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Aerobic Training Improves Hypertensive‐Myocardium Mitochondria
Author(s) -
Godoy Coto Joshua,
Pereyra Erica,
Cavalli Fiorella,
Caldiz Claudia,
Yeves Alejandra,
Ennis Irene
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2021.35.s1.04381
Subject(s) - sed , mitochondrion , bioenergetics , aerobic exercise , medicine , intracellular , endocrinology , biology , cardiology , chemistry , microbiology and biotechnology
Essential hypertension develops a maladaptive cardiac remodeling that alters myocardial ultrastructure and induces mitochondrial dysfunction. On the other hand, aerobic training promotes a beneficial adaptive remodeling improving the heart phenotype and function. Both signaling pathways converge in the mitochondria affecting the cell fate, as they play a critical role in heart function, homeostasis, and bioenergetics. Despite this, the intracellular adaptations triggered by aerobic training on hypertensive‐myocardium mitochondria are not fully understood. Objective . To determine whether swimming training improves myocardial mitochondrial array, dynamics, and function in spontaneously hypertensive rats (SHR). Methods . 3‐month‐old male SHR were randomized to sedentary (Sed) or trained (Swim) groups. After an 8‐week (5 days/week) swimming protocol, the hearts were destined to transmission electron microscopy (TEM) imaging, RT‐PCR analysis, or mitochondrial isolation. Results are presented as mean ± SEM, except TEM data as median (IQR), and considered statistically different when p<0.05. Otherwise, the p‐value is stated. Animal handling protocols were approved by the Animal Welfare Committee of our establishment and were according to the FASEB Statement of Principles for the Use of Animals in Research and Education. Results . TEM images showed increased morphological values in Swim group: cross‐sectional area (μm 2 , Swim: 0.79 (0.74), Sed: 0.72 (0.71)) and aspect ratio (Swim: 1.90 (1.13), Sed: 1.60 (0.77)). We found a mitochondria‐sarcomere disarray in Sed and it trended to be restored by the aerobic training (clusters/photo, Swim: 4.63±1.07, Sed: 8.45±0.84, p=0.057). Training also modified mitochondrial dynamics (% vs Sed): mtDNA/nDNA: 153.9±21.6 (p=0.082); PGC1‐α: 149.19±19; DRP‐1: 309.4±77.5; MFN1: 59.0±8.2; PINK1: 209.9±49.4 (p=0.063). In addition, it improved: mitochondrial membrane potential (ΔΨm) (mV, Swim: ‐175.2±5.8, Sed: ‐148.6±9.2), calcium content (nmol/mg, Swim: 151.4±21.6, Sed: 87.6±17.8), and citrate synthase activity (μmol/min*mg, Swim: 0.87±0.03, Sed: 0.64±0.05). Conclusions Our results suggest that aerobic training: improved the mitochondrial‐sarcomere array, promoted a dysfunctional mitochondrial clearance process ‐reduced fusion and enhanced biogenesis, fission, and mitophagy‐, and improved mitochondrial function ‐ΔΨm, mitochondrial Ca +2 handling, and citrate synthase activity.