Backgroup: Norepinephrine transporter (NET) is synthesized in sympathetic ganglion and arrived to presynaptic membrane of sympathetic nerve ending by axoplasmic transport. The synaptic norepinephrine concentration is regulated through norepinephrine release and norepinephrine re-uptake by NET, thus maintaining cardiac function. Regular exercise training has been associated with improvement of the sympathetic nervous system in several animal models and in some human studies. Although these data are consistent with the hypothesis that exercise training reduces the incidence of cardiovascular diseases, ameliorates cardiac function and enhances exercise performance via reduced sympathoexcitation, the mechanisms are unknown. Objective: The present study was to observe the effects of long-term exercise on NET gene expression of cardiac sympathetic ganglion in SD rats and to investigate the possible mechanism of exercise-induced improvement of cardiac sympathetic nerve function. Methods: Ten SD rats performed 12-week aerobic treadmill running (exercise group, EG) and the other ten SD rats as control group (CG) maintained resting state. After experiment and coeliac anesthesia with 1% pentobarbital (30mg/kg), exhaust time (ET) was determined during incremental treadmill test; left ventricular end-systolic diameter (LVESD), left ventricular end-diastolic diameter (LVEDD), fractional shortening (FS), left ventricular ejection fraction (LVEF) and heart rate (HR) using echocardiography; myocardial and plasma norepinephrine (NE) by high pressure liquid chromatography-electrochemical detection; cardiac sympathetic ganglion and myocardial NET mRNA level were determined by real-time fluorescent quantitation PCR; cardiac sympathetic ganglion and myocardial NET protein and myocardial tyrosine hydroxylase (TH) protein by Western blot. Results: Compared with CG, ET (42.6±4.2 vs 27.4±3.8 min, P<0.01) increased; LVEDD (7.15±0.81 vs 8.82±0.91 mm, P<0.05), FS (57.8±4.6 vs 45.0±4.3 mm/s, P<0.01) and LVEF (67.6±5.8 vs 52.4±4.7%, P<0.01) raised but HR reduced (314±37 vs 395±39 b/min, P<0.05); both plasma NE (375.7±47.2 vs 464.6±42.9 pg/ml, P<0.01) and myocardial NE (528.2±54.4 vs 664.1±39.8ng/g, P<0.01) lowered; NET mRNA (1.75±0.20 vs 1.00±0.07, P<0.01) and protein (1.82±0.17 vs 1.00±0.09, P<0.01) of sympathetic ganglion elevated; NET mRNA of heart was not detected but NET protein step-up (1.69±0.18 vs 1.00±0.08, P<0.01); TH protein was not significantly different (1.15±0.22 vs 1.00±0.12, P>0.05). Conclusion: Long-term exercise training improved cardiac construction and sympathetic nerve function, as well as enhancing exercise capacity, the mechanism of which might be related to upregulation of NET gene expression of cardiac sympathetic ganglion.