Effects of Heat Stress on Intestinal Health, Immune System and Meat Quality of Pigs

Pigs are homotherms with underdeveloped sweat glands. When the ambient temperature exceeds the upper limit of their thermoneutral zone, pigs will suffer heat stress, manifested as tail biting, rapid breathing and reduced feed intake. Their metabolism and physiological functions will be abnormal, leading to compromised growth performance: lower average daily feed intake and higher feed-to-gain ratio. Their immunity declines, the concentration of inflammatory factors in serum rises, disease resistance weakens, and morbidity and mortality increase. Meat quality deteriorates as metabolism of muscle and adipose tissues is disrupted, with reduced intramuscular fat and increased fat deposition in adipose tissue. Pigs at different growth stages have varying sensitivity to ambient temperature.

Summer in southern China features long-lasting high temperature and humidity. Poor management on pig farms under such conditions will result in impaired growth performance, weakened immunity and degraded meat quality due to heat stress, causing severe economic losses to the pig industry. The specific adverse impacts of heat stress on pigs are elaborated as follows.

1. Impacts on Pig Intestinal Health

The most intuitive manifestation of heat stress is reduced feed intake and feed conversion ratio. Within the temperature range of 20~30°C, each 1°C temperature rise leads to decreased average daily feed intake and average daily gain, accompanied by a higher feed-to-gain ratio.

1.1 Damage to Intestinal Mucosa Caused by Heat Stress

Under heat stress, the expression level of intestinal heat shock proteins in pigs is upregulated. To dissipate heat efficiently, more blood flows to peripheral tissues, resulting in intestinal hypoxia. Intestinal epithelial cells are extremely sensitive to oxygen and nutrient deficiency, which further triggers massive consumption of adenosine triphosphate (ATP), oxidative stress and nitrite stress. This alters the morphological structure and permeability of the intestine and ultimately impairs the intestinal barrier function.

In addition, heat stress significantly reduces the activity of digestive enzymes, severely hindering digestion and nutrient absorption and further suppressing pig growth. Moreover, heat stress changes the amino acid composition of endogenous intestinal proteins and increases the loss of endogenous intestinal proteins and amino acids.

1.2 Impacts on Intestinal Microflora

The intestinal microflora forms a microbial barrier, a microecological system composed of symbiotic bacteria and the host. Once the stability of this microecosystem is disrupted, opportunistic pathogens in the intestine are prone to invade the body.

2. Impacts on the Immune System of Pigs

Heat stress triggers abnormal immune responses in pigs, greatly weakening their disease resistance and increasing morbidity and mortality.

1. Heat stress destroys intestinal integrity and enhances toxin permeability: the transepithelial electrical resistance (TEER) of pig jejunum drops by 30%, endotoxin level rises by 45%, the permeability coefficient of lipopolysaccharide doubles, and alkaline phosphatase activity increases. Toxin infiltration stimulates the proliferation of immune cells, induces inflammatory reactions, and activates detoxification mechanisms in the intestine and liver.

2. Heat stress interferes with immune function through the neuroendocrine system. High temperature activates the hypothalamic-pituitary-adrenal axis, leading to hypersecretion of corticotropin-releasing hormone and pro-opiomelanocortin. These hormones act on various cytokines and immune cells, disrupting the body’s immune system.

3. Studies have found that heat stress inhibits the development of immune organs and induces apoptosis of immune cells.

3. Impacts on Pork Quality

The economic losses caused by heat stress to pig farms stem from two aspects: compromised growth performance and abnormal immune responses on the one hand, and disrupted metabolism of organs, muscles and fat on the other. Heat stress disturbs the energy balance among fat, carbohydrates and proteins, reduces the activity of several metabolic enzymes related to glycolysis in the intestine, and consequently deteriorates meat quality.

3.1 Impacts of Heat Stress on Muscle Metabolism

Persistent high temperature inhibits muscle structural and functional development, reduces muscle metabolic capacity, promotes cell apoptosis and stress responses, and thus damages meat quality.

Experts studied the effect of heat stress on the gene expression profile of porcine longissimus dorsi via sequencing technology, and found that heat stress mainly affects glucose metabolism, cytoskeletal structure and function, and stress response in muscle tissue.

According to morphological and physiological characteristics, muscle fibers are divided into type I and type II. Type I fibers are slow-twitch oxidative red fibers, while type II fibers are fast-twitch white fibers. The proportion of type I fibers is positively correlated with meat flavor. Persistent high temperature and heat stress significantly increase the quantity and proportion of white fibers while reducing those of red fibers, which impairs pork quality including meat color, drip loss, tenderness, juiciness and flavor.

3.2 Impacts of Heat Stress on Fat Metabolism

Intramuscular fat is one of the key indicators for evaluating meat quality, closely related to muscle tenderness and flavor, as well as meat traits such as muscle pH, water holding capacity and tenderness. Persistent high temperature significantly reduces intramuscular fat content in the longissimus dorsi of growing pigs and deteriorates meat quality.

Heat stress alters adipose tissue metabolism: the expression of fat catabolism-related genes is downregulated, while genes related to fat uptake and synthesis are upregulated, resulting in excessive fat deposition and altered proportions of fatty acids.