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Updated: Apr 22, 2026
Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
Published on: September 18, 2017
Effect of exercise training on Ca²⁺ release units of left ventricular myocytes of spontaneously hypertensive rats
M A Carneiro-Júnior1, J F Quintão-Júnior2, L R Drummond2
1Departamento de Ciências Fisiológicas, Universidade Federal do Espírito Santo, Vitória, ES, Brasil.
Insights
Endurance exercise training improved calcium handling in the hearts of hypertensive rats. Exercise normalized key proteins and calcium sparks, mitigating hypertension
Area of Science:
- Cardiovascular Physiology
- Molecular Cardiology
- Exercise Science
Background:
- Hypertension impairs cardiac calcium release unit function, affecting intracellular calcium handling.
- Calcium release units, crucial for cardiomyocyte contraction, are composed of sarcoplasmic reticulum calcium release channels.
- Defects in these units are linked to cardiovascular dysfunction in hypertensive states.
Purpose of the Study:
- To investigate if endurance exercise training can counteract hypertension-induced defects in cardiac calcium release units.
- To assess the impact of exercise on calcium release unit components and calcium sparks in spontaneously hypertensive rats.
- To determine the protective effects of exercise on left ventricular myocyte function under hypertensive conditions.
Main Methods:
- Spontaneously hypertensive rats and normotensive controls underwent an 8-week low-intensity treadmill running protocol.
- Gene expression analysis of ryanodine receptor type 2 (RyR2) and FK506 binding protein (FKBP12.6) was performed.
- Calcium sparks in left ventricular myocytes were measured, analyzing frequency, amplitude, and kinetics.
Main Results:
- Hypertension increased RyR2 gene expression and decreased FKBP12.6, altering calcium release unit composition.
- Exercise training reversed these gene expression changes, reducing RyR2 and normalizing FKBP12.6.
- Hypertension increased calcium spark frequency and decreased amplitude and duration; exercise partially reversed these alterations.
Conclusions:
- Endurance exercise training attenuates the detrimental effects of hypertension on cardiac calcium release units.
- Exercise normalizes key protein expression and improves calcium spark characteristics in hypertensive rat hearts.
- Regular exercise may serve as a therapeutic strategy to preserve cardiac function in hypertension.
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 hypertensive rats (4 months of age) were divided into 4 groups: normotensive (NC) and hypertensive control (HC), and normotensive (NT) and hypertensive trained (HT) animals (7 rats per group). NC and HC rats were submitted to a low-intensity treadmill running protocol (5 days/week, 1 h/day, 0% grade, and 50-60% of maximal running speed) for 8 weeks. Gene expression of the ryanodine receptor type 2 (RyR2) and FK506 binding protein (FKBP12.6) increased (270%) and decreased (88%), respectively, in HC compared to NC rats. Endurance exercise training reversed these changes by reducing RyR2 (230%) and normalizing FKBP12.6 gene expression (112%). Hypertension also increased the frequency of Ca²⁺ sparks (HC=7.61 ± 0.26 vs NC=4.79 ± 0.19 per 100 µm/s) and decreased its amplitude (HC=0.260 ± 0.08 vs NC=0.324 ± 0.10 ΔF/F0), full width at half-maximum amplitude (HC=1.05 ± 0.08 vs NC=1.26 ± 0.01 µm), total duration (HC=11.51 ± 0.12 vs NC=14.97 ± 0.24 ms), time to peak (HC=4.84 ± 0.06 vs NC=6.31 ± 0.14 ms), and time constant of decay (HC=8.68 ± 0.12 vs NC=10.21 ± 0.22 ms). These changes were partially reversed in HT rats (frequency of Ca²⁺ sparks=6.26 ± 0.19 µm/s, amplitude=0.282 ± 0.10 ΔF/F0, full width at half-maximum amplitude=1.14 ± 0.01 µm, total duration=13.34 ± 0.17 ms, time to peak=5.43 ± 0.08 ms, and time constant of decay=9.43 ± 0.15 ms). Endurance exercise training attenuated the deleterious effects of hypertension on calcium release units of left ventricular myocytes.
