These data suggest that: 1) EIB is prevalent in several Olympic winter sports and affects nearly one of every four elite winter sport athletes; 2) the winter sport with the highest incidence of EIB is cross-country skiing; 3) in general, EIB is more prevalent in female versus male elite winter sport athletes; and 4) athletes may compete successfully at the international level despite having EIB.

The term exercise-induced bronchospasm (EIB) describes the acute transient airway narrowing that occurs during and most often after exercise in 10 to 50% of elite athletes, depending upon the sport examined. Although multiple factors are unquestionably involved in the EIB response, airway drying caused by a high exercise-ventilation rate is primary in most cases. The severity of this reaction reflects the allergic predisposition of the athlete, the water content of the inspired air, the type and concentration of air pollutants inspired, and the intensity (or ventilation rate) of the exercise. The highest prevalence of EIB is seen in winter-sport populations, where athletes are chronically exposed to cold dry air and/or environmental pollutants found in indoor ice arenas. When airway surface liquid lost during the natural warming and humidification process of respiration is not replenished at a rate equal to the loss, the ensuing osmolarity change stimulates the release of inflammatory mediators and results in bronchospasm; this cascade of events is exacerbated by airway inflammation and airway remodelling. The acute EIB response is characterised by airway smooth muscle contraction, membrane swelling, and/or mucus plug formation. Evidence suggests that histamine, leukotrienes and prostanoids are likely mediators for this response. Although the presence of symptoms and a basic physical examination are marginally effective, objective measures of lung function should be used for accurate and reliable diagnosis of EIB. Diagnosis should include baseline spirometry, followed by an appropriate bronchial provocation test. To date, the best test to confirm EIB may simply be standard pulmonary function testing before and after high-intensity dry air exercise. A 10% post-challenge fall in forced expiratory volume in 1 second is used as diagnostic criteria. The goal of medical intervention is to limit EIB exacerbation and allow the athlete to train and compete symptom free. This is attempted through daily controller medications such as inhaled corticosteroids or by the prophylactic use of medications before exercise. In many cases, EIB is difficult to control. These and other data suggest that EIB in the elite athlete is in contrast with classic asthma.

Self-reported symptoms by elite athletes are not reliable in identifying EIA. Reference range criterion for FEV1 decrement in the elite athlete postexercise contrasts current recommended guidelines. Moreover, a large number of false negatives may occur in this population if EIA screening is performed with inadequate exercise and environmental stress.

Sweating has a variety of functions in mammals including pheromone action, excretion of waste products and maintenance of the skin surface ecosystem. In a small number of mammalian species, which includes humans and the Equidae, it also has an important role in thermoregulation. This review is focused specifically on the thermoregulatory role of sweat in Equidae and the causes of sweating failure (anhidrosis). The first part describes the glandular appearance, sweat composition, and output rates; and considers the latest theories on the glandular control and secretory mechanisms. It is concluded that the glands are not directly innervated but are controlled by the interplay of neural, humoral and paracrine factors. The secretory mechanism is not as simple as previously thought and is mediated by the dynamic interaction of activating pathways, including autocrine control not only of the secretory process but probably also of secretory cell reproduction, growth, and death.

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Ultrastructural examination of sweat glands from the human loin before and during heat-induced activity indicated that the sweat is formed from the contents of disrupted cells as well as from the products of secretion. The principal secretory processes appear to be fluid transport and exocytosis of vesicles. However, configurations suggesting microapocrine secretion were also observed. It is concluded that the mechanisms involved in sweat production in man are fundamentally similar to those in animals and the terms 'apocrine' and 'eccrine' should be discarded. The myoepithelial cells which were contracted at the onset of sweating appeared to be under less tension after 3 h of continuous activity.

The present finding of the absence of structural defects in the glands indicates that future studies should concentrate on the investigation of neurohumoral or secretory cell metabolic abnormalities.

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