Cardiovascular disease (CVD) gets prevalent with advancing age. It is one of the important leading causes of death in many countries. Recent studies have found central pulse wave velocity (carotid-femoral PWV, cfPWV) and adiponectin (ADN) are both predictive markers for cardiovascular diseases clinically. Adiponectin has been found to link with anti-inflammatory effects and ameliorate atherosclerosis. Previous study suggested eccentric exercise could induce transient arterial stiffening; however, it is still unknown whether such effects are exercise type dependent and interact with ADN response. Purpose: to determine the effects of muscle damage induced by acute downhill running and eccentric resistance exercise on cfPWV and ADN, as well as its relationship. Methods: eighteen apparent healthy males were randomly assigned into downhill running (EE, n=9) and eccentric resistance exercise (RE, n=9) groups. Peak oxygen uptake (VO2peak= 50.5 ± 7.6 ml/kg/min) and one prepetition maximum of inclined leg press (1RM= 222.4 ± 55.2 kg) were determined respectively prior to experiment. EE group performed 30 minutes of the downhill running at -10° of slope that could elicit 75% of individual VO2peak, whereas RE group performed 120% 1RM eccentric contractions for 6 reps × 10 sets. cfPWV, ADN, creatine kinese (CK), and C-reactive protein (CRP) were measured pre-exercise, 90 minutes, 24 and 48 hours post-exercise. Results: CK of EE and RE group were significantly higher than the pre-exercise; PWV of two groups were also significantly higher on 24 (5.47 ± 0.59 m/s) and 48 hours post-exercise (5.44 ± 0.68 m/s) as compared to pre-exercise (5.18 ± 0.47 m/s) (p< .05) respectively. Compared with pre-exercise, ADN and CRP did no altered after performing eccentric exercise (p> .05); however, ΔcfPWV was correlated with ΔADN (r = -.51, p< .05) 90 minutes post-exercise. Conclusion: both downhill running and eccentric resistance exercise increased muscle damage and cfPWV, but did not altered adiponectin response, suggesting that such transient central arterial stiffening effects appeared not directly associated with adiponectin.