Hyperthermia and not hypoxia may reduce sperm motility and morphology following testicular hyperthermia

Abstract

ABSTRACT:The mammalian testis typically operates on the brink of hypoxia; the long-standing dogma is that increased testicular temperature increases metabolism, but blood flow is unaffected and the resulting hypoxia reduces sperm motility and morphology. In rats and mice, oxygen (O 2 ) content of inspired air affected O 2 content of testes, enabling the latter to range from approximately 50 to more than 200% of physiologic concentrations. A ram model was used to test the hypotheses that hypoxia would disrupt sperm motility and morphology and that hyperoxia would prevent hyperthermia-induced reductions in sperm motility and morphology. Eighteen Canadian Arcott rams (approximately 10 months old) were used in a 2 × 3 factorial, with factors being scrotal insulation (insulated or not insulated) and O 2 concentrations in inspired air (14, 21 or 85%). Six rams, three with and three without scrotal insulation, were placed in each of three enclosed areas for 30 h to expose them to their respective oxygen concentrations, with scrotal insulation removed at the end of the exposure. Semen was collected by electro-ejaculation twice before insulation, bi-weekly for four weeks starting one week after exposures, and then once weekly for two weeks. There were effects of insulation, time and an insulation × time interaction for motile sperm and sperm that had normal morphology or head or midpiece defects (P < 0.01 for each). Sperm motility and morphology exhibited alterations between approximately two and five weeks after insulation, with mean progressively motile and morphologically normal sperm decreasing from approximately 55 to 35% and from 80 to 30%, respectively, and with head and midpiece defects increasing from approximately 3 to 50% and from 10 to 20% (P < 0.05 for each). The hypotheses that hypoxia would disrupt sperm quality and production, whereas hyperoxia would prevent hyperthermia-induced reductions in sperm quality and production, were not supported. This is apparently the first report that heat-stress induced damage to sperm was due to increased temperature per se and not testicular hypoxia, calling into question a long-standing paradigm.

Increased testicular blood flow maintains oxygen delivery and avoids testicular hypoxia in response to reduced oxygen content in inspired air

“…In conclusion, under acute hypoxic conditions (13% oxygen in inspired air), the testis maintained oxygen delivery and uptake by increasing blood flow and oxygen extraction, with no indications of a shift to anaerobic metabolism. Similarly, in our previous study in conscious rams, exposure of control rams (no scrotal insulation) to 85, 21 and 14% oxygen for 30 h had no significant effect on semen quality 13 . Thus, we concluded that the testis compensated for decreased oxygen concentrations in inspired air, although this needs additional confirmation.…”

“…Although hyperemia was reported when testes not covered by the scrotum were exposed to increased temperatures 12 , this was not regarded as sufficient evidence to challenge the classical view that hypoxia mediates damage caused by testicular hyperthermia. In a previous preliminary study 13 , conscious rams breathed inspired air containing 85, 21 or 14% oxygen for 30 h. Half of the rams had an insulated scrotum (a well-established model to increase testicular temperature); in those rams, percentages of morphologically normal sperm and motile sperm were significantly decreased from ~2 to 5 wk after exposure. Furthermore, in that study, hyperoxia did not mitigate effects of scrotal insulation, nor did hypoxia cause subsequent decreases in morphologically normal or motile sperm.…”

Scrotal thermography to assess the seminal quality in Nelore and Girolando bulls

“…It is known that the thermoregulation mechanisms of the male reproductive organ are not totally efficient (Losano et al, 2018). In the case of thermal stress, the increase in scrotal/testicular temperature occurs, thereby increasing cellular metabolism in the testicles, which leads to a higher O 2 need (Kastelic, Wilde, Rizzoto, & Thundathil, 2017). Testicular blood supply is limited and will not be enough to supply the increase in O 2 demand in testicular cells, which leads to cell death and testicular degeneration, affecting both spermatogenesis and androgenesis (Paul, Teng, & Saunders, 2009).…”

>b<Perfil de microRNAs presentes no sêmen e embriões bovinos e sua relação com a fertilidade>/b<

“…Em humanos e em animais de produção, para que a espermatogênese ocorra de maneira ideal é necessário que a temperatura testicular esteja de 2 a 6º C abaixo da temperatura corporal ALVES et al, 2016a), o que se denomina de termorregulação testicular. Embora a etiopatogenia da degeneração testicular tenha sido questionada recentemente (KASTELIC et al, 2017), até o momento acredita-se que a perda da termorregulação testicular, ocasionada pelo aumento da temperatura testicular, ocasiona aumento do metabolismo celular sem aumento na oxigenação testicular levando à hipóxia (PAUL et al, 2008;TENG;SAUNDERS, 2009). Essa condição resultará em estresse oxidativo das células presentes no epitélio seminífero, o que pode levar a prejuízos na qualidade espermática como queda de motilidade, aumento da porcentagem de espermatozoides anormais, danos ao DNA espermático e diminuição na concentração sérica de testosterona (ALVES et al, 2015(ALVES et al, , 2016a.…”