Heat Stress and the HPA Axis in Laying Hens: How the Body’s Alarm System Works

Heat stress (HS) is one of the most significant environmental stressors limiting productivity in poultry. Especially during summer, the combination of high temperature and humidity disrupts the physiological balance of laying hens, negatively affecting production performance, immune health, and overall welfare.

Because chickens lack sweat glands and have limited mechanisms for heat dissipation, they are particularly vulnerable to thermal stress. To preserve internal stability (homeostasis), the body initiates a series of physiological responses and, at the centre of these is the hypothalamic–pituitary–adrenal (HPA) axis.

The HPA Axis: The Body’s “Emergency Button”

The HPA axis bridges the central nervous system and the endocrine system, controlling the organism’s ability to cope with stress. When exposed to environmental threats such as heat stress:

1. The hypothalamus releases corticotropin-releasing hormone (CRH).
2. The pituitary gland secretes adrenocorticotropic hormone (ACTH).
3. The adrenal glands increase production of corticosterone: the principal stress hormone in chickens.

Corticosterone in birds serves a role similar to cortisol in mammals and is responsible for most systemic stress responses.

“No system can remain on high alert indefinitely.”

While short-term HPA activation supports adaptation, chronic activation leads to production losses and physiological disorders.

Physiological Effects of HPA Axis Activation Under Heat Stress

1. Increased Stress Hormones

Heat stress activates the HPA axis from the hypothalamus to the adrenal glands, leading to a marked rise in plasma corticosterone levels.

• Increases protein catabolism.
• Stimulates gluconeogenesis, raising blood glucose.
• Suppresses the proliferation of immune cells.
• Reduces secretion of reproductive (LH, FSH) and growth hormones.

These changes, particularly under prolonged exposure, result in substantial performance losses in hens.

2. Metabolic and Haematological Changes

With elevated glucocorticoids, the following alterations are observed:

• Hyperglycaemia: Corticosterone stimulates hepatic glucose production.
• Hypoalbuminaemia: Protein synthesis in the liver is suppressed.
• Increased AST and ALT: Indicate liver stress and cell damage due to heat load.
• Elevated NEFA and β-hydroxybutyrate: Reflect a metabolic shift toward fat utilisation for energy.
• Electrolyte imbalance (hyponatraemia, hyperkalaemia): Disrupts cellular conductivity and muscle function.

3. Increased Oxidative Stress

Chronic activation of the HPA axis elevates oxidative load. High corticosterone increases mitochondrial activity and the production of reactive oxygen species (ROS), resulting in:

• Depletion of antioxidant enzymes (SOD, catalase, glutathione peroxidase).
• Increased malondialdehyde (MDA) levels.
• Lipid peroxidation, DNA damage, and cell death.

These effects are particularly pronounced in broilers due to their rapid metabolic rate.

4. Suppression of the Reproductive System

The rise in corticosterone caused by heat stress suppresses reproductive hormones:

• Reduced LH and FSH secretion → slower follicle development and ovulation.
• Decreased progesterone and oestrogen → poor egg quality and weaker shells.
• Lower vitellogenin synthesis → impaired yolk formation.

Consequently, egg production declines, shell strength decreases, and breakage rates increase.

5. Effects on the Immune System

HPA axis activation has a suppressive impact on immunity:

• Shrinkage of lymphoid organs (thymus, bursa, spleen).
• Reduced lymphocyte production; increased heterophil-to-lymphocyte (H/L) ratio, a key stress indicator.
• Lower IgG, IgM, and IgA concentrations.
• Decreased T and B cell proliferation.
• Weakened vaccine responses and higher infection susceptibility.

This makes birds more vulnerable to pathogens and secondary infections.

Not Just Heat: A Silent System Breakdown

For chickens, heat stress is not merely an environmental challenge; it is a multi-system physiological crisis. The HPA axis lies at its core. Short-term activation is adaptive, but when chronic, it causes serious damage to the reproductive, immune, and metabolic systems.

Therefore, intervention should not focus solely on reducing temperature; it must also target the body’s physiological responses.

What Can Be Done?

• Environmental control (ventilation, cooling systems) is essential but not sufficient.
• Nutritional support plays a crucial role in managing heat stress:
  • Antioxidant supplementation
  • Electrolyte balance support
  • Natural compounds that modulate HPA activity (such as phytobiotics and adaptogens)

Remember: heat stress is not just a problem of temperature regulation; it is a battle for homeostasis. Winning that battle requires not only cooling the environment but also strategically supporting the body’s adaptive systems.