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Physiological effects of heat stress

Physiological effects of heat stress

This condition compromises pig health, resulting in a drop in performance

by Jennifer DuCray

Stress is the sum of all biological reactions to mental, emotional and physical stimuli that disrupt an animal’s homeostasis (state of balance) as it relates to bodily functions. A myriad of internal and external stimuli can affect this homeostasis. Once disrupted, the body elicits physiological stress responses involving the immune system to try to re-establish balance.

In the summer months, an environmental stressor that is on many swine producers’ minds is heat. Heat stress will cause an animal to redistribute blood to the periphery of its body to maximize radiant heat dissipation to maintain a safe body temperature.

The redistribution of blood causes the constriction of blood vessels supplying the gastrointestinal (GI) tract. The resulting epithelial barrier dysfunction (loss of tight junctions) causes compromised intestinal integrity due to decreases in nutrient and blood flow.

This situation leads the pig to decrease its feed and water consumption, causing dehydration. In turn, the resulting osmotic imbalance (meaning the diffusion of water across a membrane) intensifies the damage and sloughing of intestinal cells. The intestinal epithelial barrier consists of tight junctions and secretory proteins that selectively absorb nutrients and prevent the absorption of harmful molecules or toxins from the contents of the intestines.

The breakdown of this barrier will elicit an immune response due to the increase of harmful molecules and toxic substances, including bacterial lipopolysaccharide (endotoxin, LPS) and mycotoxins from the lumen passing through the intestinal barrier and entering the bloodstream. The activation of the animal’s immune response will also increase energy costs, meaning less energy will go toward growth and performance.

Heat stress and the resulting damage to the intestinal barrier can also increase maintenance requirements due to:

  • amplified energy expenditure from panting
  • changes in body temperature, as maintaining a safe body temperature becomes the top priority
  • pregulated biological processes (activation and maintenance of the immune function) in an attempt to maintain homeostasis

Increased body temperature significantly affects biological systems. A 1-degree C (1.8-degree F) change in body temperature alone can increase caloric needs by 7 to 15 percent, according to 1978 research from Matthew J. Kluger.

The swine industry experiences significant annual economic loss due to heat stress. These losses can be attributed to reduced growth and efficiency, decreased fertility, increased veterinary costs, decreased carcass value and increased mortality.

Heat stress can also alter normal metabolism by increasing lipid production and decreasing muscle mass. Paradoxically, heat stress can also increase basal concentrations of the anabolic hormone insulin and increase insulin sensitivity, despite decreases in feed intake. This situation leads to reduced basal plasma non-esterified fatty acids (NEFA) concentrations, which are a significant source of energy for animals under stress conditions. Lack of NEFA causes animals to increase their production of and reliance on glucose as a fuel source by other measures, including the catabolic breakdown of muscles.

Heat stress can significantly affect the productivity of pigs over the subsequent couple of months. However, many of the physiological responses to heat stress are like other stressors. For example, pigs experience many of the gut health challenges and decreases in productivity discussed here when they experience weaning stress, abrupt dietary change or a prolonged out-of-feed event. Therefore, we must meet the animals’ nutritional requirements to help them through stressful events with minimal effects on productivity.


Kluger, M.J. (1978). “The evolution and adaptative value of fever: Long regarded as a harmful by-product of infection, fever may instead be an ancient ally against disease, enhancing resistance and increasing chances of survival.” American Scientist, 66(1), 38-43.

Jennifer DuCray is a product manager for Kemin Animal Health and Nutrition – North America. Jennifer graduated with a Bachelor of Science in Chemistry from Colorado State University and started with Kemin in 2009.


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