A new paradigm regarding testicular thermoregulation in ruminants?

Increased testicular temperature reduces percentages of morphologically normal and motile sperm and fertility. Specific sperm defects appear at consistent intervals after testicular hyperthermia, with degree and duration of changes related to intensity and duration of the thermal insult. Regarding pathogenesis of testicular hyperthermia on sperm quality and fertility, there is a long-standing paradigm that: 1) testes operate near hypoxia; 2) blood flow to the testes does not increase in response to increased testicular temperature; and 3) an ensuing hypoxia is the underlying cause of heat-induced changes in sperm morphology and function. There are very limited experimental data to support this paradigm, but we have data that refute it. In 2 × 3 factorial studies, mice and rams were exposed to two testicular temperatures (normal and increased) and three concentrations of O₂ in inspired air (hyperoxia, normoxia and hypoxia). As expected, increased testicular temperature had deleterious effects on sperm motility and morphology; however, hyperoxia did not prevent these changes nor did hypoxia replicate them. In two follow-up experiments, anesthetized rams were sequentially exposed to: 1) three O₂ concentrations (100, 21 and 13% O₂); or 2) three testicular temperatures (33, 37 and 40 °C). As O₂, decreased, testis maintained O₂ delivery and uptake by increasing testicular blood flow and O₂ extraction, with no indication of anaerobic metabolism. Furthermore, as testicular temperature increased, testicular metabolic rate nearly doubled, but increased blood flow and O₂ extraction prevented testicular hypoxia and anaerobic metabolism. In conclusion, our data, in combination with other reports, challenged the paradigm that testicular hyperthermia fails to increase testicular blood flow and the ensuing hypoxia disrupts spermatogenesis.