Figure 5.

Both oxidative and reductive stress stimulate adipocytes’ thermogenesis and browning during exercise. In an oxidative stress state, ROS opens the UCP1 proton channel on the mitochondrial inner membrane to initiate thermogenesis by the thiol oxidation of UCP1 at cystine (Cys253). In a state of reductive stress, lactate as a reducing agent produced by exercise stimulates browning by up-regulating UCP1 expression through the AMPK pathway or directly promoting the proliferation of beige/brown precursor cells. In the exercise cycling of energy supply and expenditure (including one bout of exercise and chronic regular exercise), ROS initiates adipose thermogenesis immediately to compensate the daily energy expenditure, whereas lactate increases adipocytes mitochondrial biogenesis and browning through the adaptive up-regulation of UCP1.