight was similarly higher in MetS groups vs. Lean. RVH groups achieved significant stenosis and developed hypertension. Mitochondrial matrix density and ATP production were lower and H2O2 production higher in RVH groups versus Lean and MetS. Lean+RVH (but not MetS+RVH) activated mitophagy, which was associated with decreased myocardial expression of mitophagy-related microRNAs. MetS groups exhibited higher numbers of inter-mitochondrial junctions (IMJs), which could have prevented membrane depolarization/activation of mitophagy in MetS+RVH. Cardiac fibrosis, hypertrophy (increased left ventricular muscle mass), and diastolic function (decreased E/A ratio) were greater in MetS+RVH versus Lean+RVH. Conclusions Superimposition of MetS on swine RVH induces myocardial mitochondrial damage and dysfunction. MetS+RVH failed to activate mitophagy, resulting in greater cardiac remodeling, fibrosis, and diastolic dysfunction. Mitochondrial injury and impaired mitophagy may constitute important mechanisms and potential therapeutic targets to ameliorate cardiac damage and dysfunction in patients with coexisting MetS and RVH.

scholarly journals 5TNF-α and IL-1β Neutralization Ameliorates Angiotensin II-Induced Cardiac Damage in Male Mice

Endocrinology ◽  
2014 ◽  
Vol 155 (7) ◽  
pp. 2677-2687 ◽  
Author(s):  
Yueli Wang ◽  
Yulin Li ◽  
Yina Wu ◽  
Lixin Jia ◽  
Jijing Wang ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Adhesion Molecule ◽  
Cardiac Fibrosis ◽  
Smooth Muscle Actin ◽  
Cardiac Injury ◽  
Intercellular Adhesion Molecule ◽  
Ang Ii ◽  
Cardiac Damage ◽  
Inflammatory Infiltration ◽  
Tnf Α

Inflammation is a key event in hypertensive organ damage, and TNF-α and IL-1β are elevated in hypertension. In this study, we evaluated the effects of TNF-α and IL-1β elevation on hypertensive cardiac damage by treatment with a bifunctional inflammatory inhibitor, TNF receptor 2-fragment crystalization-IL-1 receptor antagonist (TFI), which can neutralize these 2 cytokines simultaneously. A mouse hypertension model of angiotensin II (Ang II) infusion (1500 ng/kg·min for 7 d) was induced in wild-type mice. TNF-α and IL-1β were inhibited by TFI administration (5 mg/kg, every other day), the effects of inhibition on cardiac damage were examined, and its mechanism on inflammatory infiltration was further studied in vivo and in vitro. Ang II infusion induced cardiac injury, including increased macrophage infiltration, expression of inflammatory cytokines (IL-12, IL-6, etc), and cardiac fibrosis, such as elevated α-smooth muscle actin, collagen I, and TGF-β expression. Importantly, the Ang II-induced cardiac injury was suppressed by TFI treatment. Moreover, TFI reduced the expression of adhesion molecules (intercellular adhesion molecule-1 and vascular cell adhesion molecule-1) and monocyte chemotactic protein-1 expression in Ang II-treated hearts. Additionally, blockade of TNF-α and IL-1β by TFI reduced monocyte adherence to endothelia cell and macrophage migration. This study demonstrates that blocking TNF-α and IL-1β by TFI prevents cardiac damage in response to Ang II, and targeting these 2 cytokines simultaneously might be a novel tool to treat hypertensive heart injury.

scholarly journals PO-271 Effects of accumulated exercise with different intensities on insulin resistance in mice

2018 ◽  
Vol 1 (5) ◽  
Author(s):  
Yuli Zhang ◽  
Songtao Wang ◽  
Fei Liang ◽  
Xiangyu Shuai ◽  
Weibao Liang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
High Intensity ◽  
Exercise Intervention ◽  
Exercise Program ◽  
Exercise Group ◽  
The Body ◽  
Moderate Intensity ◽  
Control Group ◽  
Continuous Exercise

Objective The aim of this study was to investigate the effect of 8-week moderate-intensity and high-intensity accumulated exercise on insulin resistance in mice, compared with the moderate intensity continuous exercise with equal workload, which will provide an experimental reference for seeking a more reasonable and effective exercise program to break sedentary behavior and improve metabolic diseases such as IR. Methods Eighty 4-week-old C57BL/6J mice were randomly divided into normal diet group (group C) and high-fat diet group (group H), fed with different diet. At the 10th weekend, insulin resistance model was judged by OGTT curve (AUC) and fasting blood glucose. All mice with insulin resistance were randomly divided into four groups: IR control group (IC), IR moderate-intensity continuous exercise group (IE), IR moderate-intensity accumulated exercise group (IM), IR high-intensity accumulated exercise group (IH), retained normal diet control group (C), with 12 mice for each group. All groups were fed with normal feed. The three exercise-related group performed an 8-week’s treadmill exercise program with equal workload (involve preparation and relaxation activities,0°platform slope, 5 days/week). For IE group, mice run 50min continuously with the velocity of 11m/min. For IM group，mice exercised 12.5 min per session, total 4 sessions per day, with 3-hour’s interval and the velocity of 11m/min. The IH group performed an alike exercise program with IM group, except the running speed (19m/min) and exercise time (7.5min). On the 8th weekend of exercise, FBG, OCTT, FINS, HOME- IR, and ISI were tested for each groups. Results 1. Compared with group C, body weight, FBG and OGTT-AUC were significantly increased in group H (P<0.05 or P<0.01). 76% mice were induced to insulin resistance successfully.  2. Before and after exercise intervention of 8 weeks, there were no significant changes in body weight and OGTT-AUC, while the FBG was significantly increased in IC group (P<0.05). Body weight, FBG, and OGTT-AUC significantly decreased in IE group, IM group and IH group (P<0.05 or P<0.01). 3. After 8 weeks of exercise intervention, the FBG in the IE group, IM group, and IH group were significantly lower than that in C group (P<0.05 or P<0.01). Compared with the IC group, the FBG, FINS, OGTT-AUC, and HOME-IR in IM group, IH group and IE group were lower than those in the IC group (P<0.05 or P<0.01). Compared with the IE group, the body weight and HOME-IR index of IH group were significantly lower than those in IE group (P<0.01). Compared with IH group, the HOME-IR in IH group was lower than that in IM group (P<0.05); There was no significant difference between IM group and IE group. Conclusions 1. Chronic moderate-intensity continuous exercise, moderate-intensity accumulated exercise, and high-intensity accumulated exercise all can effectively improve the glucose metabolism and insulin resistance in IR mice. 2.Compared with moderate-intensity accumulated exercise and moderate-intensity continuous exercise, the high-intensity accumulated exercise with equal workload is more effective in reducing the body weight and improving insulin resistance in IR mice.  

Inhibition of IκB phosphorylation prevents load-induced cardiac dysfunction in mice

2012 ◽  
Vol 303 (12) ◽  
pp. H1435-H1445 ◽  
Author(s):  
Tetsu Tanaka ◽  
Masahito Ogawa ◽  
Jun-ichi Suzuki ◽  
Asuka Sekinishi ◽  
Akiko Itai ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Cardiac Dysfunction ◽  
Cardiac Fibrosis ◽  
Nuclear Translocation ◽  
Pressure Overload ◽  
Treated Group ◽  
Left Ventricular ◽  
Matrix Metalloproteinase 2 ◽  
Cardiomyocyte Hypertrophy ◽  
Iκb Kinase

Pressure overload is known to be a cause of cardiac hypertrophy that often transits to heart failure. Although nuclear factor (NF)-κB is a key factor in the progression of cardiac hypertrophy, its pathophysiology is yet to be elucidated. Thus, we aimed to show that inhibition of NF-κB activation improves pressure overload-induced cardiac dysfunction. To assess the effect of inhibition on NF-κB activation in pressure overload cardiac hypertrophy, we used IMD-1041 in a murine thoracic aortic constriction (TAC) model. IMD-1041 inhibits the phosphorylation of IκB via inhibition of IκB kinase-β. IMD-1041 (100 mg·kg−1·day−1) or vehicle was administered orally into mice once a day, and mice were euthanized on day 42 after TAC. TAC resulted in left ventricular wall thickening, cardiac dysfunction, and increases of heart and lung weight, whereas IMD-1041 significantly suppressed the development of cardiac hypertropy 6 wk after TAC. Histologically, developed cardiac fibrosis and cardiomyocyte hypertrophy occurred in the vehicle-treated group, whereas IMD-1041 significantly attenuated these changes. IMD-1041 suppressed the expression of p65-positive cells and nuclear translocation of p65 induced by TAC compared with vehicle. Matrix metalloproteinase-2 activity increased in the vehicle + TAC-treated group; however, it was suppressed in the IMD-1041 + TAC-treated group. IMD-1041 treatment from day 28 to day 42 after TAC significantly attenuated the decrease in the percentage of fractional shortening and cardiac fibrosis without an antihypertrophic effect. In conclusion, IMD-1041 may be useful for preventing pressure overload-induced cardiac dysfunction and the transition of cardiac hypertrophy to contraction failure via suppression of NF-κB activation.

scholarly journals Disruption of COX-2 modulates gene expression and the cardiac injury response to doxorubicin

2006 ◽  
Vol 291 (2) ◽  
pp. H532-H536 ◽  
Author(s):  
Tomas G. Neilan ◽  
Glen A. Doherty ◽  
Gang Chen ◽  
Catherine Deflandre ◽  
Hester McAllister ◽  
...  
Keyword(s):  
Gene Expression ◽  
Protein Kinase ◽  
Cardiac Dysfunction ◽  
Cell Apoptosis ◽  
Cardiac Fibrosis ◽  
Cardiac Injury ◽  
Cardiac Cell ◽  
Wild Type ◽  
Cox 2 ◽  
Prostacyclin Analog

To determine the role of cyclooxygenase (COX)-2 in anthracycline-induced cardiac toxicity, we administered doxorubicin (Dox) to mice with genetic disruption of COX-2 (COX-2−/−). After treatment with Dox, COX-2−/− mice had increased cardiac dysfunction and cardiac cell apoptosis compared with Dox-treated wild-type mice. The expression of the death-associated protein kinase-related apoptosis-inducing protein kinase-2 was also increased in Dox-treated COX-2−/− animals. The altered gene expression, cardiac injury, and dysfunction after Dox treatment in COX-2−/− mice was attenuated by a stable prostacyclin analog, iloprost. Wild-type mice treated with Dox developed cardiac fibrosis that was absent in COX-2−/− mice and unaffected by iloprost. These results suggest that genetic disruption of COX-2 increases the cardiac dysfunction after treatment with Dox by an increase in cardiac cell apoptosis. This Dox-induced cardiotoxicity in COX-2−/− mice was attenuated by a prostacyclin analog, suggesting a protective role for prostaglandins in this setting.

scholarly journals Effects of an Evidence-based Exercise Intervention on Clinical Outcomes in Breast Cancer Survivors: A Randomized Controlled Trial

2020 ◽  
Vol 22 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Junga Lee ◽  
Florence Vicil
Keyword(s):  
Breast Cancer ◽  
Cancer Survivors ◽  
Cardiorespiratory Fitness ◽  
Breast Cancer Survivors ◽  
Exercise Intervention ◽  
Handgrip Strength ◽  
Exercise Group ◽  
Moderate Intensity ◽  
Evidence Based ◽  
Strength Exercise

OBJECTIVES The number of breast cancer survivors throughout the world has increased. Breast cancer survivors need to know how to exercise to improve their clinical outcomes. The purpose of this study was to find the effects of an evidence-based combined exercise intervention on the fitness levels of breast cancer survivors.METHODS A total of 38 female breast cancer survivors were randomly assigned to an exercise group (n=19) or a control group who did usual care (n=19). Subjects in the exercise group participated eight weeks of moderate intensity aerobic exercise and bodyweight strength exercise three times per week. Weight, body mass index (BMI), cardiorespiratory fitness, handgrip strength, and flexibility were measured to assess the effects of the exercise intervention.RESULTS Women who completed the exercise intervention had decreased weight and BMI and increased cardiorespiratory fitness, handgrip strength, and flexibility.CONCLUSIONS Breast cancer survivors had improved health outcomes. A combined exercise intervention of moderate intensity three times per week for eight weeks can help breast cancer survivors improve their health. Participating in aerobic exercise and bodyweight strength exercise, which provide dynamic movements and use large muscle groups with no equipment, can help increase physical fitness levels of breast cancer survivors.

scholarly journals Cardiovascular Metrics Associated With Prevention of Aging-Related Parkinsonian Signs Following Exercise Intervention in Sedentary Older Rats

2021 ◽  
Vol 13 ◽  
Author(s):  
Ella A. Kasanga ◽  
Joel Little ◽  
Tamara R. McInnis ◽  
Nicoleta Bugnariu ◽  
J. Thomas Cunningham ◽  
...  
Keyword(s):  
Exercise Intervention ◽  
Treadmill Exercise ◽  
Motor Impairment ◽  
Rest Period ◽  
Male Rats ◽  
Moderate Intensity ◽  
Physically Active ◽  
Exercise Regimen ◽  
Active Lifestyles ◽  
Intensity Of Exercise

Preservation of motor capabilities is vital to maintaining independent daily living throughout a person's lifespan and may mitigate aging-related parkinsonism, a progressive and prevalent motor impairment. Physically active lifestyles can mitigate aging-related motor impairment. However, the metrics of physical activity necessary for mitigating parkinsonian signs are not established. Consistent moderate intensity (~10 m/min) treadmill exercise can reverse aging-related parkinsonian signs by 20 weeks in a 2-week on, 2-week off, regimen in previously sedentary advanced middle-aged rats. In this study, we initiated treadmill exercise in sedentary 18-month-old male rats to address two questions: (1) if a rest period not longer than 1-week off exercise, with 15 exercise sessions per month, could attenuate parkinsonian signs within 2 months after exercise initiation, and the associated impact on heart rate (HR) and mean arterial pressure (MAP) and (2) if continuation of this regimen, up to 20 weeks, will be associated with continual prevention of parkinsonian signs. The intensity and frequency of treadmill exercise attenuated aging-related parkinsonian signs by 8 weeks and were maintained till 23 months old. The exercise regimen increased HR by 25% above baseline and gradually reduced pre-intervention MAP. Together, these studies indicate that a practicable frequency and intensity of exercise reduces parkinsonian sign severity commensurate with a modest increase in HR after exercise. These cardiovascular changes provide a baseline of metrics, easily measured in humans, for predictive validity that practicable exercise intensity and schedule can be initiated in previously sedentary older adults to delay the onset of aging-related parkinsonian signs.

Abstract 19037: Exercise Reduces 24-hr Blood Pressure and Albuminuria in Patients with Moderate Diabetic Kidney Disease

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Ulf G Bronas ◽  
Marc Weber ◽  
Paul Drawz ◽  
John Bantle ◽  
Daniel Duprez ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Kidney Disease ◽  
Exercise Training ◽  
Exercise Intervention ◽  
Intervention Group ◽  
Exercise Group ◽  
Moderate Intensity ◽  
Control Group ◽  
Inverse Association ◽  
Moderate Intensity Exercise

Introduction: Observational studies have shown an inverse association between physical function and CVD mortality in patients with chronic kidney disease (CKD) through unknown mechanisms. We have previously reported a significant exercise-induced reduction in resting blood pressure (BP) in 85 patients with stage 2-4 type 2 diabetes related CKD (DKD). The efficacy of exercise to reduce 24-hour ambulatory blood pressure (ABP) and albumin-creatinine ratio (ACR) is unclear. The purpose of this study was to test the hypothesis that 12wks of exercise would reduce 24-hr ABP and ACR in patients with stage 3-4 DKD and hypertension, compared to the control group. Methods: We randomly assigned 28 participants (21 male, age 62.9 yrs, BMI 34.8 kg/m2) with stage 3-4 DKD and hypertension (141(17)/75 (10) mmHg) to either 12-wks of moderate-intensity exercise training, 4x/wk for 45 minutes (n=15) or a usual medical care control group (n=13). The primary endpoint was change in 24-hr ABP at 12-wks. Results: There were no significant differences between groups in baseline demographic or medical variables. There were no changes in pharmacological variables at 12-week follow-up; group comparisons were analyzed by ANCOVA using baseline and exercise performed as covariates. Systolic BP levels and ACR were significantly reduced in the exercise-intervention group compared to the control group (Table 1). Reductions in diastolic BP levels were not significant between groups. Heart rate variables did not differ between groups. There was a strong inverse association between change in aerobic capacity and change in systolic and diastolic BP levels in the exercise group only (r=-.56, p=.039, and -.66, p=.011). Conclusion: This study suggests that exercise training imparts a favorable modulation of BP levels and ACR in patients with stage 3-4 DKD, potentially providing insight into the cardioprotective effect of exercise in this population.

scholarly journals Exercising before a nap benefits memory better than napping or exercising alone

SLEEP ◽  
2020 ◽  
Vol 43 (9) ◽  
Author(s):  
Melodee Mograss ◽  
Monica Crosetta ◽  
Joanne Abi-Jaoude ◽  
Elizaveta Frolova ◽  
Edwin M Robertson ◽  
...  
Keyword(s):  
Visual Recognition ◽  
Exercise Intervention ◽  
Exercise Group ◽  
Moderate Intensity ◽  
Long Term Memory ◽  
Learning Session ◽  
Beneficial Effects ◽  
Exercise Condition ◽  
Equivalent Time ◽  
Main Effects

Abstract Sleep leads to the enhancement of memory, and physical exercise also improves memory along with beneficial effects on sleep quality. Potentially, sleep and exercise may operate independently upon memory; alternatively, they may operate synergistically to boost memory above and beyond exercise or sleep alone. We tested this hypothesis in 115 young healthy adults (23 ± 3.9 years) randomly allocated to one of the four conditions in a 2 (exercise vs. no exercise) × 2 (nap vs. no nap) design. The exercise intervention consisted of a 40-minute, moderate intensity cycling, while the no exercise condition was an equivalent period of rest. This was followed by a learning session in which participants memorized a set of 45 neutral pictures for a later test. Subsequently, participants were exposed to either a 60-minute sleep period (nap) or an equivalent time of resting wakefulness, followed by a visual recognition test. We found a significant interaction between the effects of exercise and nap (p = 0.014, η p2 = 0.053), without significant main effects of exercise or nap conditions. Participants who experienced both exercise plus nap were significantly more accurate (83.8 ± 2.9) than those who only napped (81.1 ± 5.4, p = 0.027) and those who only exercised (78.6 ± 10.3, p = 0.012). Within the combined nap plus exercise group, higher recognition accuracies were associated with higher sleep spindle densities (r = 0.46, p = 0.015). Our results demonstrate that short-term exercise and a nap improve recognition memory over a nap or exercise alone. Exercise and sleep are not independent factors operating separately upon memory but work together to enhance long-term memory.

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