Insufficient oxidative capacity, or mitochondrial dysfunction, may contribute to the development of high blood pressure by stimulating increased blood flow. To test this hypothesis, we examined the prospective association of lactate, a product of glycolysis and marker of oxidative capacity, with incident hypertension in 5,554 participants from the Atherosclerosis Risk in Communities (ARIC) Study. Participants had no diagnosed hypertension and blood pressures <140/<90 mm Hg at baseline (1996-1998). Incident hypertension was assessed during annual telephone calls and defined as a self-reported physician diagnosis of hypertension or hypertension medication use. Analyses were performed with Cox proportional hazards models. The mean age was 61.9 years, and the mean lactate was 0.08 mmol/L. The population was 45.1% male and 12.8% black. During a median follow-up period of 11.9 years (range: 26.9 days to 13.4 years), there were 3,849 new cases of hypertension. The unadjusted 10-yr cumulative incidences across quartiles 1-4 of lactate were 14.6, 18.3, 21.5, and 32.3%. After adjustment for traditional hypertension risk factors, including baseline systolic and diastolic blood pressure, the highest quartile of baseline lactate was associated with 1.18 times the hazard of the lowest quartile (95% CI: 1.07, 1.31; P-trend = 0.001) (Figure). This association was stronger (HR 1.42; 95% CI: 1.23, 1.63) in participants with blood pressures <120/<80 mm Hg. Mild elevations in lactate precede hypertension even in a normotensive population. These findings have important implications for early detection of hypertension risk in healthy adults.