Fig. 5

Mechanisms in EP-induced autophagy assisting cardioprotection by intermittent ischemia–hypoxia. Autophagy is initiated by intermittent ischemia–hypoxia of EP by inducing upregulation of Beclin1 levels. The process of autophagy was complete because of the degradation of autophagy substrate p62. High-intensity exercise can also induce autophagy by continuous ischemia–hypoxia. However, it fails to increase LC3II/LC3I ratio, and to decrease p62, which relate to autophagy obstacles. Preraised autophagy by EP-induced ischemia–hypoxia plays an adaptive role in subsequent acute stress, allowing heart to be protected