Priyank Tiwari
Marketsandmarkets

As climate change intensifies global temperatures, heat stress poses a growing threat to poultry health, gut integrity, and overall productivity. Understanding the physiological mechanisms—from respiratory alkalosis to compromised immunity—is key to implementing effective housing and nutritional mitigation strategies that safeguard flock performance.

Heat stress in poultry occurs when birds struggle to maintain a balance between body heat production and heat loss due to high environmental temperatures. This condition affects all types of poultry at different stages of growth and can lead to significant welfare and productivity challenges. When birds are within their thermoneutral zone (typically 18–27°C), they can regulate heat efficiently from their body. However, exceeding the upper critical temperature forces birds to lose heat actively, primarily through panting. If heat production surpasses the birds’ maximum heat loss capacity—either acutely or chronically—it can result in severe physiological distress and even mortality.

In poultry production, particularly in fast-growing species like broiler chickens, heat stress in chickens becomes a critical concern. Their high metabolic rate generates substantial body heat, while their decreasing surface area relative to body weight limits heat dissipation. This imbalance impairs feed conversion efficiency, performance, and overall production profitability. Additionally, heat stress in poultry triggers oxidative stress and inflammation, negatively affecting gut health and immune function. With climate change intensifying temperature extremes, heat stress in poultry is becoming an even greater challenge worldwide. When birds fail to regulate their body temperature effectively, they experience a negative heat balance, leading to reduced productivity and increased economic losses. Effective heat stress management strategies—including optimized environmental controls and nutritional interventions—are essential to maintaining poultry health and performance. Climate change has increased the prevalence and intensity of heat stress conditions in most poultry production areas all over the world.

The optimum temperature for poultry animals’ well-being and performance –the so-called thermoneutral zone– is between 18 and 22°C. When birds are kept within this temperature range, they do not have to spend energy on maintaining constant body temperature. Heat stress is the result of unsuccessful thermoregulation in the animals, as they produce a higher quantity of heat than they can lose. It means that there is a negative balance between the net amount of heat produced by the animal and its capacity to dissipate this body heat to the environment.

Heat stress can be classified into two main categories, acute and chronic:

• Acute heat stress refers to a short and fast increase in environmental temperature (a few hours), in general, poultry animals show a degree of resilience to acute heat stress.
• Chronic heat stress is when the high temperatures persist for more extended periods (several days), and their compensatory mechanisms are not sufficient to maintain tissue integrity and thus health and performance are hindered.

When the environmental temperature is above the thermoneutral zone, the animals activate thermoregulation mechanisms to lose heat through behavioral, biochemical, and physiological changes and responses. Panting and exposure of low/non-feathered body areas (raising wings) are the main behavioral mechanisms in which chickens regulate their body temperature when exposed to heat stress. These actions help the chickens to cool down, at a high toll: high energy demands, dehydration, respiratory alkalosis, lethargy, decrease in feed intake, loss of intestinal function and oxidative stress. The cardiovascular system also responds to high temperatures by deviating blood to the peripheral areas of the body to maximize the dissipation of heat. This implicates a reduced supply of nutrients and oxygen to the gastrointestinal tract, hindering its functions and provoking inflammation and oxidative stress. The hypothalamic-pituitary-adrenal (HPA) axis gets activated, increasing the levels of circulating corticosterone, skeletal protein synthesis and the immune system is suppressed, therefore the animals stop growing and are more susceptible to disease.

Heat stress also changes the gene expression of cytokines, upregulates heat shock proteins (HSP), and reduces the concentration of thyroid hormones. When heat stress persists, these cascades of cellular reactions result in tissue damage and malfunction. The animals exposed to heat stress suffer adverse effects in terms of performance, which are widely known and include high mortality, lower growth, and production and a decline in meat and egg quality. Heat stress is a common reality in poultry production; its effects are quite complex and harmful and depend on the intensity and duration of the exposure to high temperatures.

By lowering feed digestibility, increasing gut permeability, and compromising immunity, heat stress leaves animals more susceptible to gut-health related issues such as dysbacteriosis and necrotic enteritis – and thus may increase the need to use antibiotics. Additionally, the passage of LPS through the permeable gut induces inflammation and further damage to animal welfare, health and performance.

Mitigation strategies, including support to the gut oxidative balance and lowering LPS-induced inflammation are crucial to support poultry animals in these critical periods.

Panting due to heat stress can cause an acid-base imbalance in the blood of layers, resulting in thinner and weaker eggshell. Hyperventilation in birds to regulate body temperature leads to excessive loss of CO2 gas from the lungs and blood, resulting in an increase in blood pH or a shift towards alkalinity, a condition referred to as respiratory alkalosis. A rise in blood pH levels reduces the activity of carbonic anhydrase enzyme, causing a decrease in the transfer of calcium and carbonate ions from the blood to the shell gland. The addition of calcium to the diet alone cannot rectify this issue. A reduction in feed intake and an increase in phosphorus loss leads to a decrease in calcium consumption, which is another factor contributing to thin eggshells. To restore acid-base balance, use of potassium chloride, ammonium chloride, or sodium bicarbonate is recommended. Heat stress reduction in poultry can be achieved by implementing various strategies. Two key strategies are housing management and nutritional management. Housing management involves adjusting the environment in which the birds are kept, including ventilation, temperature control, and lighting. Nutritional management involves providing birds with a balanced diet that includes specific nutrients that can help them cope with heat stress. Both strategies can be effective in reducing heat stress and maintaining performance. Monitoring the temperature and humidity at farm is a critical task during implementation of heat stress mitigation strategies.