An increased incidence of upper respiratory tract infections is often reported by individuals undertaking prolonged strenuous exercise and by athletes during periods of heavy training (Gleeson, 2000; Mackinnon, 2000). Therefore, we examined the effects of acute exhaustive exercise performed during normal, intensified and recovery training periods on several aspects of immune function including neutrophil and monocyte oxidative burst, lymphocyte proliferation and T-cell cytokine production.
Following approval by the South Birmingham Local Research Ethics Committee, seven healthy endurance-trained men (age 30 ± 2 years, body mass 75 ± 3 kg, maximal oxygen uptake (×{special}O2max) 4.55 ± 0.11 l min-1; means ± S.E.M.) completed three trials consisting of cycling exercise at a work rate equivalent to 74 % ×{special}O2max until volitional fatigue. The trials took place before and after a 6-day period of intensified training (IT) and after 2 weeks of light recovery training (RT). Normal training (NT) consisted of ~10 h of cycling per week; during IT the training load was increased on average by 73 %. During RT, exercise was limited to no more than 3 h per week for 2 weeks. Training intensity and duration were confirmed by the use of heart rate monitors. Venous blood samples were collected at rest, during and after the exercise trials. Following stimulation with phorbol 12-myristate 13-acetate (PMA) and ionomycin, samples were stained for T-lymphocyte surface antigens (CD3), and intracellular interferon (IFN)-λ and analysed using flow cytometry. Neutrophil and monocyte oxidative burst activity (reactive oxygen species production) were assessed using E. coli (as stimulant) and flow cytometry. Lymphocyte proliferation was determined by [3H]thymidine incorporation using phytohemagluttinen as the mitogen and expressed as the stimulation index (stimulated to unstimulated ratio). A two-way (trial X time) repeated measure ANOVA was used to compare means with post hoc Tukey or paired t tests as appropriate.
Time to exhaustion in the exercise trials was 107 ± 7, 85 ± 5 and 100 ± 7 min during NT, IT and RT periods, respectively (P < 0.01, NT vs IT). Following acute exhaustive exercise on the NT trial the circulating number of IFN-λ+ T-cells (P < 0.05), and the amount of IFN-λ produced per T-cell (P < 0.05) was decreased. The circulating number of T-cells producing IFN-λ was lower at rest following the IT period compared with normal training (P < 0.05), though the amount of IFN-λ produced per T-cell was unchanged (Table 1). Neutrophil oxidative burst activity and lymphocyte proliferation both fell after acute exercise by about 30 % (P < 0.05) and both neutrophil and monocyte oxidative burst were lower (P < 0.05) at rest after the IT period compared with NT (Table 1). All measured immune functions were back to normal after 2 weeks of RT.
These results indicate that resting immune function is decreased after only 6 days of intensified training and these effects are reversible with two weeks of relative rest. In general the immune response to an acute bout of exhaustive exercise was not affected by the weekly training load.
This work was supported by GlaxoSmithKline.
