The effect of preconditioning with high intensity interval training on cardioprotection and left ventricular function against Ischemia-reperfusion injury in male rats

Cardiac ischemia-reperfusion (IR) is one of the main causes of death in the world. Since exercise training is one of the practical ways to improve cardioprotection against these injuries, the purpose of the present study was to investigate the effect of preconditioning with a short term of high-intensity interval training on cardioprotection, left ventricular function and possible mechanisms.
In this study, 48 male rats (8-10 weeks and 250-300 g) were randomly divided into 5 groups: control (C), high-intensity interval training (H), sham (Sh), control談ⅺ梚reperfusion (CIR) and high-intensity interval training談ⅺ梚reperfusion (HIR). The high-intensity interval training protocol consisted of 5 consecutive treadmill running in 6×2 min high intermittence with 85-90% vo2max and 5×2 min slow intermittence with 55-60% Vo2max. Rats in CIR and HIR groups were exposed to cardiac IR injury. Infarct size, lactate dehydrogenase, creatine kinase, Kloth, and TRPC6 expression were measured and data were analyzed by one way ANOVA and Tukey's post-hoc tests.
The results of this study showed a significant decrease in infarct size and enzymes of cardiac injury in the training group during IR. Also, the results demonstrated that the reduction of ventricular function in the training group (HIR) was less than CIR group. As well, the results showed the significant increase in Klotho levels after training and lower expression of TRPC6 channels during IR in training group.
Short-term high-intensity interval training could reduce infarct size by one-third compared with the untrained group (CIR) (a decrease of 33.45%) and it could prevent noticeable reduction of cardiac function in IR injury. Based on the results, an increase in klotho following training and, consequently, lower expression of TRPC6 during IR, could be a mechanism for increasing cardioprotection and to reduce cardiac dysfunction.