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Abstract Introduction It remains unclear if naturally occurring respiratory muscle (RM) work influences leg diffusive O2 transport during exercise in heart failure patients with reduced ejection fraction (HFrEF). In this retrospective study, we hypothesized that RM unloading during submaximal exercise will lead to increases in locomotor muscle O2 diffusion capacity (DMO2) contributing to the greater leg VO2. Methods Ten HFrEF patients and 10 healthy control matched participants performed two submaximal exercise bouts (i.e., with and without RM unloading). During exercise, leg blood flow was measured via constant infusion thermodilution. Intrathoracic pressure was measured via esophageal balloon. Radial arterial and femoral venous blood gases were measured and used to calculate leg arterial and venous content (CaO2 and CvO2, respectively), VO2, O2 delivery, and DMO2. Results From CTL to RM unloading, leg VO2, O2 delivery, and DMO2 were not different in healthy participants during submaximal exercise (all, p > .15). In HFrEF, leg VO2 (CTL: 0.7 ± 0.3 vs. RM unloading: 1.0 ± 0.4 L/min, p < .01), leg O2 delivery (CTL: 0.9 ± 0.4 vs. RM unloading: 1.4 ± 0.5 L/min, p < .01), and leg DMO2 (CTL: 31.5 ± 11.4 vs. RM unloading: 49.7 ± 18.6 ml min−1 mmHg−1) increased from CTL to RM unloading during submaximal exercise (all, p < .01), whereas CaO2‐CvO2 was not different (p = .51). The degree of RM unloading (i.e., % decrease in esophageal pressure‐time integral during inspiration) was related to the % increase in leg DMO2 with RM unloading (r = −.76, p = .01). Conclusion Our data suggest RM unloading leads to increased leg VO2 due to greater convective and diffusive O2 transport during submaximal exercise in HFrEF patients.