In contrast to associations with other cardiometabolic risk factors, the extent to which breastfeeding is associated with cardiorespiratory fitness (CRF) is unclear. Moreover, whether any such association persists throughout the life course has never been investigated before. We have therefore examined the associations between breastfeeding (yes/no, duration) and CRF as estimated from field and laboratory tests and expressed by the level of VO 2 max from late childhood, through adolescence to young adulthood in 892 (50.8% female) participants in the Northern Ireland Young Hearts Project. This is a population-based cohort study conducted in a region with very low rates of breastfeeding within the UK and the western world. Longitudinal data were analyzed with weighted generalized estimating equations, to correct estimates for selective attrition bias (with inverse probability of attrition weights). All estimates were adjusted for the participants age, sex, socio-economic status and important perinatal confounders (birthweight z-scores, gestational age, maternal age and parity, and mode of delivery). Participants’ mean levels of CRF were 45.6±4.9, 43.9±6.9 and 32.8±9.7 mL/kg/min at the ages of 12, 15 and 22 years, respectively. On average, and as compared with participants who were never breastfed (n=746), those who were breastfed (n=146) had significantly higher levels of CRF, from childhood to adulthood: 1.23 mL/min/kg (95%CI: 0.22, 2.24). Further adjustments for potential mediators, i.e. participants’ lifestyle risk factors (physical activity, smoking alcohol and dietary habits) and body size (height) and composition (fat and fat-free masses) during growth, did not appreciably attenuate this association: 1.14 mL/min/kg (95%CI: 0.29, 1.99). Analyses by duration of breastfeeding did not reveal increasing benefits with increasing duration, however: +1.10 and +1.20 mL/kg/min if <=3 and >3 months vs. none, respectively. There were no significant interactions between breastfeeding and participants’ sex or age at the time of CRF assessments, indicating that the decreases in CRF were similar across the different breastfeeding groups, with those who were not breastfed displaying consistently lower levels throughout the longitudinal period. Finally, those who were breastfed had lower lifelong risk of poor CRF as defined according to age and sex-specific reference values of VO 2 max: RR=0.70 (0.49, 0.97) and RR=0.73 (0.51, 0.99) in models adjusted for confounders and potential mediators, respectively. In conclusion, breastfeeding may have lifelong beneficial effects on CRF and thereby cardiovascular health. These findings may have important public health and clinical implications and should reinforce breastfeeding promotion policies, particularly where uptake rates remain low. The mechanisms through which breastfeeding affect CRF need to be further explored though.