ArticleJournal of applied physiology (Bethesda, Md. : 1985)2009
Exercise training during diabetes attenuates cardiac ryanodine receptor dysregulation.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.
- Reprogramming heart failure: physiological orchestration and mechanistic decoding of exercise benefits.BMC cardiovascular disorders · 2025Pooled it
- Metabolic stress exacerbates CaExperimental physiology · 2026Article
- Lymphatic pumping failure in the arm precedes dermal backflow and breast cancer-related lymphedema.Breast cancer research : BCR · 2026Article
- Cardiac Cell Remodeling in Obesity and Diabetes.Handbook of experimental pharmacology · 2026Review
- Ablation of mitochondrial calcium uniporter alleviates cardiac dysfunction in type 1 diabetes.Cell calcium · 2026Article
- Calcium Signaling and Cardiac Adaptation to Stress: Focus on Pregnancy and Diabetes.Biomolecules · 2025Review
- Exercise Empowerment: A Multifaceted Anatomy in Managing Diabetic Myocardial Disorder.Journal of cardiovascular translational research · 2025Review
- Exercise in Diabetic Cardiomyopathy: Its Protective Effects and Molecular Mechanism.International journal of molecular sciences · 2025Review
- Ginsenoside Rb1 reduces oxidative/carbonyl stress damage and dysfunction of RyR2 in the heart of streptozotocin-induced diabetic rats.BMC cardiovascular disorders · 2024Article
- Protein carbonylation causes sarcoplasmic reticulum CaPflugers Archiv : European journal of physiology · 2024Article
- Protein carbonylation causes sarcoplasmic reticulum Ca2+ overload by increasing intracellular Na+ level in ventricular myocytes.Research square · 2024Article
- Diabetes-induced chronic heart failure is due to defects in calcium transporting and regulatory contractile proteins: cellular and molecular evidence.Heart failure reviews · 2023Review
- Differential changes in cyclic adenosine 3'-5' monophosphate (cAMP) effectors and major CaJournal of cellular and molecular medicine · 2023Article
- The high-intensity interval training (HIIT) and curcumin supplementation can positively regulate the autophagy pathway in myocardial cells of STZ-induced diabetic rats.BMC research notes · 2023Article
- Emerging Therapy for Diabetic Cardiomyopathy: From Molecular Mechanism to Clinical Practice.Biomedicines · 2023Review
- Effects of High-Intensity Interval Training and Continuous Training on Exercise Capacity, Heart Rate Variability and Isolated Hearts in Diabetic Rats.Arquivos brasileiros de cardiologia · 2023Article
- CaPflugers Archiv : European journal of physiology · 2022Review
- Heart failure in diabetes.Metabolism: clinical and experimental · 2021Review
- Calcium signaling in endocardial and epicardial ventricular myocytes from streptozotocin-induced diabetic rats.Journal of diabetes investigation · 2021Article
- Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The present study was undertaken to assess the effects of exercise training (ExT) initiated after the onset of diabetes on cardiac ryanodine receptor expression and function. Type 1 diabetes was induced in male Sprague-Dawley rats using streptozotocin (STZ). Three weeks after STZ injection, diabetic rats were divided into two groups. One group underwent ExT for 4 wk while the other group remained sedentary. After 7 wk of sedentary diabetes, cardiac fractional shortening, rate of rise of left ventricular pressure, and myocyte contractile velocity were reduced by 14, 36, 44%, respectively. Spontaneous Ca(2+) spark frequency increased threefold, and evoked Ca(2+) release was dyssynchronous with diastolic Ca(2+) releases. Steady-state type 2 ryanodine receptor (RyR2) protein did not change, but its response to Ca(2+) was altered. RyR2 also exhibited 1.8- and 1.5-fold increases in phosphorylation at Ser(2808) and Ser(2814). PKA activity was reduced by 75%, but CaMKII activity was increased by 50%. Four weeks of ExT initiated 3 wk after the onset of diabetes blunted decreases in cardiac fractional shortening and rate of left ventricular pressure development, increased the responsiveness of the myocardium to isoproterenol stimulation, attenuated the increase in Ca(2+) spark frequency, and minimized dyssynchronous and diastolic Ca(2+) releases. ExT also normalized the responsiveness of RyR2 to Ca(2+) activation, attenuated increases in RyR2 phosphorylation at Ser(2808) and Ser(2814), and normalized CaMKII and PKA activities. These data are the first to show that ExT during diabetes normalizes RyR2 function and Ca(2+) release from the sarcoplasmic reticulum, providing insights into mechanisms by which ExT during diabetes improves cardiac function.
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