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Busting myths about athlete immunity and low energy availability

In our recent paper, “Does REDs exist?”, we raise some important questions about the REDs concept and supporting evidence (1). This blog covers whether low energy availability (LEA), considered the cause of REDs, leads to ‘immunosuppression’ or ‘immunological dysfunction’ in athletes, as has been suggested. Interest in this topic has been stoked by observations that leanness and LEA are associated with the recall of illness symptoms in athletes.

Are infections a serious problem for athletes?

YES. For most of us, suffering a respiratory infection, such as a common cold, is an unwelcome nuisance. However, for an elite athlete, respiratory and gastrointestinal infections limit their availability to train and take part in major competition. Medal winning athletes typically report fewer and shorter lasting infections. Clearly, infection is incompatible with success in elite sport.

Athletes often choose to train and compete despite suffering acute infection symptoms with potentially serious implications for health and performance. For example, competing in distance running events with recent ‘below-the-neck’ systemic symptoms (e.g., fever, cough etc) doubles the likelihood of not finishing the event. From a practical standpoint, athletes suffering ‘below-the-neck’ symptoms should avoid heavy exercise as it may extend an ongoing infection and lead to serious medical complications.

Are athletes particularly susceptible to infections?

Sometimes YES. Unfortunately, definitive evidence is lacking to support the popular belief that athletes are more susceptible to infections than non-athletes. This is because studies have rarely compared infection symptoms in athletes with a non-athletic control group. Other study weaknesses include small sample sizes, short monitoring periods, unstandardised infection symptom recording and effects of confounders — for example, respiratory infection symptoms can have a non-infectious cause such as hay fever.

Risk factors for infection in athletes are broadly similar to those in the wider population; including, the common cold season and foreign travel, when pathogen exposure increases, and factors that compromise immunity by activating the body’s stress pathways (see section below on 'A multifactorial approach to maintaining athlete immune health') including psychological stress, anxiety, depression and poor sleep. Its logical to conclude that ‘yes’ elite athletes are often particularly susceptible to infection as they experience increased pathogen exposure (e.g., when travelling for training camps and competition) and increased psychological stress and poor sleep around the time of important competition.

Does exercise cause 'immunosupression' in athletes?

NO. As far back as the 1980’s, it was a commonly held belief amongst scientists, athletes and support staff, that heavy exercise caused ‘immunosuppression’, increasing infection susceptibility in athletes. I now look back to when I wrote my PhD in the late 1990’s and think this was scaremongering because the terms commonly used at the time, ‘immunosuppression’ and ‘immunological dysfunction’ have such strong clinical connotations. These terms are being used frequently in papers on REDs and LEA. After more than 40 years of exercise immunology research, evidence is lacking that otherwise healthy athletes suffer ‘immunosuppression’ because of the exercise they do. The statistically significant, yet transient, immune changes induced by heavy exercise would largely be considered ‘unremarkable’ by a clinical immunologist — the athlete would not be considered ‘immunosuppressed’. Nevertheless, factors related to psychological well-being and the athlete’s lifestyle may decrease immune function, potentially increasing susceptibility to opportunistic, common or garden infections like the common cold, which is, after all, ‘common’.

A multifactorial approach to maintaining athlete immune health

Exercise immunologists have now adopted a multifactorial approach to understanding athlete immune health, broadening their interests beyond heavy exercise, acknowledging important roles for mental health, sleep and nutrition. Poor mental health (e.g., stress, anxiety, depression and mood disturbance) and poor sleep, just like other stressors, activate the body’s stress pathways (via the hypothalamic-pituitary-adrenal axis and sympathetic nervous system) increasing stress hormones like cortisol which in-turn alter immune function (see Figure 3 in our latest paper). Seminal studies in the general population show dose-response relationships between psychological stress and common cold and sleep quantity and quality and common cold after intra-nasal inoculation with rhinovirus.

Aligning with a multifactorial approach to athlete immune health, in our paper (1), and in another upcoming blog, we discuss the concept of ‘allostasis’ and how one or more different stressors combined can result in ‘allostatic load’, which over time causes ‘wear and tear’ to many of the body’s systems, including the immune system. As discussed below (see section below on 'Does low energy availability cause ‘immunosuppression’ in athletes?'), it’s likely that other stressors account for reports of increased infection in athletes with LEA.

Is nutrition important for athlete immune health?

YES. Nutrient availability influences immunity because macronutrients (carbohydrate, fat and protein) are involved in immune cell metabolism and protein synthesis (e.g., to make antibodies and cytokines) and micronutrients (e.g., vitamin C, D etc.) in antioxidant defences (2).

Varied diet — Athletes are recommended to follow a varied diet that avoids deficiencies of any of the macro- or micro-nutrients required for proper immune function, irrespective of their dietary preference/requirements (e.g., carnivorous, omnivorous, vegetarian diets, lactose intolerance etc.).

Adequate protein — Ensuring adequate protein intake is particularly important to support immunity. Protein deficiency is widely considered responsible for the ‘immunosuppression’ and clinical infection in severe malnutrition and starvation (e.g., in Kwashiorkor patients). Well-preserved immunity and infection resistance in anorexia nervosa patients is likely because protein intake is adequate —carbohydrate and fat are typically reduced. Anorexia nervosa patients suffer ‘immunosuppression’ and increased infection only when body weight decreases dramatically, by 40% or more, when there is clear evidence of decreased cellular immunity.

Does low energy availability cause 'immunosupression' in athletes?

UNLIKELY. As we discuss in our paper (1), direct evidence is currently lacking to support the notion that LEA, of the magnitude often reported in athletes, causes ‘immunosuppression’ or ‘immunological dysfunction’ as claimed. These terms (discussed above) have clinical connotations — otherwise healthy athletes are not clinically immunosuppressed.

A handful of survey studies show that leanness and LEA are associated with the recall of illness symptoms in athletes. Besides the fact that these findings are limited to association, and the challenges assessing energy availability in athletes, these studies lack comparator control and adopted unstandardised recall of infection symptoms over a 1–3-month period. Infection symptoms should be monitored daily using a validated common cold questionnaire.

In female athletes with an LEA determination, protein intake appears to be sufficient to support immunity, typically exceeding recommendations for endurance athletes (1.2–1.7 g·kg−1·day−1). As such, there must be some other explanation for the increased illness reports in athletes with LEA. It is conceivable that poor mental health, highly prevalent in female athletes with LEA, plays a role. For example, anxiety, stress, depression and overall recovery state explained most of the variance in illness symptoms in one study in female athletes with LEA. A multidimensional approach to supporting athlete immune health is needed (see section above on 'A multifactorial approach to maintaining athlete immune health').

Professor Neil Walsh

@ProfNeilWalsh