The negative impact of direct scrotal heating on male fertility has previously been documented and here we have extended on this work by investigating the effects of whole body heating on male fertility. For this purpose, adult male mice were exposed to an elevated ambient temperature of 35ºC under two exposure models. The first involved acute exposure for 24 hours, followed by recovery periods of between 1 day and 6 weeks. The alternative heating regimen involved a daily exposure of 8 hours for periods of 1 or 2 weeks. Collectively our models identified elevated sperm mitochondrial ROS generation (p < 0.05), increased sperm membrane fluidity (p < 0.05) as well as DNA damage in the form of single strand breaks (p < 0.001) and oxidative DNA damage (p < 0.05); characteristic of an oxidative stress cascade. This DNA damage was detected in, and possibly originated from, pachytene spermatocytes (p < 0.001) and round spermatids (p < 0.001) isolated from testes after 1 day recovery. Despite these lesions, the spermatozoa of heat treated mice exhibited no differences in their ability to achieve hallmarks of capacitation or to fertilise the oocyte and support development of embryos to the blastocyst stage (all p > 0.05). Collectively, our acute heat stress model supports the existence of heat susceptible stages of germ cell development, with the round spermatids being most perturbed and spermatogonial stem cells exhibiting resistance to this insult. Such findings were complemented by those generated from our chronic heat stress model, which further supported the vulnerability of the round spermatid population.