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

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 (O2) content of inspired air...

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Main Authors: J.P. Kastelic, R.E. Wilde, G. Rizzoto, J.C. Thundathil
Format: Article
Language:English
Published: Czech Academy of Agricultural Sciences 2017-08-01
Series:Veterinární Medicína
Subjects:
Online Access:https://vetmed.agriculturejournals.cz/artkey/vet-201708-0003_hyperthermia-and-not-hypoxia-may-reduce-sperm-motility-and-morphology-following-testicular-hyperthermia.php
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author J.P. Kastelic
R.E. Wilde
G. Rizzoto
J.C. Thundathil
author_facet J.P. Kastelic
R.E. Wilde
G. Rizzoto
J.C. Thundathil
author_sort J.P. Kastelic
collection DOAJ
description 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 (O2) content of inspired air affected O2 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 O2 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.
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spelling doaj.art-527ab83e03274d8083e7334f96ba2e282023-02-23T03:50:40ZengCzech Academy of Agricultural SciencesVeterinární Medicína0375-84271805-93922017-08-0162843744210.17221/124/2016-VETMEDvet-201708-0003Hyperthermia and not hypoxia may reduce sperm motility and morphology following testicular hyperthermiaJ.P. Kastelic0R.E. Wilde1G. Rizzoto2J.C. Thundathil3Faculty of Veterinary Medicine, University of Calgary, Calgary, CanadaAgriculture and Agri-Food Canada, Lethbridge Research Centre, Lethbridge, CanadaFaculty of Veterinary Medicine, University of Calgary, Calgary, CanadaFaculty of Veterinary Medicine, University of Calgary, Calgary, CanadaThe 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 (O2) content of inspired air affected O2 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 O2 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.https://vetmed.agriculturejournals.cz/artkey/vet-201708-0003_hyperthermia-and-not-hypoxia-may-reduce-sperm-motility-and-morphology-following-testicular-hyperthermia.phpscrotal/testicular thermoregulationscrotal insulationtesticular hypoxiasemen qualityram
spellingShingle J.P. Kastelic
R.E. Wilde
G. Rizzoto
J.C. Thundathil
Hyperthermia and not hypoxia may reduce sperm motility and morphology following testicular hyperthermia
Veterinární Medicína
scrotal/testicular thermoregulation
scrotal insulation
testicular hypoxia
semen quality
ram
title Hyperthermia and not hypoxia may reduce sperm motility and morphology following testicular hyperthermia
title_full Hyperthermia and not hypoxia may reduce sperm motility and morphology following testicular hyperthermia
title_fullStr Hyperthermia and not hypoxia may reduce sperm motility and morphology following testicular hyperthermia
title_full_unstemmed Hyperthermia and not hypoxia may reduce sperm motility and morphology following testicular hyperthermia
title_short Hyperthermia and not hypoxia may reduce sperm motility and morphology following testicular hyperthermia
title_sort hyperthermia and not hypoxia may reduce sperm motility and morphology following testicular hyperthermia
topic scrotal/testicular thermoregulation
scrotal insulation
testicular hypoxia
semen quality
ram
url https://vetmed.agriculturejournals.cz/artkey/vet-201708-0003_hyperthermia-and-not-hypoxia-may-reduce-sperm-motility-and-morphology-following-testicular-hyperthermia.php
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AT grizzoto hyperthermiaandnothypoxiamayreducespermmotilityandmorphologyfollowingtesticularhyperthermia
AT jcthundathil hyperthermiaandnothypoxiamayreducespermmotilityandmorphologyfollowingtesticularhyperthermia