Are athletes susceptible to common cold?

 

Ryoichi Nagatomi

Lab of Health & Sports Science, Division of Biomedical Engineering for Health & Welfare, Tohoku University Graduate School of Biomedical Engineering, Seiryomachi 2-1, Aoba-ku, Sendai 980-8575, Japan

 

Elite athletes are believed to suffer higher incidence of common cold. Majority of common cold symptoms is caused by infection of common cold viruses causing upper respiratory tract illness.  Although fluctuation in salivary IgA concentration is reported to have some association with common cold incidence, high prevalence of asymptomatic IgA deficiency without apparent susceptibility to upper respiratory infection suggests that fluctuation in the concentration of salivary IgA may not directly explain the higher incidence of common cold symptoms among elite athletes. Natural killer cells are known to confront with viruses such as herpes virus and cytomegalovirus that continuously infect human cells. Natural killer deficient patients, however, does not show higher susceptibility to common cold viruses. Therefore large fluctuation in the circulating number of natural killer cells due to prolonged or high intensity exercise may not directly explain the susceptibility to common cold.

In search for potential causes for common cold susceptibility, it came to our attention that human rhinovirus, which causes more than 30% of human adult common cold symptoms during autumn and winter seasons, propagates in fibroblasts cultured at a lower temperature. Temperatures at upper airway such as oral and nasal cavities are lower than the core temperature, and have large individual differences. The upper airway temperature largely drops after strenuous exercise, possibly due to altered distribution of blood flow.

Human rhinovirus infected fibroblasts undergo apoptosis only when cultured at lower temperature, but not at 37ºC. Microarray analysis comparing the expression profile of mRNA in rhinovirus infected fibroblasts at 33ºC and 37ºC revealed a marked suppression of anti-apoptotic factor which also interfere with viral capsid formation. Although we still don’t know the mechanism by which lower temperature suppresses cellular defense system, since such anti-viral mechanism could also be shared with other viruses we suggest that temperature dependent cellular anti-viral protection may account, if not all, for common cold susceptibility of athletes.

 

Key words: common cold, human rhinovirus, apoptosis