Objective    To determine the effects of acute hypobaric hypoxia on AMP-activated protein kinase (AMPK) phosphorylation and glycogen content in rat myocardium.     Methods    Totally 16 rats were randomly divided into control and acute hypoxia group (n=8). The rats in hypoxia group were submitted to simulated 5 000 m of high altitude in a hypobaric chamber for 24 h. After the rats were sacrificed and their heart was take

n out. Cardiac function and pulmonary artery pressure were measured

blood glucose and lactate as well as myocardial glycogen content was determined. Both ventricular myocardial GLUT4 protein and AMPK and phosphorylated AMPK (pAMPK) was detected by Western blotting.     Results    Compared with the control group

pulmonary arterial pressure was significantly increased

the right ventricular performance was enhanced notably

while left ventricular systolic pressure and  dp/dt

max

had no obvious change in hypoxia group. Twenty-four hours’ hypoxic exposure induced an increase of blood glucose (5.6±0.6 mmol/L in control group vs 7.5±0.5 mmol/L in acute hypoxia group

P0.05) and myocardial glycogen content (right ventricular myocardium: 4.78±1.29 mg/g in control group vs 6.55±1.20 mg/g in hypoxia group

left ventricular myocardium: 4.15±0.77 mg/g in control group vs 5.73±1.57 mg/g in hypoxia group

P0.05). Ventricular GLUT4 protein was enhanced in both groups after 24 h hypoxic exposure. Although AMPK was not changed

the phosphorylated AMPK was weakened

and the ratio of pAMPK/AMPK was decreased significantly after 24 h hypoxic exposure.     Conclusion    Acute hypoxia exposure leads to a decrease of myocardial AMPK phosphorylation

which indicates energy balance in the myocardium

and the elevated myocardial glycogen content may be involved in the reduction of AMPK phosphorylation.