Male fertility is declining in developed countries, as well as in developing countries. External factors linked to lifestyle, such as eating disorders, negatively affect spermatogenesis, both at central and gonadal levels. The overconsumption of high‐energy diets (HED) alters the functioning of the male reproductive axis and consequently affects the testicular physiology, disrupting its metabolism and bioenergetic capacity. Testicular metabolism presents unique characteristics, partly because of its cellular heterogeneity and to the specific functions that each cell type plays within the testicular environment. Disruption of the tightly regulated metabolic pathways leads to adverse reproductive outcomes, such as inefficient energy supply to germ cells, sperm defects or spermatogenesis arrest. Testicular metabolic alterations induced by HED intake may also lead to mitochondrial dysfunction, which is closely associated to reactive oxygen species (ROS) overproduction and oxidative stress. ROS easily target spermatozoa DNA and lipids, contributing to decreased sperm quality. Thus, understanding the detrimental effects of HED overconsumption on the pathways underlying testicular metabolism and sperm production is imperative; otherwise, one may favour a transgenerational amplification of subfertility. Herein, we present an up‐to‐date overview of the effects of HED on testicular metabolism, sperm parameters and the subsequent consequences for male fertility.