Emeritus Professor Maree Gleeson

OBJECTIVE: To investigate relationships between training mileage and intensity, and the type, incidence, severity, and duration of respiratory illness in distance runners, and the impact of illness on submaximal and maximal running performance. DESIGN: A longitudinal observational study of distance runners with serial monitoring of training loads and clinical patterns of illness. SETTING: A 4-month winter training period in the Southern Hemisphere. PARTICIPANTS: A total of 20 highly trained (elite) male middle-distance and distance runners competing at the national and international levels. MAIN OUTCOME MEASURES: Training was quantified by mileage (km), intensity (scale, 1-5), and load (volume x intensity). Symptoms and signs of respiratory illness (type, duration, and severity) were verified by a physician at a weekly review. Performance was monitored by measuring submaximal and maximal oxygen uptake and time to exhaustion on a incremental treadmill test. RESULTS: A majority of subjects (15/20) experienced 1 or more episodes of respiratory illness (mean, 2.5 episodes; range, 1-5), with 79% of symptoms classified as upper respiratory in origin. There were no significant differences in mean weekly mileage (P = 0.43), training intensity (P = 0.85), or training load (P = 0.45) between healthy runners and those affected by illness. Mean weekly (88 +/- 46 km) and mean monthly (373 +/- 163 km) mileages prior to each episode of illness were similar to the overall study means (95.5 +/- 36.4 km and 382 +/- 146 km). There were no substantial relationships between mean weekly training mileage, intensity, or training load and the number of illnesses reported (all r < 0.20). Neither submaximal nor maximal running performance was significantly affected by the presence of illness. CONCLUSIONS: Differences in training mileage, intensity, and load were not associated with the incidence of respiratory illness in highly trained middle-distance and distance runners. Runners with mild illness can be reassured that symptoms will not necessarily impair submaximal and maximal performance.

During a prospective study of the ontogeny of the mucosal immune system using saliva, one subject acquired a selective IgA deficiency at 3 years 6 months of age. Prior to this time the infant had normal ontogeny patterns for salivary immunoglobulins and the salivary IgA was confirmed to be dimeric IgA containing secretory component. Two respiratory tract infections at 3 years 4 months and 3 years 5 months were reported prior to the collection of a saliva sample which was deficient in IgA. All subsequent saliva collections remained IgA deficient. Serum and saliva collected at 11 years of age confirmed persistent IgA deficiency. There was a family history of organ-specific autoimmune disease. The prospectively collected data indicate in this subject that the IgA deficiency was not congenital, but was acquired closely associated with two episodes of respiratory tract infections, against a genetic background of disturbed immune regulation. Copyright © 1994, Wiley Blackwell. All rights reserved

The development of secretory IgA was followed in saliva of 263 children from birth to age 5, and in cross sectional studies of Australian school children and Papua New Guinea highland children from birth to age 5. Salivary IgA first appeared after the first week of life, peaking at 6 weeks, and falling again at 12 weeks, then rising to a peak around age 5-7, to remain at adult levels. A transient period of absent salivary IgA occurred sometime during the first 4 years in a few individuals. 5 factors were found to affect the pattern of development of IgA: the mucosal IgM response, mucosal permeability, feeding, environmental exposure, and nutritional status. The presence of IgA was associated with IgM, but not albumin, suggesting that it is secreted by plasma cells locally, rather than by transudation. On the other hand, presence of IgG in saliva was associated with that of albumin, a marker of mucosal permeability. Feeding infants formula accelerated the appearance of IgA, suggesting that this is an immune response to formula contents or to altered gut flora. In Papua New Guinea, malnourished children had lower total IgA and specific IgA antibody to E. coli and H. influenza than did normal children. The environmental stimuli of birth and entering school were both marked by dramatic increases in IgA levels. Age-matched children from Papua New Guinea had 2-3 times higher IgA levels than Australian children.

OBJECTIVE: To assess the adequacy of investigation and later review of patients with serum monoclonal proteins detected in our laboratory. METHOD: To review all monoclonal proteins detected and to search through the laboratory computerized records for evidence of further investigation and later review. RESULTS: Nine per cent of monoclonal proteins detected were not followed up at all. A urine examination to detect Bence-Jones protein was not requested in 12% of those regularly followed up. The mean age of the patients studied was 69 years, but there were eight patients under 60 years who had multiple myeloma.

A large number of studies have failed to show whether exercise-induced perturbations in immune function are associated with the incidence of infection. "Sports immunology", examining the interaction of physical, psychological and environmental stress on immunity, is emerging as a sub-discipline of sports medicine. A series of studies by our research team has profiled the immune responses of elite swimmers during training. Serum immunoglobulin and IgG subclass levels were lower in swimmers than controls. Suppression of mucosal immune parameters has been associated with the risk of upper respiratory tract infection. Swimmers with a lower pre-season salivary IgA and/or lower pre-exercise salivary IgA level were more likely to contract an URTI during a 7-month training period. In a shorter 12-week study, infected swimmers had a mean salivary IgM concentration that dropped more sharply after a single training session. Significant declines in natural killer cell count and neutrophil oxidative activity were not associated with URTI. Despite systemic and mucosal immunosuppression a cohort of swimmers were also able to mount an antibody response to pneumococcal vaccine equivalent to that of sedentary individuals. Observations of chronic suppression of aspects of host defence and the significant relationship between changes in mucosal immune parameters and URTI, provide a framework for assessment of the immune status of athletes. The underlying causes of upper respiratory tract distress symptoms may be infective, inflammatory or allergic in origin: a differential diagnosis has implications for treatment and management. © Georg Thieme Verlag.