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High-Intensity Interval and Aerobic Training Alleviate Cardiac Pathology, Apoptosis, and Atrial Fibrillation in Rats
Sina Rokhsati1, Nazanin Shahsavari1, Shahram Rabbani2
1Department of Exercise Physiology, Faculty of Physical Education and Sport Sciences, University of Tehran, Tehran 1417935840, Iran.
Insights
High-intensity interval training (HIIT) and aerobic training (AT) improve cardiovascular health in chronic kidney disease (CKD) rats by modulating FGF23 and Klotho levels, reducing cardiac issues, and improving mineral metabolism.
Area of Science:
- Nephrology
- Cardiology
- Exercise Physiology
Background:
- Chronic kidney disease (CKD) is associated with significant metabolic and cardiovascular complications.
- Fibroblast growth factor 23 (FGF23) and Klotho dysregulation are central to CKD pathophysiology.
- Understanding the impact of exercise on these pathways is crucial for managing CKD complications.
Purpose of the Study:
- To investigate the effects of high-intensity interval training (HIIT) and moderate aerobic training (AT) on FGF23, Klotho, mineral metabolism, apoptosis, and atrial fibrillation (AF) in a rat model of CKD.
- To evaluate exercise as a non-pharmacological intervention for CKD-related cardiovascular and metabolic disturbances.
Main Methods:
- A rat model of CKD was established using 5/6 nephrectomy.
- Thirty-five Wistar rats were divided into control, sham, CKD, CKD + HIIT, and CKD + AT groups.
- Exercise interventions (HIIT or AT) were conducted for eight weeks, followed by measurements of cardiac parameters, blood biomarkers (FGF23, Klotho, minerals), apoptosis markers (BAX, Bcl2), and AF.
Main Results:
- Both HIIT and AT reduced heart weight and attenuated CKD-induced increases in FGF23 and decreases in Klotho.
- Exercise interventions improved mineral metabolism (phosphate, PTH, vitamin D) and modulated apoptosis markers (decreased BAX, increased Bcl2).
- Cardiac function was improved, and the duration of atrial fibrillation (AF) was reduced in exercise groups.
Conclusions:
- Exercise, including both HIIT and AT, can ameliorate cardiovascular and metabolic complications associated with CKD.
- Modulation of the FGF23 and Klotho pathways appears to be a key mechanism by which exercise exerts its beneficial effects.
- Exercise represents a promising non-pharmacological strategy for managing CKD patients.
Abstract:
Chronic kidney disease (CKD) leads to metabolic and cardiovascular complications, and the dysregulation of key biomolecules, namely fibroblast growth factor 23 (FGF23) and Klotho, plays a central role. This study investigated the effects of high-intensity interval training (HIIT) and moderate aerobic training (AT) on FGF23, Klotho, mineral metabolism, apoptosis markers (BAX, Bcl2), and atrial fibrillation (AF) in a rat CKD model. The study used 35 Wistar rats randomly assigned to control (CTL), sham (SH), CKD, CKD + HIIT, and CKD + AT groups. CKD was induced by 5/6 nephrectomy surgery. Exercise interventions consisted of eight weeks of HIIT (80-100% of maximum speed, 24-54 min/week) or AT (45-55% of maximum speed, 40-60 min/week), conducted three times weekly on a treadmill. We measured heart weight, blood levels of FGF23, Klotho, and mineral metabolism markers, as well as the heart expression of apoptosis proteins (i.e., BAX, Bcl2) and atrial fibrillation (AF). Both exercise types reduced the heart weight and heart/body weight ratio; attenuated CKD-induced elevations in FGF23 and reductions in Klotho; improved blood levels of phosphate, PTH, and vitamin D; and modulated apoptotic markers by decreasing BAX and increasing Bcl2 levels. Exercise improved cardiac function and reduced the AF duration. These findings emphasize that exercise could be a helpful non-pharmacological intervention to ameliorate CKD-induced cardiovascular and metabolic disturbances through the modulation of the FGF23 and Klotho pathways.
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