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Heat stress (HS) in mammals results from an imbalance in heat accumulation and dissipation. Fertility impairments consequential to HS have been recognized for decades in production animals, and more recently, observations have been extended to other species, including women. There are several systemic impacts of HS that can independently affect reproduction, including metabolic endotoxemia, reduced plane of nutrition, and endocrine disruption. At the level of the ovary, molecular pathways are altered by HS, such as inflammation, JAK-STAT, PI3K, oxidative stress, cell death, and heat shock response. Taken together, impaired ovarian function contributes to seasonal infertility that results from HS. This review paper describes the physiological and endocrine systemic impacts of HS that may independently and collaboratively impair fertility in the porcine model. The review then details ovarian intracellular events that are altered during HS and finally determines future needs in this area of research. [ABSTRACT FROM AUTHOR]

Oxidative stress contributes to heat stress (HS)-mediated alterations in skeletal muscle; however, the extent to which biological sex mediates oxidative stress during HS remains unknown. We hypothesized muscle from males would be more resistant to oxidative stress caused by HS than muscle from females. To address this, male and female pigs were housed in thermoneutral conditions (TN; 20.8 ± 1.6°C; 62.0 ± 4.7% relative humidity; n = 8/sex) or subjected to HS (39.4 ± 0.6°C; 33.7 ± 6.3% relative humidity) for 1 (HS1; n = 8/sex) or 7 days (HS7; n = 8/sex) followed by collection of the oxidative portion of the semitendinosus. Although HS increased muscle temperature, by 7 days, muscle from heat-stressed females was cooler than muscle from heat-stressed males (0.3°C; P < 0.05). Relative protein abundance of 4-hydroxynonenal (4-HNE)-modified proteins increased in HS1 females compared with TN (P = 0.05). Furthermore, malondialdehyde (MDA)-modified proteins and 8-hydroxy-20-deoxyguanosine (8-OHdG) concentration, a DNA damage marker, was increased in HS7 females compared with TN females (P = 0.05). Enzymatic activities of catalase and superoxide dismutase (SOD) remained similar between groups; however, glutathione peroxidase (GPX) activity decreased in HS7 females compared with TN and HS1 females (P = 0.03) and HS7 males (P = 0.02). Notably, HS increased skeletal muscle Ca2þ deposition (P = 0.05) and was greater in HS1 females compared with TN females (P < 0.05). Heat stress increased sarco(endo)plasmic reticulum Ca2þ ATPase (SERCA)2a protein abundance (P < 0.01); however, Ca2þ ATPase activity remained similar between groups. Overall, despite having lower muscle temperature, muscle from heat-stressed females had increased markers of oxidative stress and calcium deposition than muscle from males following identical environmental exposure. NEW & NOTEWORTHY Heat stress is a global threat to human health and agricultural production. We demonstrated that following 7 days of heat stress, skeletal muscle from females was more susceptible to oxidative stress than muscle from males in a porcine model, despite cooler muscle temperatures. The vulnerability to heat stress-induced oxidative stress in females may be driven, at least in part, by decreased antioxidant capacity and calcium dysregulation. [ABSTRACT FROM AUTHOR]

Environmental heat stress (HS) can impair muscle mitochondrial function which may contribute to negative health outcomes, but little is known about potential treatments to rescue mitochondrial function during HS. To test the hypothesis that thyroid hormone (T3) would protect mitochondrial function during HS, samples were collected from the right ventricle (RV) of 3-mo-old, crossbred gilts under 4 different environmental conditions: thermoneutral (TN; 22°C; n = 8); 1 d HS (HS1; 38°C; n = 7); oral supplementation of 1.33 μg kg body weight (BW)-1. d-1 Cytomel (liothyronine sodium) during the 1 d HS (HS1TH; n = 8); and 7 d HS (HS7; n = 8). The oxidative portion of the semitendinosus (ST) was also collected from all groups plus a 5th group: oral supplementation of Cytomel during 7 d HS (HS7TH, n = 8). Mitochondrial volume density was estimated by citrate synthase (CS) activity, and oxidative phosphorylation (OP) and electron transfer (E) capacities were determined via high resolution respirometry. Data were analyzed using mixed linear models in SAS v9.4 with treatment group as a fixed effect and pig (treatment) as a random effect. Within the RV, the contribution of OP supported by complex I (PCI) to maximal E was less in HS1TH gilts compared with all other groups (P ≤ 0.02), and the contribution of E supported by complex II (ECII) to maximal E was greater in TN than HS1 or HS7 (P ≤ 0.02) and tended to be greater in TN compared with HS1TH gilts (P = 0.07). Within the ST, integrative (relative to tissue wet weight) PCI was greatest in TN gilts (vs. HS7 and HS7TH, P ≤ 0.0002; vs. HS1 and HS1TH, P ≤ 0.06) and least in HS7 and HS7TH (vs. HS1 and HS1TH, P ≤ 0.05). Integrative maximal P (PCI+II) was greatest in TN pigs (compared with HS1TH, HS7, and HS7TH, P ≤ 0.05; compared with HS1, P = 0.09). Integrative maximal E (ECI+II) was also greatest in TN gilts than all other groups (P ≤ 0.05) while ECII was greater in TN pigs compared with HS7 and HS7TH (P ≤ 0.009) and tended to be greater than HS1 and HS1TH (P ≤ 0.09). In ST, intrinsic (relative to CS activity) PCI and PCI+II were greater in TN compared with HS1, HS1TH, and HS7 pigs (P ≤ 0.03) and PCI+II tended to be greater in TN than HS7TH (P ≤ 0.06). Intrinsic ECI+II and ECII were greater in TN compared with all other treatment groups (P ≤ 0.04). These results suggest that T3 supplementation did not protect mitochondrial function from negative impacts of HS in skeletal muscle but may have modified electron transfer through complex I in cardiac muscle which may have implications on oxidative stress. [ABSTRACT FROM AUTHOR]