Testicular hyperthermia increases blood flow that maintains aerobic metabolism in rams

Abstract

There is a paradigm that testicular hyperthermia fails to increase testicular blood flow and that an ensuing hypoxia impairs spermatogenesis. However, in our previous studies, decreases in normal and motile spermatozoa after testicular warming were neither prevented by concurrent hyperoxia nor replicated by hypoxia. The objective of the present study was to determine the effects of increasing testicular temperature on testicular blood flow and O2 delivery and uptake and to detect evidence of anaerobic metabolism. Under general anaesthesia, the testicular temperature of nine crossbred rams was sequentially maintained at ~33°C, 37°C and 40°C (±0.5°C; 45min per temperature). As testicular temperature increased from 33°C to 40°C there were increases in testicular blood flow (13.2±2.7 vs 17.7±3.2mLmin−1 per 100g of testes, mean±s.e.m.; P<0.05), O2 extraction (31.2±5.0 vs 47.3±3.1%; P<0.0001) and O2 consumption (0.35±0.04 vs 0.64±0.06mLmin−1 per 100g of testes; P<0.0001). There was no evidence of anaerobic metabolism, based on a lack of change in lactate, pH, HCO3− and base excess. In conclusion, these data challenge the paradigm regarding scrotal–testicular thermoregulation, as acute testicular hyperthermia increased blood flow and tended to increase O2 delivery and uptake, with no indication of hypoxia or anaerobic metabolism.

Review of the impact of heat stress on reproductive performance of sheep

“…Hypoxia is suggested as a mechanism through which hyperthermia induces germ cell damage [72,74]. However, while an early study [74] reported no increase in testicular blood flow when ram testes were heated, a recent study demonstrated increased testicular blood flow and oxygen extraction in anaesthetised rams with sequential increases in testicular temperature to 40°C [115]. Spermatozoa are vulnerable to oxidative stressinduced damage, including membrane lipid peroxidation and DNA damage [116], and scrotal heat stress in rodents induced expression of oxidative stress markers [113,117].…”