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The dynamic interactions between nitric oxide (NO) and myoglobin (Mb) in the cardiovascular system have received considerable attention. The loss of Mb, the principal O₂ carrier and a NO scavenger/producer, in the heart of some red-blooded fishes provides a unique opportunity for assessing this globin’s role in NO homeostasis and mitochondrial function. We measured Mb content, activities of enzymes of NO and aerobic metabolism [NO Synthase (NOS) and citrate synthase, respectively] and mitochondrial parameters [Complex-I and -I+II respiration, coupling efficiency, reactive oxygen species production/release rates and mitochondrial sensitivity to inhibition by NO (i.e., NO IC₅₀)] in the heart of three species of red-blooded fish. The expression of Mb correlated positively with NOS activity and NO IC₅₀, with low NOS activity and a reduced NO IC₅₀ in the Mb-lacking lumpfish (<i>Cyclopterus lumpus</i>) as compared to the Mb-expressing Atlantic salmon <i>(Salmo salar)</i> and short-horned sculpin <i>(Myoxocephalus scorpius</i>). Collectively, our data show that NO levels are fine-tuned so that NO homeostasis and mitochondrial function are preserved; indicate that compensatory mechanisms are in place to tightly regulate [NO] and mitochondrial function in a species without Mb; and strongly suggest that the NO IC₅₀ for oxidative phosphorylation is closely related to a fish’s hypoxia tolerance.