Monocyte function has been reported to fall temporarily after prolonged strenuous exercise (Baum et al. 1997). Increases in plasma cortisol and prolactin concentration after prolonged strenuous exercise may be partly responsible for exercise-induced alterations in monocyte function (Woods, 2000). Prolonged exercise in hot conditions has been shown to elevate plasma cortisol (Mitchell et al. 2002), prolactin (Bridge et al. 2003) and the circulating monocyte count (Severs et al. 1996) to a greater extent than prolonged exercise in cool conditions. We therefore wished to examine the influence of prolonged strenuous exercise in hot and humid conditions on monocyte function (lipopolysaccharide (LPS)-stimulated TNF-α release) in endurance trained males.

With local ethics committee approval, thirteen well trained male cyclists (age 28 ± 2 years, body mass 75.4 ± 1.4 kg, Î{special}J{special}_,max 61.2 ± 2.3 ml kg^-1 min^-1, mean ± S.E.M.) volunteered to participate in the study. On two occasions, in random order and separated by one week, subjects reported to the laboratory at 1230 h following a 4 h fast. Subjects cycled for 2 h on a stationary ergometer at 55 % peak power output (194 ± 4 W) in an environmental chamber on one occasion at a temperature and humidity of 20.4 ± 0.1°C and 60 ± 1 % (CONTROL) and on another occasion 30.3 ± 0.1°C and 76 ± 1 % (HOT). Venous blood samples were collected at pre, post and 2 h post-exercise. Plasma cortisol, prolactin and TNF-α concentrations were determined using ELISA. Blood monocyte counts were performed using a Beckman Coulter counter. Monocyte function was assessed by measuring the plasma TNF-α concentration in unstimulated samples and after treatment of a 1 ml aliquot of whole blood with 50 µl LPS stimulant (10 mg ml^-1) for 1 h at 37°C. Results were analysed using a two-factor (trial X time) repeated measures ANOVA with post hoc Tukey’s HSD. Statistical significance was accepted at P < 0.05.

Final rectal temperatures were 38.1 ± 0.1°C (CONTROL) and 38.7 ± 0.1°C (HOT: P < 0.01). Plasma cortisol concentration increased post-exercise (P < 0.01) and was significantly higher on the HOT trial at post and 2 h post-exercise (P < 0.01). Plasma prolactin concentration increased post-exercise (P < 0.01) and was significantly higher on the HOT trial at post-exercise (P < 0.01). Circulating monocyte counts increased post-exercise (P < 0.01) and were significantly higher on the HOT trial at post and 2 h post-exercise (CONTROL: pre-exercise 0.4 ± 0.0, post-exercise 0.8 ± 0.1; HOT: pre-exercise 0.4 ± 0.0, post-exercise 0.9 ± 0.1 X 10⁹ cells l^-1, P < 0.01). Plasma TNF-α concentration increased post-exercise (P < 0.01). LPS-stimulated TNF-α release increased 2 h post-exercise (P < 0.01). LPS-stimulated TNF-α release per monocyte decreased post-exercise (CONTROL: pre-exercise 3.4 ± 0.4, post-exercise 2.5 ± 0.4; HOT: pre-exercise 4.1 ± 0.7, post-exercise 1.7 ± 0.2 fg. Cell^-1, P < 0.01). The post-exercise decrease in LPS-stimulated TNF-α release per monocyte tended to be greater on the HOT trial but this did not reach statistical significance (interaction: P = 0.06 ANOVA).

These data suggest that prolonged strenuous exercise results in a decrease in LPS-stimulated monocyte TNF-α release (on a per cell basis) and that performing the exercise in hot and humid conditions does not significantly alter this response.