PURPOSE: While vigorous exercise is well known to stimulate erythropoiesis, the hematological response to exercise detraining remains incompletely understood. We sought to characterize red blood cell (RBC) mediated determinants of oxygen carry capacity, including RBC population dynamics, during a period of detraining. METHODS: Recreational marathon runners participated in a structured 18-week training program (~7-8 h/w) then completed the 2016 Boston Marathon. Participants then reduced total exercise exposure to <2 h/w (no single session >1 hour) for 8 weeks. Exercise testing, carbon monoxide rebreathing tests and venous blood draws were performed 10-14 days before, and at 4 and 8 weeks after the marathon. Mixed linear modeling adjusting for age and marathon finish time was used to compare data across time points. RESULTS: Twenty-two runners (age = 34.5 ± 7.5 y, 50% men) completed the study protocol. Detraining was confirmed by serial reductions in time to exhaustion during treadmill testing (p<0.01, Figure 1). Plasma volume significantly declined by 4 weeks. In contrast, total hemoglobin mass (tHbmass) and serum ferritin remained stable. By 4 weeks, glycated hemoglobin was significantly elevated while RBC mean corpuscular volume was significantly reduced, indicating an increase in mean RBC age. By 8 weeks, there was a significant decrease in the RBC clearance threshold (Vc). CONCLUSION: tHbmass, a primary determinant of oxygen carrying capacity, appears to be stable during 8 weeks of exercise detraining. We speculate that this phenomenon is mediated by a subtle decrease in RBC production rate, and that an extended Vc after 8 weeks occurs to defend tHbmass in the absence of a sufficient erythropoietic stimulus.Figure 1: Changes in exercise capacity and hematologic parameters in response to 8 weeks of exercise detraining following completion of the Boston Marathon.