Age-related physiological decline emerges at different chronological ages across individuals. While physiological aging is linked to the functional decay of stem cells that sustain tissue regeneration, the basis of aging variation across individuals remains unclear. Using high throughput single cell technologies to compare mice of the same chronological age that exhibited early or delayed hematopoietic aging, we identified a small subset of “anti-aging” HSCs in delayed aging mice that counteracted the progression of aging by reducing myelopoiesis. Our molecular analyses revealed that some HSCs in mice with early aging onset show upregulation of genes involved in aging, myeloid differentiation, and stem cell proliferation. Delayed aging was instead linked to the upregulation of genes involved in stem cell regulation and response to external signals. Altogether, our findings suggest that modulation of myelopoiesis in select HSCs plays a major role in triggering or delaying the onset of hematopoietic aging in individuals.