Document Type : Original Article
Department of Physical Education and Sport Science, Jolfa Branch, Islamic Azad University, Jolfa, Iran
Department of Biochemistry, School of Medicine, Tabriz Branch, Islamic Azad University, Tabriz, Iran
Neuroscience Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
4Department of Kinesiology, College of Agriculture, Health and Natural Resources, University of Connecticut, Connecticut, USA
The purpose of this study was to investigate the effect of moderate-intensity training on the calcineurin/ nuclear factor of activated t-cells (NFAT) pathway and factors affecting it in the middle-age Wistar rats.
Materials and Methods
In this experimental study, 40 young (n=10, 4-month-old) and middle-aged (n=30, 13-15 months old) Wistar rats were included in this experimental study. All young and 10 middle-aged rats did not training and served as a control comparision; while the remaining 20 middle-aged rats were trained at moderate intensity for 4-weeks (n=10) or 8-weeks (n=10) on a treadmill (speed: 16 m/minutes, slope: 0%, distance: 830 m, duration: 54 minutes).
Calcineurin tissue expression was increased in the middle-aged control rats compared to the young control rats (P=0.001). Expression of sarco/endoplasmic reticulum Ca2+ -ATPase (SERC2A), natriuretic peptide receptor-A (NPR-A), phospholamban (PLB), plasma membrane Ca2+ ATPase (PMCA4b), and p-AKT was significantly decreased in the heart tissue of middle-aged control compared to the young control rats (P=0.001). Furthermore, transforming growth factor beta (TGF-β), including transient receptor potential canonical 6 (TRPC6), were up-regulated in the heart tissue of middle-aged control compared to the young control rats (P=0.001). However, aerobic training inhibited this pathway and reversed all changes in the trained middle-aged rats.
Aerobic training effectively inhibited the calcineurin/NFATc pathway and modulated intracellular Ca2+ levels at least partially by restoring NPR-A, SERCA2, p-PLB, and p-AKT, and decreasing TRPC6 and TGF-β levels.