Trans-sodium crocetinate (TSC), the isomer of the carotenoid compound crocetin, is found markedly to increase survival in hemorrhagic shock subsequent to 50–60% blood loss, mainly via restored resting oxygen consumption (VO2), blood pressure and heart rate. The proposed mechanism is that TSC increases oxygen diffusivity, and thus availability, in plasma. If this were found to be a prominent feature in the oxygen transfer from blood to skeletal muscle fiber mitochondria, increased VO2 during exercise would be expected because of reduced partial pressure of venous oxygen (increased utilization), which we aimed to elucidate in this study. Male Sprague-Dawley rats were intravenously injected with 0.3 mL kg−1 TSC (40 µg mL−1) or placebo and immediately thereafter tested on a ramped treadmill test protocol. Rats were introduced to the experimental protocols beforehand. Administration of TSC had a neutral effect on submaximal and maximal VO2 (VO2max) as well as running performance measured as maximal running time and maximal aerobic running velocity. Thus, in this study we cannot report any effects of TSC on steady-state submaximal VO2 or VO2max at exhaustive exercise.