Heat stress (HS) jeopardizes pig health, reduces performance variables, and results in a fatter carcass. Whether HS directly or indirectly (via reduced feed intake) is responsible for the suboptimal production is not known. Crossbred gilts (n = 48; 35 ± 4 kg BW) were housed in constantly climate-controlled rooms in individual pens and exposed to 1) thermal-neutral (TN) conditions (20°C; 35% to 50% humidity) with ad libitum intake (n = 18), 2) HS conditions (35°C; 20% to 35% humidity) with ad libitum intake (n = 24), or 3) pair-fed [PF in TN conditions (PFTN), n = 6, to eliminate confounding effects of dissimilar feed intake (FI)]. Pigs in the TN and HS conditions were sacrificed at 1, 3, or 7 d of environmental exposure, whereas the PFTN pigs were sacrificed after 7 d of experimental conditions. Individual rectal temperature (Tr), skin temperature (Ts), respiration rates (RR), and FI were determined daily. Pigs exposed to HS had an increase (P < 0.01) in Tr (39.3°C vs. 40.8°C) and a doubling in RR (54 vs. 107 breaths per minute). Heat-stressed pigs had an immediate (d 1) decrease (47%; P < 0.05) in FI, and this magnitude of reduction continued through d 7; by design the nutrient intake pattern for the PFTN controls mirrored the HS group. By d 7, the TN and HS pigs gained 7.76 and 1.65 kg BW, respectively, whereas the PFTN pigs lost 2.47 kg BW. Plasma insulin was increased (49%; P < 0.05) in d 7 HS pigs compared with PFTN controls. Compared with TN and HS pigs, on d 7 PFTN pigs had increased plasma NEFA concentrations (110%; P < 0.05). Compared with TN and PFTN controls, on d 7 circulating N(τ)-methylhistidine concentrations were increased (31%; P < 0.05) in HS pigs. In summary, despite similar nutrient intake, HS pigs gained more BW and had distinctly different postabsorptive bioenergetic variables compared with PFTN controls. Consequently, these heat-induced metabolic changes may in part explain the altered carcass phenotype observed in heat-stressed pigs.

Stress, a ubiquitous part of daily human life, has varied biological effects which are increasingly recognized as including modulation of commensal microorganisms residing in the gastrointestinal tract, the gut microbiota. In turn, the gut microbiota influences the host stress response and associated sequelae, thereby implicating the gut microbiota as an important mediator of host health. This narrative review aims to summarize evidence concerning the impact of psychological, environmental, and physical stressors on gut microbiota composition and function. The stressors reviewed include psychological stress, circadian disruption, sleep deprivation, environmental extremes (high altitude, heat, and cold), environmental pathogens, toxicants, pollutants, and noise, physical activity, and diet (nutrient composition and food restriction). Stressors were selected for their direct relevance to military personnel, a population that is commonly exposed to these stressors, often at extremes, and in combination. However, the selected stressors are also common, alone or in combination, in some civilian populations. Evidence from preclinical studies collectively indicates that the reviewed stressors alter the composition, function and metabolic activity of the gut microbiota, but that effects vary across stressors, and can include effects that may be beneficial or detrimental to host health. Translation of these findings to humans is largely lacking at present. This gap precludes concluding with certainty that transient or cumulative exposures to psychological, environmental, and physical stressors have any consistent, meaningful impact on the human gut microbiota. However, provocative preclinical evidence highlights a need for translational research aiming to elucidate the impact of stressors on the human gut microbiota, and how the gut microbiota can be manipulated, for example by using nutrition, to mitigate adverse stress responses.

Excessive heat exposure reduces intestinal integrity and post-absorptive energetics that can inhibit wellbeing and be fatal. Therefore, our objectives were to examine how acute heat stress (HS) alters intestinal integrity and metabolism in growing pigs. Animals were exposed to either thermal neutral (TN, 21°C; 35–50% humidity; n = 8) or HS conditions (35°C; 24–43% humidity; n = 8) for 24 h. Compared to TN, rectal temperatures in HS pigs increased by 1.6°C and respiration rates by 2-fold (P<0.05). As expected, HS decreased feed intake by 53% (P<0.05) and body weight (P<0.05) compared to TN pigs. Ileum heat shock protein 70 expression increased (P<0.05), while intestinal integrity was compromised in the HS pigs (ileum and colon TER decreased; P<0.05). Furthermore, HS increased serum endotoxin concentrations (P = 0.05). Intestinal permeability was accompanied by an increase in protein expression of myosin light chain kinase (P<0.05) and casein kinase II-α (P = 0.06). Protein expression of tight junction (TJ) proteins in the ileum revealed claudin 3 and occludin expression to be increased overall due to HS (P<0.05), while there were no differences in claudin 1 expression. Intestinal glucose transport and blood glucose were elevated due to HS (P<0.05). This was supported by increased ileum Na+/K+ ATPase activity in HS pigs. SGLT-1 protein expression was unaltered; however, HS increased ileal GLUT-2 protein expression (P = 0.06). Altogether, these data indicate that HS reduce intestinal integrity and increase intestinal stress and glucose transport.

Heat stress can compromise intestinal integrity and induce leaky gut in a variety of species. Therefore, the objectives of this study were to determine if heat stress (HS) directly or indirectly (via reduced feed intake) increases intestinal permeability in growing pigs. We hypothesized that an increased heat-load causes physiological alterations to the intestinal epithelium, resulting in compromised barrier integrity and altered intestinal function that contributes to the overall severity of HS-related illness. Crossbred gilts (n=48, 43±4 kg BW) were housed in constant climate controlled rooms in individual pens and exposed to 1) thermal neutral (TN) conditions (20°C, 35-50% humidity) with ad libitum intake, 2) HS conditions (35°C, 20-35% humidity) with ad libitum feed intake, or 3) pair-fed in TN conditions (PFTN) to eliminate confounding effects of dissimilar feed intake. Pigs were sacrificed at 1, 3, or 7 d of environmental exposure and jejunum samples were mounted into modified Ussing chambers for assessment of transepithelial electrical resistance (TER) and intestinal fluorescein isothiocyanate (FITC)-labeled lipopolysaccharide (LPS) permeability (expressed as apparent permeability coefficient, APP). Further, gene and protein markers of intestinal integrity and stress were assessed. Irrespective of d of HS exposure, plasma endotoxin levels increased 45% (P<0.05) in HS compared with TN pigs, while jejunum TER decreased 30% (P<0.05) and LPS APP increased 2-fold (P<0.01). Furthermore, d 7 HS pigs tended (P=0.06) to have increased LPS APP (41%) compared with PFTN controls. Lysozyme and alkaline phosphatase activity decreased (46 and 59%, respectively; P<0.05) over time in HS pigs, while the immune cell marker, myeloperoxidase activity, was increased (P<0.05) in the jejunum at d 3 and 7. These results indicate that both HS and reduced feed intake decrease intestinal integrity and increase endotoxin permeability. We hypothesize that these events may lead to increased inflammation, which might contribute to reduced pig performance during warm summer months.

Acute heat stress (HS) and heat stroke can be detrimental to the health, well-being, and performance of mammals such as swine. Therefore, our objective was to chronologically characterize how a growing pig perceives and initially copes with a severe heat load. Crossbred gilts (n=32; 63.8±2.9 kg) were subjected to HS conditions (37°C and 40% humidity) with ad libitum intake for 0, 2, 4, or 6 h (n=8/time point). Rectal temperature (Tr), respiration rates (RR), and feed intake were determined every 2 h. Pigs were euthanized at each time point and fresh ileum and colon samples were mounted into modified Ussing chambers to assess ex vivo intestinal integrity and function. Transepithelial electrical resistance (TER) and fluorescein isothiocyanate-labeled dextran (FD4) permeability were assessed. As expected, Tr increased linearly over time (P<0.001) with the highest temperature observed at 6 h of HS. Compared to the 0-h thermal-neutral (TN) pigs, RR increased (230%; P<0.001) in the first 2 h and remained elevated over the 6 h of HS (P<0.05). Feed intake was dramatically reduced due to HS and this corresponded with significant changes in plasma glucose, ghrelin, and glucose-dependent insulinotropic peptide (P<0.050). At as early as 2 h of HS, ileum TER linearly decreased (P<0.01), while FD4 linearly increased with time (P<0.05). Colon TER and FD4 changed due to HS in quadratic responses over time (P=0.050) similar to the ileum but were less pronounced. In response to HS, ileum and colon heat shock protein (HSP) 70 mRNA and protein abundance increased linearly over time (P<0.050). Altogether, these data indicated that a short duration of HS (2-6 h) compromised feed intake and intestinal integrity in growing pigs. KeywordsAnimal Science, appetite, heat stress, intestinal integrity, swine ABSTRACT: Acute heat stress (HS) and heat stroke can be detrimental to the health, well-being, and performance of mammals such as swine. Therefore, our objective was to chronologically characterize how a growing pig perceives and initially copes with a severe heat load. Crossbred gilts (n = 32; 63.8 ± 2.9 kg) were subjected to HS conditions (37°C and 40% humidity) with ad libitum intake for 0, 2, 4, or 6 h (n = 8/time point). Rectal temperature (T r ), respiration rates (RR), and feed intake were determined every 2 h. Pigs were euthanized at each time point and fresh ileum and colon samples were mounted into modified Ussing chambers to assess ex vivo intestinal integrity and function. Transepithelial electrical resistance (TER) and fluorescein isothiocyanate-labeled dextran (FD4) permeability were assessed. As expected, T r increased linearly over time (P < 0.001) with the highest temperature observed at 6 h of HS. Compared to the 0-h thermal-neutral (TN) pigs, RR increased (230%; P < 0.001) in the first 2 h and remained elevated over the 6 h of HS (P < 0.05). Feed intake was dramatically reduced due to HS and this corresponded with significant changes in plasma glucose, ghrelin, and glucose-dependent insulinotropic peptide (P < ...