Several structural and functional features keep bull testes 2°C to 6°C below body temperature, essential for the production of morphologically normal, motile and fertile sperm. The testicular vascular cone (TVC), located above the testis, consists of a highly coiled testicular artery surrounded by a complex network of small veins (pampiniform plexus). The TVC functions as a counter-current heat exchanger to transfer heat from the testicular artery to the testicular vein, cooling blood before it enters the testis. Bulls with increased TVC diameter or decreased distance between arterial and venous blood, have a greater percentage of morphologically normal sperm. Both the scrotum and testes are warmest at the origin of their blood supply (top of scrotum and bottom of testis), but they are cooler distal to that point. In situ, these opposing temperature gradients result in a nearly uniform testicular temperature (top to bottom), cooler than body temperature. The major source of testicular heat is blood flow, not testicular metabolism. High ambient temperatures have less deleterious effects on spermatogenesis in Bos indicus v. Bos taurus bulls; differences in TVC morphology in B. indicus bulls confer a better testicular blood supply and promote heat transfer. There is a long-standing paradigm that testes operate on the brink of hypoxia, increased testicular temperature does not increase blood flow, and the resulting hypoxia reduces morphologically normal and motile sperm following testicular hyperthermia. However, in recent studies in rams, either systemic hypoxia or increased testicular temperature increased testicular blood flow and there were sufficient increases in oxygen uptake to prevent tissue hypoxia. Therefore, effects of increased testicular temperature were attributed to testicular temperature per se and not to secondary hypoxia. There are many causes of increased testicular temperature, including high ambient temperatures, fever, increased recumbency, high-energy diets, or experimental insulation of the scrotum or the scrotal neck. It is well known that increased testicular temperatures have adverse effects on spermatogenesis. Heat affects all germ cells and all stages of spermatogenesis, with substantial increases in temperature and/or extended intervals of increased testicular temperature having the most profound effects. Increased testicular temperature has adverse effects on percentages of motile, live and morphologically normal sperm. In particular, increased testicular temperature increases the percentage of sperm with abnormal morphology, particularly head defects. Despite differences among bulls in the kind and percentage of abnormal sperm, the interval from increased testicular temperature to the emergence of specific sperm defects is consistent and predictable. Scrotal surface temperatures and structural characteristics of the testis and TVC can be assessed with IR thermography and ultrasonography, respectively.

The objective was to determine effects of feed restriction and refeeding on reproductive development and energy balance in pre-pubertal male rats. Sprague Dawley rats (n = 32, 24 days old, ~65 g), were randomly allocated into four treatments (n = 8/treatment): (1) Control (CON, ad libitum feed; (2) Mild Restriction (MR, rats fed 75% of CON consumption); (3) Profound Restriction (PR, 50% of CON consumption); or (4) Refeeding (RF, 50% restriction for 14 days, and then ad libitum for 7 days). Feed restriction delayed reproductive development and decreased energy balance and tissue accretion, with degree of reproductive and metabolic dysfunctions related to restriction severity. In RF rats, refeeding largely restored testis weight, sperm production (per gram and total), plasma IGF-1, leptin and insulin concentrations and energy expenditure, although body composition did not completely recover. On Day 50, more CON and RF rats than PR rats were pubertal (5/6, 4/5 and 1/6, respectively; plasma testosterone >1 ng/mL) with the MR group (4/6) not different. Our hypothesis was supported: nutrient restriction of pre-pubertal rats delayed reproductive development, induced negative energy balance and decreased metabolic hormone concentrations (commensurate with restriction), whereas short-term refeeding after profound restriction largely restored reproductive end points and plasma hormone concentrations, but not body composition.

Despite a long-standing assertion that mammalian testes operate near hypoxia and increased testicular temperature causes frank hypoxia, we have preliminary evidence that changes are due to hyperthermia per se. The objective was to determine how variations in inspired oxygen concentration affected testicular blood flow, oxygen delivery and extraction, testicular temperature and lactate production. Eight rams were maintained under general anesthesia, with successive decreases in oxygen concentration in inspired air (100, 21 and 13%, respectively). As oxygen concentration decreased from 100 to 13%, there were increases in testicular blood flow (9.6 ± 1.7 vs 12.9 ± 1.9 ml/min/100 g of testis, P < 0.05; mean ± SEM) and conductance (normalized flow; 0.46 ± 0.07 to 1.28 ± 0.19 ml/min/mm Hg/100 g testis (P < 0.05). Increased testicular blood flow maintained oxygen delivery and increased testicular temperature by ~1 °C; this increase was correlated to increased testicular blood flow (r = 0.35, P < 0.0001). Furthermore, oxygen utilization increased concomitantly and there were no significant differences among oxygen concentrations in blood pH, HCO₃− or base excess, and no effects of venous-arterial differences in lactate production. In conclusion, under acute hypoxic conditions, testes maintained oxygen delivery and uptake by increasing blood flow and oxygen extraction, with no evidence of anaerobic metabolism. However, additional studies are needed to determine longer-term responses and potential evidence of anaerobic metabolism at the molecular level.

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; 45 min 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 ± 3.2 mL min-1 per 100 g 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 ± 0.06 mL min-1 per 100 g 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.