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Sex complicates the effect and treatment of heat stress
Author(s) -
Rudolph Tori,
Lozano Johana Mayorga,
Rhoads Robert P.,
Baumgard Lance H.,
Selsby Joshua T.
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.05453
Subject(s) - oxidative stress , malondialdehyde , heat stress , placebo , autophagy , antioxidant , chemistry , medicine , oxidative phosphorylation , skeletal muscle , reactive oxygen species , endocrinology , andrology , biology , biochemistry , zoology , apoptosis , pathology , alternative medicine
Global temperature is continuing to rise, and resultant heat stress (HS) poses a major threat to human health. Using large animal models, we have shown that 12 and 24 h, and 7 d of heat exposure induced oxidative stress and impaired autophagy in oxidative skeletal muscle but not glycolytic muscle. We and others have implicated mitochondrial dysfunction in this process. We hypothesized that treatment with a mitochondrially targeted antioxidant, MitoQ, would decrease oxidative stress and alleviate cellular dysfunction during HS. To address this hypothesis, 3 mo old castrated male pigs (59 ± 1.0m kg; n=8/group) were administered either placebo or MitoQ (40 mg/day) divided into two daily doses every 12 h beginning 48 h prior to environmental treatment and continuing through environmental exposure. Half of the placebo‐ and half of the MitoQ‐treated pigs were assigned to thermoneutral (TN; 20°C) or HS (35°C) conditions for 24 h. The red portion of the semitendinosus (STR) was collected for subsequent analysis. Unexpectedly, malondialdehyde (MDA) concentration, a marker of oxidative stress, was unaffected by treatment or environment. Additionally, LC3A/B‐I was decreased 0.5‐fold (p<0.05) during HS, LC3A/B‐II was similar, and the ratio of LC3A/B‐II/I was increased 1.5‐fold (p<0.05) in HS; p62 was similar between treatment groups. These data suggest increased degradation of autophagosomes in HS males, which may explain maintenance of redox balance but conflicts with previous findings in female pigs; a scenario which raises the possibility of a sex effect on the muscular response to HS. To probe this idea, we compared STR from these HS males to archived HS STR from female pigs treated with a similar experimental design and environmental protocol described above. We confirmed our previous findings of oxidative stress and dysfunctional autophagy in females, and maintenance of redox balance with increased degradation of autophagosomes in males. In total, these data suggest that muscle from female pigs is more susceptible to detrimental effects of environment‐induced hyperthermia than muscle from male pigs. Support or Funding Information Supported by USDA grant 2017‐05931