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Eccentric exercise (EE) is known to induce damage and dysfunction in skeletal muscle. However, the possible role of mitochondrial (dys)function, including the vulnerability to mitochondrial permeability transition pore (MPTP) opening, is unclear. Therefore, this study aimed to analyze the impact of a single acute bout of downhill running on skeletal muscle mitochondrial function. Thirty 12-week-old Charles River CD1 male mice were randomly assigned into control (C) or exercised groups. EE consisted of 120 min of downhill treadmill running at a -16° gradient. Exercised animals were sacrificed immediately (Ecc0h) and 48 h (Ecc48h) after the end of the running bout. Plasma and skeletal muscles were then obtained. Muscle mitochondrial function, including oxygen consumption prior to and after anoxia and reoxygenation, membrane potential, and MPTP opening, were evaluated. Respiratory chain complexI, II, and V activities were determined. EE significantly increased plasma creatine kinase activity (119.4 ± 5.6 vs. 1061.3 ± 46.3 vs. 256.8 ± 15.3 U·L-1, C, Ecc0h and Ecc48h, respectively) and myoglobin and interleukin-6 content. Impaired state 3 and respiratory control ratio (8.4 ± 0.4 vs. 5.6 ± 0.9 vs. 8.4 ± 0.5, C, Ecc0h and Ecc48h, respectively), as well as increased susceptibility to MPTP opening, seen by cyclosporin A-sensitive high swelling amplitude, lower time to maximal swelling velocity (313.8 ± 17.7 vs. 244.5 ± 19.4 vs. 298.5 ± 8.7 s, C, Ecc0h and Ecc48h, respectively), and calcium release immediately after the end of exercise (C vs. Ecc0h) were observed. EE induced a transient impairment in the activity of complex V (C vs. Ecc0h). No significant changes from the C group were observed 48 h after the end of EE (C vs. Ecc48h) in any analyzed parameters. In conclusion, prolonged EE transiently impaired mice skeletal muscle mitochondrial function and increased susceptibility to calcium-induced MPTP opening. [ABSTRACT FROM AUTHOR]