In humans, testicular temperature must be ~3 ºC below body core temperature for production of high-quality, fertile sperm. Increased testicular temperature can be caused by several known pathologies (e.g. varicocele) or behaviours (e.g. hot baths; sitting for several hours). Consequently, leading to low sperm quality and infertility. Furthermore, due to global climate change and intense heat episodes, heat stress is nearly universally a major issue in mammals. Therefore, there is a need to elucidate pathophysiological pathways involved in heat stress impairing testicular function and spermatogenesis in men. The model of choice for this study is the bovine, which include a heat resistant (Bos indicus) and a heat sensitive (Bos taurus) breed. Our hypothesis is that testicular cells respond differently to heat stress and heat resistant animals will present better cell defense mechanisms with lower expression of apoptotic markers. Furthermore, microRNA profile from sperm cells will differ, based on the stage of the cycle when the stress took place. Lastly, paternal heat stress will impact embryo quality, development and gene expression. The data obtained through this proposal will be fundamental to answer important questions regarding how paternal heat stress impacts fertility in men. Furthermore, it will allow the identification of potential heat resistance markers. The results obtained, will support development of treatments for infertility and improving sperm quality.