When ambient heat turns calf growth into maintenance | Dellait

Álvaro García

Heat stress is usually discussed in the context of lactating cows. Milk production declines, reproductive performance suffers, and respiration rates rise as cows struggle to dissipate excess body heat. Because these losses are visible and economically immediate, the effects of summer heat on mature cows receive most of the industry’s attention.

Calves, however, are often overlooked when it comes to summer heat. This is partly because the signs in young animals are less obvious. A preweaned calf does not show a drop in the milk tank, nor does it carry the metabolic burden of a high-producing lactating cow. In fact, calves often continue drinking milk or eating starter even under elevated temperatures, creating the impression that they are tolerating the heat well. But that impression can be misleading.

Where are your calves being raised right now?

Regions currently (June 2026) experiencing elevated temperature and humidity may expose calves to varying degrees of heat stress risk. Actual heat stress depends not only on ambient temperature, but also on humidity, solar radiation, air movement, and housing conditions. 

Heat stress in calves may not always reduce feed intake enough to explain the losses in growth commonly observed during hot weather. Research suggests that the actual cost of heat stress in young animals is not simply lower nutrient intake, but rather a shift in how nutrients are used. Energy that should support growth is instead redirected toward maintaining thermal balance, supporting immune activation, and repairing tissue damage.

This distinction matters because growth during the preweaning period is not just about adding body weight. It determines skeletal development, mammary gland growth, immune competence, and future milk production. Anything that slows this process can have lasting effects.

Earlier work has already shown that summer heat reduces preweaning performance through increased maintenance requirements and lower nutrient-use efficiency (Garcia 2020). More recent evidence now suggests that part of this loss may be driven by intestinal inflammation and immune activation.

Heat changes where energy goes

One of the most important concepts in calf nutrition is that nutrients are never used for just one purpose. Energy must first meet maintenance requirements before it can support growth. Under normal environmental conditions, this balance favors tissue accretion. Once maintenance is covered, the remaining nutrients can be directed toward frame growth, muscle deposition, organ development, and the initial stages of mammary development. Heat stress changes that balance. To maintain body temperature, calves increase respiratory rate and activate evaporative cooling mechanisms. Unlike sweating, which is limited in cattle, panting becomes the primary pathway for dissipating heat. This process is effective, but it comes at an energetic cost. Respiration rate increases, maintenance requirements rise, and a greater portion of available energy is diverted away from growth.

Recent work presented by A. Rius at the 2026 ASAS Physiology Symposium demonstrated just how significant that shift can be. Using production data from normothermic and hyperthermic calves, his group modeled energy utilization and found that heat stress increased thermoregulatory energy requirements by approximately 17% of metabolizable energy for maintenance. Under thermoneutral conditions, calves allocated approximately 56% of their total energy requirements toward frame growth. In hyperthermic calves, that number dropped to only 40%, creating an energy differential of 1.2 Mcal of metabolizable energy daily.

Heat-stressed calves showed declines in average daily gain and feed efficiency of up to 35%, even when feed intake remained unchanged. This finding challenges the traditional assumption that poor summer growth is merely a feeding problem. In many cases, the calf may consume adequate nutrients, but those nutrients are no longer available for efficient growth.

This helps explain why increasing milk or starter intake during periods of heat stress does not always fully recover lost performance. The limitation may not be nutrient supply alone, but how the calf is forced to use those nutrients.

Table 1. Physiological effects of heat stress in preweaned dairy calves

Heat stress damages the gut

If heat stress simply increased maintenance requirements, the biological cost would already be important. But this research suggests its effects go much deeper. One of the most significant findings was its impact on intestinal integrity. Calves exposed to elevated temperatures showed a 20 to 24% increase in intestinal permeability, meaning the gut became more “leaky” and less able to maintain its normal barrier function. This matters because the intestinal lining is not only a digestive surface, but also one of the body’s main defenses against pathogens and toxins.

As body temperature rises, blood flow is redirected toward peripheral tissues to help dissipate heat. This reduces blood flow to the gastrointestinal tract, creating localized hypoxia and nutrient deprivation in the intestinal mucosa. The result is structural damage that compromises both nutrient absorption and barrier function. Rius’ data confirmed these changes, showing flattened jejunal villi and increased crypt depth in heat-stressed calves—classic indicators of intestinal stress. In practical terms, this means calves may continue eating, but their ability to digest and absorb nutrients efficiently may already be impaired.

The consequences extend beyond digestion. A weakened intestinal barrier allows greater movement of endotoxins and bacterial components into circulation, activating the immune system. That immune response is metabolically expensive, requiring energy and nutrients that would otherwise support growth. In other words, heat stress does not simply make calves hotter. It can damage the intestine, trigger inflammation, and redirect nutrients away from growth and toward maintenance and tissue repair.

Reducing the biological cost of heat

If heat stress shifts nutrients away from growth and toward maintenance, the next question becomes how producers can reduce that biological cost. The first line of defense remains environmental management. Shade, adequate ventilation, improved air movement, and unrestricted access to clean water are still the foundation of heat abatement. Calves housed in hutches, particularly under direct solar radiation, may experience heat loads well above ambient temperature, making simple adjustments in shade, hutch orientation, and airflow especially valuable for lowering heat accumulation and reducing thermoregulatory stress.

Hydration and nutritional management are equally important. As respiratory evaporation increases, calves lose more water and electrolytes, making constant access to fresh water essential. Strategic electrolyte supplementation may help support hydration and reduce part of that physiological burden. At the same time, the greater energetic cost of staying cool makes nutrient density more important. Calves may continue consuming milk or starter, but the efficiency of converting those nutrients into growth declines. Maintaining adequate protein and energy density can help offset some of these losses during prolonged heat exposure.

Emerging research suggests there may be another important nutritional target: the gut itself. If heat stress compromises intestinal integrity and increases inflammation, strategies aimed at supporting gut health become highly relevant. Prebiotics may help stabilize the microbial ecosystem and reinforce gut barrier function, while postbiotics may strengthen epithelial integrity and modulate inflammatory responses. Together, these approaches may help reduce intestinal permeability and preserve the calf’s ability to use nutrients for growth rather than diverting them toward tissue repair and immune activation.

Heat stress starts earlier than we think

For many producers, heat stress becomes a concern only when visible signs appear calves panting, reduced starter intake, lethargy, or obvious dehydration. But by the time these signs are present, part of the biological damage may already be underway. Recent research suggests that heat stress in calves begins much earlier, with subtle shifts in energy partitioning, increased thermoregulatory costs, compromised intestinal integrity, and activation of inflammatory pathways. These changes may be invisible at first, but their effects are measurable in reduced growth and poorer efficiency.

This matters because early-life growth has consequences far beyond weaning. Improved preweaning average daily gain has consistently been associated with greater milk production in first lactation. When heat stress suppresses growth during this critical window, the cost is not limited to lost weight. It may also affect structural development, immune competence, and the foundation for future performance.

Heat abatement in calves, therefore, is not simply about comfort. It is about protecting growth efficiency and preserving the biological resources needed to build the future dairy cow. A calf under heat stress may continue drinking milk and consuming starter, creating the impression that little has changed. But internally, nutrients that should be building frame, muscle, and mammary tissue may instead be diverted toward cooling the body, repairing the gut, and supporting inflammation. And when that happens, heat does not simply slow growth, it turns growth into maintenance.

The full list of references used in this article is available upon request.

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