Mitochondria are crucial organelles of eukaryotic aerobic cells (somatic and germ cells) because they produce adenosine triphosphate (ATP) and are modulators of ion homeostasis, generators of free radicals and regulators of cell death. Numerous studies reported that mitochondrial functionality was associated with sperm quality. Indeed, mitochondrial activities regulate many important sperm functions including sperm motility, hyperactivation, capacitation, acrosome reaction, and fertilization [1]. The exact mechanisms that link mitochondrial activities and sperm functions are often poorly understood or remain debated. Sperm mitochondria are arranged in the midpiece close to the flagellar. It seemed obvious that mitochondrial injuries can result in decreased sperm motility since motility is an ATP-dependent process, thus reliant on the energetic function of mitochondria for powering the flagellar motion. However, increasing evidence suggests that the dependence on mitochondria-derived ATP for human sperm motility is not unique and that glycolysis may replace mitochondrial oxidative phosphorylation [2]. Furthermore, spermatozoa can adapt their metabolic pathways depending on the availability of substrates. This is feasible since sperm mitochondria possess specific enzyme isoforms with distinct kinetics [2]. In addition to their role as an ATP producer, mitochondria regulate the lifespan of spermatozoa. Reduction in mitochondrial activities judged by the drop in the mitochondrial membrane potential (Δψm) has been regarded as an early cell death event [3]. The relevance of sperm mitochondria in fertility may also be associated with their role in the intermediate metabolism as producer of reactive oxygen species (ROS) or as regulator of intracellular calcium homeostasis, which are known to regulate proper sperm functions [4].