A fever is an elevated body temperature, a controlled response the body uses to fight off infection. This temporary rise in temperature creates an environment unfavorable to invading viruses or bacteria. It seems counterintuitive that a person with a high fever often does not sweat, since sweating is the body’s primary cooling mechanism. This lack of sweating is due to a deliberate re-calibration of the body’s internal thermal regulation system.
How the Body Regulates Temperature Normally
The human body maintains a core temperature of about 98.6°F (37°C), which is necessary for biological processes to function correctly. When the body becomes too warm, it relies on two main physiological mechanisms to dissipate excess heat. The first is the production of sweat, which cools the skin through evaporative cooling as the moisture turns to vapor.
The second mechanism is vasodilation, where blood vessels near the skin’s surface widen. This allows more warm blood to flow close to the exterior, dumping heat into the surrounding environment through radiation and convection. These two cooling responses are the body’s standard, reflexive actions whenever the core temperature exceeds its established comfort zone.
The Role of the Hypothalamus in Raising the Set Point
The central control for temperature management is the hypothalamus, a small region in the brain that acts as the body’s master thermostat. This organ monitors the blood temperature and maintains the core temperature at a specific target, known as the set point. When the body encounters a pathogen, the immune system launches a defense, releasing signaling molecules called pyrogens.
These pyrogens, such as cytokines, travel through the bloodstream to the hypothalamus. There, they trigger the synthesis of prostaglandin E2 (PGE2), which acts as the chemical messenger that alters the thermostat’s setting. PGE2 instructs the body to raise the core temperature set point, perhaps from 98.6°F to a higher target like 102°F. This action of resetting the set point is the defining mechanism of a fever.
Why the Elevated Set Point Stops Sweating
The elevated set point is the reason why sweating ceases during the rising phase of a fever. Once the hypothalamus resets its target temperature upward, the current body temperature is perceived as too low relative to the new set point. Even if the body temperature is 99°F, the brain interprets this as cold if the new target is 102°F.
Because the body believes it is too cold, the hypothalamus engages mechanisms intended to generate and conserve heat. The cooling response, including sweating and vasodilation, is suppressed to prevent heat loss. Simultaneously, the body initiates shivering and chills, which are muscle contractions designed to rapidly produce heat. Blood vessels near the skin constrict (vasoconstriction) to shunt warm blood away from the surface, conserving heat. The lack of sweating is a consequence of the body actively trying to reach its new, higher thermal goal.
The Sweating Phase When the Fever Breaks
Sweating returns during the final stage of a fever, a phase known as defervescence or when the fever “breaks.” This change occurs once the immune system has cleared the infection or when fever-reducing medication, such as acetaminophen, inhibits the production of PGE2. The pyrogen signals diminish, and the hypothalamus rapidly resets the set point back down to the normal 98.6°F.
The body’s core temperature, which may still be elevated at 102°F, is suddenly much higher than the normal set point. The regulatory system recognizes a state of overheating. To rapidly drop the temperature, the hypothalamus triggers the activation of all available cooling mechanisms. This response includes intense vasodilation and profuse sweating, which quickly brings the core temperature back down to the normal range.