Reproductive Criteria of Beef Bulls during and after Exposure to Increased Ambient Temperature

Meyerhoeffer, D. C.; Wettemann, R. P.; Coleman, S. W.; Wells, M. E.

doi:10.2527/jas1985.602352x

Cited by 72 publications

(41 citation statements)

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“…Similar changes occurred at corresponding times in previous studies that involved increased testicular temperatures in bulls and rams (Howarth 1969;Meyerhoeffer et al 1985;Saab et al 2011;Rocha et al 2015;Hamilton et al 2016) with some apparent differences in the magnitude of changes and the interval from the thermal insult to recovery, attributed to the degree and duration of testicular heating and perhaps species-specific characteristics (Skinner and Louw 1966;Rathore 1970;Brito et al 2004;Nichi et al 2006). Furthermore, in this study, sperm damage occurred during the final stages of spermatogenic development in the testis (Howarth 1969;Cardoso and Queiroz 1988;Senger 2003).…”

Section: Discussionsupporting

confidence: 64%

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

Kastelic¹,

Wilde²,

Rizzoto³

et al. 2017

Vet. Med.

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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.

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Section: Discussionsupporting

confidence: 64%

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

Kastelic¹,

Wilde²,

Rizzoto³

et al. 2017

Vet. Med.

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“…HSPA1B plays a crucial role in the promotion of cell survival through refolding of damaged and unfolded proteins generated by stressful stimuli (Jäättelä 1999, Akerfelt et al 2007) and protects cells against DNA damage (Kotoglou et al 2009). Moreover, HSPA1B is involved in lightening the damage of hyperthermia on spermatogenesis and post-ejaculatory function of sperm (Meyerhoeffer et al 1985). It can protect cells from various stresses by inhibiting stress-induced apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Expressions of miR-15a and its target gene HSPA1B in the spermatozoa of patients with varicocele

Mou

et al. 2014

Reproduction

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Hyperthermia and oxidative stresses are the two central elements contributing to varicocele-related sperm damage. Growing evidence indicates that microRNAs (miRNAs) are involved in the regulation of the heat and oxidative stress responses. In this study, we analyzed the expressions of several stress-related miRNAs in the sperm and found that the expression of miR-15a was significantly decreased in patients with varicocele compared with the control. Furthermore, miR-15a repressed the expression of HSPA1B, which is a typical stressinduced chaperone protein, through directly binding its 3 0 -UTR. The expressions of miR-15a and HSPA1B exhibited an inverse correlation in sperm. Our results provide a valuable insight into the varicocele-related sperm impairment and male infertility, and may help to develop potential therapeutic targets and novel biomarkers for male infertility.

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“…Meyerhoeffer et al (1985) reported that exposure to elevated ambient temperatures resulted in decreased bull semen quality as evidenced by a reduced percentage of motile sperm, reduced sperm output and an increased percentage of abnormal and aged sperm. Production Milk.…”

Section: Reproductionmentioning

confidence: 99%

Metabolic and hormonal acclimation to heat stress in domesticated ruminants

Bernabucci

Lacetera

Baumgard

et al. 2010

Animal

738

492

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Environmentally induced periods of heat stress decrease productivity with devastating economic consequences to global animal agriculture. Heat stress can be defined as a physiological condition when the core body temperature of a given species exceeds its range specified for normal activity, which results from a total heat load (internal production and environment) exceeding the capacity for heat dissipation and this prompts physiological and behavioral responses to reduce the strain. The ability of ruminants to regulate body temperature is species-and breed-dependent. Dairy breeds are typically more sensitive to heat stress than meat breeds, and higher-producing animals are more susceptible to heat stress because they generate more metabolic heat. During heat stress, ruminants, like other homeothermic animals, increase avenues of heat loss and reduce heat production in an attempt to maintain euthermia. The immediate responses to heat load are increased respiration rates, decreased feed intake and increased water intake. Acclimatization is a process by which animals adapt to environmental conditions and engage behavioral, hormonal and metabolic changes that are characteristics of either acclimatory homeostasis or homeorhetic mechanisms used by the animals to survive in a new 'physiological state'. For example, alterations in the hormonal profile are mainly characterized by a decline and increase in anabolic and catabolic hormones, respectively. The response to heat load and the heat-induced change in homeorhetic modifiers alters post-absorptive energy, lipid and protein metabolism, impairs liver function, causes oxidative stress, jeopardizes the immune response and decreases reproductive performance. These physiological modifications alter nutrient partitioning and may prevent heat-stressed lactating cows from recruiting glucose-sparing mechanisms (despite the reduced nutrient intake). This might explain, in large part, why decreased feed intake only accounts for a minor portion of the reduced milk yield from environmentally induced hyperthermic cows. How these metabolic changes are initiated and regulated is not known. It also remains unclear how these changes differ between short-term v. long-term heat acclimation to impact animal productivity and well-being. A better understanding of the adaptations enlisted by ruminants during heat stress is necessary to enhance the likelihood of developing strategies to simultaneously improve heat tolerance and increase productivity.Keywords: ruminants, heat stress, metabolism, acclimation, adaptation ImplicationsHeat stress is a significant financial burden to animal agriculture in most areas of the world. Acclimation to heat stress imposes behavioral, physiological and metabolic adjustments to reduce the strain and enhances the likelihood of surviving the stress, and it also frequently reduces ruminant performance and compromises health. Improving our knowledge of physiological and metabolic mechanisms of acclimation may contribute to the development and adoption of proce...

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Reproductive Criteria of Beef Bulls during and after Exposure to Increased Ambient Temperature

Cited by 72 publications

References 0 publications

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

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

Expressions of miR-15a and its target gene HSPA1B in the spermatozoa of patients with varicocele

Metabolic and hormonal acclimation to heat stress in domesticated ruminants

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