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Moving Toward Solid Ground on Exercise and Immune Defense Against Viral Infection


Exercise and Sport Sciences Reviews: October 2009 - Volume 37 - Issue 4 - p 155
doi: 10.1097/JES.0b013e3181b7ba03
Commentary to Accompany

Montana State University, Bozeman, MT

Authors for this section are recruited by Commentary Editor: George A. Brooks, Ph.D., FACSM, Department of Integrative Biology, University of California, Berkeley, CA 94720 (E-mail:

The onset of the seasonal influenza epidemic begins each year in October, and our interest in preventing viral infections is renewed each year about this time. The recent and ongoing outbreak of the H1N1 virus, more commonly known as the swine flu virus, provides us with an additional incentive to consider our vulnerability to respiratory tract viral infections. Although it is difficult to find a physiological system that is not improved by an appropriate exercise stimulus, the immune system has been difficult to characterize with respect to the influence of exercise on defense against viral infections. In this issue of Exercise and Sport Sciences Reviews, Martin et al. (2) provide an account of the challenges to characterizing the influence of exercise on risk and severity of respiratory tract viral infections. Based on their research in mice, the authors also propose one of the first hypotheses to describe the potential mechanisms underlying modulation of immune function that is consistent with the observational data regarding exercise and illness incidence in humans.

The basic pattern for incidence and severity of infection to decrease with moderate exercise and to increase with severe exercise is consistently supported in observational studies (described in greater detail by Martin et al. [2]). However, there is substantial debate regarding many aspects of this topic. For example, Bermon (1) hypothesized that nonpathogenic (not viral or bacterial) local inflammation in the upper respiratory tract (URT) after intense exercise may be the underlying cause of many subsequent upper respiratory illnesses. This hypothesis calls into question whether infection is present in the studies in which URT infection (URTI) symptoms are reported in the absence of a detectable pathogen. Alternatively, it may be argued that failing to detect a specific pathogen does not rule out infection as the cause of URTI symptoms. As most observational studies have not attempted to measure the presence of pathogens, the debate regarding inflammation versus infection as the link between exercise severity and the appearance of respiratory tract illness symptoms mainly has been based on indirect evidence. The research described by Martin et al. (2) certainly does not end this debate, but it does provide evidence of improved outcome with moderate exercise and worsened outcome with severe exercise after exposure to a true respiratory tract virus.

In addition to demonstrating the dose-response relationship of exercise to respiratory tract viral infection responses, Martin et al. (2) also provide evidence for the mechanism underlying this relationship. In a nutshell, they hypothesize that severe exercise elicits inflammation and endocrine responses that inhibit cell-mediated immunity, particularly by shifting the T-helper (TH) lymphocyte balance toward Type 2 (TH2) and away from Type 1 (TH1) function. This shift decreases cell-mediated immunity and may allow for increased severity of respiratory tract and other viral infections. Some elements of this hypothesis were previously proposed by Smith (3) who suggested a link among cytokine responses, predominance of TH2 activity, and increased susceptibility to URTI with overtraining syndrome. However, Martin et al. (2) provide direct evidence to support these related hypotheses. An additional exciting component underlying the collective hypotheses of Bermon (1), Smith (3), and Martin et al. (2) is the common link between inflammation and the occurrence of illness. On one hand, inflammation may cause illness symptoms even in the absence of infection and, on the other hand, cytokines and endocrine factors regulating inflammation also may limit the ability of the innate immune system to fight respiratory tract viral infections.

Further research is needed to clarify additional details of moderate and severe exercise doses in humans, the mechanisms modulating defense against viral infections, and the types of viruses for which this relationship exists. This may allow us both to use exercise as a tool to limit the impact of viral epidemics and to avoid exercise that may increase our susceptibility to viruses.

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1. Bermon S. Airway inflammation and upper respiratory tract infection in athletes: Is there a link? Exerc. Immunol. Rev. 2007; 13:6-14.
2. Martin SA, Pence BD, Woods JA. Exercise and respiratory tract viral infections. Exerc. Sport Sci. Rev. 2009; 37:157-164.
3. Smith LL. Overtraining, excessive exercise, and altered immunity. Is there a T helper-1 versus T helper 2 lymphocyte response? Sports Med. 2003; 33:347-64.
©2009 The American College of Sports Medicine