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Syncope and Acclimatization

The incidence of heat syncope declines with each day of exercise-heat exposure. This parallels the circulatory adaptations that occur during the first – days of heat acclimatization plasma volume expansion, decreased heart rate; see table This phenomenon is illustrated in figure which has been redrawn from a very early study of the body’s adaptive responses during heat acclimation.

Incidence of syncope among subjects living in a hot environment foreach day and undergoing exercise trials.

Reprinted Forty-five male test subjects lived in the heat for days, and underwent lengthy exercise trials each day. After nearly half of these males experienced syncope on day , investigators saw a rapid decline in these events until days -, when no one fainted. Although heat syncope may be associated with heat exhaustion and sometimes may be treated by replacing lost water and salt, heat syncope usually is categorized as a distinct syndrome because fainting may occur in individuals who have normal fluid-electrolyte status.

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Causes of Heat Syncope

If fainting occurs after exercise, when environmental conditions are mild, heat syncope per se is not involved. The possible causes for this type of syncope are numerous, and are classified as either cardiac or noncardiac. The former category includes heart valve obstruction, electrical conduction abnormalities arrhythmias, and nerve dysfunction. The latter includes metabolic low blood sugar, neurologic seizure, and psychiatric causes. However, vasovagal syncope is probably the most common type of fainting seen among athletes. The term vasovagal refers to the effect of the vagus nerves on veins and the heart. These nerves emerge from the medulla and pass downward through the neck, near the jugular vein, to various autonomic ganglia. From there, the vagus fibers innervate muscles of the thoracic and abdominal organs, where they control heart rate and almost all abdominal activities. Vigorous contractions of the ventricle in response to prolonged standing, dehydration, exercise, and increased blood levels of the hormone epinephrine see post are believed to initiate a vasovagal reaction by activating cardiovascular receptors that sense movement and/or force. These receptors are thought to initiate a reflex in the brain specifically, the medulla that produces vasovagal syncope. This state results from a strong activation of parasympathetic signals to slow the heart and sympathetic signals to dilate peripheral blood vessels, causing decreased cardiac output and blood pressure plus the classic symptoms of pallor, nausea, blurred vision, and fainting. The enhanced tone of the vagus nerve in endurance athletes probably explains why they are more susceptible to exercise-induced vasovagal syncope than nonathletes. Although this type of fainting is not life-threatening, the falls resulting from such vasovagal events can be dangerous. When athletes experience syncope repeatedly, it is more likely that cardiac complications or disease are involved, but proper diagnosis and medications may improve the possibility that the athletes can return to their sport.

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