Pathogenesis and mitigation of the deleterious effects of heat stress on bull reproduction

Bull testes must be 2 to 6 0C below body temperature for morphologically normal, motile and fertile sperm. Scrotal/testicular thermoregulation is complex, including a coiled testicular artery, surrounded by the venous pampiniform plexus comprising the testicular vascular cone, a counter-current heat exchanger. In addition, heat radiation from the scrotum, sweating, complementary arterial blood supplies, and temperature gradients in the scrotum and testes all contribute to testicular cooling. Despite a long-standing paradigm that mammalian testes are close to hypoxia and blood flow does not increase in response to testicular heating, in recent studies in mice, rams and bulls, warming the testes stimulated increased blood flow, with no indications of testicular hypoxia. Furthermore, hypoxia did not replicate the changes and hyperoxia did not provide protection. Therefore, we concluded that testicular hyperthermia and not secondary hypoxia affects spermatogenesis and sperm quality. Increasing testicular temperature causes many cellular and subcellular changes. As testicular temperature increases, the proportion of defective sperm increases; recovery is dependent upon the nature and duration of the thermal insult. Environmental control of temperature (shade, sprinklers, air conditioning) and some chemical approaches (e.g., melatonin and L-arginine) have promise in reducing the effects of heat stress on bull reproduction.