Upregulation of Ryanodine Receptor Calcium Channels (RyR2) in Rats with Induced Diabetes after 4 Weeks of High Intensity Interval Training
Article Notes and Dates
International Cardiovascular Research Journal: March 31, 2016,
; e10311.Published Online: March 01, 2016
Article Type: Research Article; Received: May 09, 2015; Revised: August 18, 2015; Accepted: September 01, 2015
To Cite :
M A , Faramarzi
H , Gaeini
A A, Asghar Ravasi
A , Izadi
M R , et al. Upregulation of Ryanodine Receptor Calcium Channels (RyR2) in Rats with Induced Diabetes after 4 Weeks of High Intensity Interval Training,
Int Cardio Res J.
Copyright © 2016, Shiraz University of Medical Sciences. .
Background: To date, not sufficient information is available regarding the effect of High Intensity Interval Training (HIIT) on diabetes-induced myocardial dysfunctions.
Objectives: The present study aimed to evaluate the effect of 4-week HIIT on change in expression levels of ryanodine receptor calcium channel (RyR2) and ATPase calcium pump (SERCA2a) in diabetic rats.
Materials and Methods: This study was conducted on 24 Wistar rats with average weight of 245 ± 10 g. The rats were randomly divided into a sedentary diabetic group and a trained diabetic group. Training was started two weeks after diabetes induction by Streptozotocin (STZ) injection. The training program consisted of 4 weeks running on a treadmill and was considered to be intense for the two groups’ diabetic rats. After all, the animals’ characteristics and myocardial gene expression were compared using independent t-test.
Results: Measurement of gene expression by Real Time-PCR revealed that cardiac mRNA expression of RyR2 was enhanced in the HIIT group. The results also revealed a significant (P = 0.03) difference between the hearts of the sedentary controls and the trained group regarding RyR2 levels. However, no significant difference was observed between the two groups with respect to SERCA2a levels (P = 0.14).
Conclusions: The study results showed that treatment with HIIT could prevent and/or minimize the loss in expression of RyR2 and SERCA2a.