Patients with chronic obstructive pulmonary disease (COPD) experience a delayed recovery from skeletal muscle fatigue following exhaustive exercise that likely contributes to their progressive loss of mobility. As this phenomenon is not well understood, this study sought to examine post-exercise peripheral oxygen (O₂) transport and muscle metabolism dynamics in patients with COPD, two important determinants of muscle recovery. Twenty four subjects, 12 non-hypoxemic patients with COPD and 12 healthy subjects with a sedentary lifestyle, performed dynamic plantar flexion exercise at 40% of maximal work rate (WR_max) with phosphorus magnetic resonance spectroscopy (³¹P-MRS), near-infrared spectroscopy (NIRS), and vascular Doppler ultrasound assessments. The mean response time of limb blood flow at the offset of exercise was significantly prolonged in patients with COPD (Controls:56±27s; COPD:120±87s; P<0.05). In contrast, the post-exercise time constant for capillary blood flow was not significantly different between groups (Controls:49±23s; COPD:51±21s; P>0.05). The initial post-exercise convective O₂ delivery (Controls:0.15±0.06 L.min^-1; COPD:0.15±0.06 L.min^-1) and the corresponding oxidative adenosine triphosphate (ATP) demand (Controls: 14±6 mM.min^-1; COPD: 14±6 mM.min^-1) in the calf were not significantly different between controls and patients with COPD (P>0.05). The PCr resynthesis time constant (Controls:46±20 s; COPD:49±21 s), peak mitochondrial phosphorylation rate, and initial proton efflux were also not significantly different between groups (P>0.05). Therefore, despite perturbed peripheral hemodynamics, intracellular O₂ availability, proton efflux, and aerobic metabolism recovery in the skeletal muscle of non-hypoxemic patients with COPD are preserved following plantar flexion exercise and, thus, are unlikely to contribute to the delayed recovery from exercise in this population.