Human T lymphocyte migration towards the supernatants of human rhinovirus infected airway epithelial cells: influence of exercise and carbohydrate intake.

Physical stress induces a marked redistribution of T lymphocytes that may be influenced by carbohydrate (CHO) availability, yet the effect of these on T lymphocyte migration towards infected tissue is unknown. Therefore, the aim of this study was to determine the effect of strenuous exercise and CHO ingestion on subsequent ex vivo lymphocyte migration towards the supernatants of a Human Rhinovirus (HRV)-infected bronchial epithelial cell line. In a randomised, cross-over, double-blind design, 7 trained males ran for 2 h at 60% VO2peak on two occasions with regular ingestion of either a 6.4% w/v glucose and maltodextrin solution (CHO trial) or placebo solution (PLA trial). Plasma glucose concentration was higher on CHO than PLA after exercise (P<0.05). Migration of CD4+ and CD8+ cells and their CD45RA+ and CD45RO+ subpopulations towards supernatants from HRV-infected cells decreased following exercise (main effect for exercise, P<0.01 for CD4+, CD4+CD45RA+ and CD4+CD45RO+; P<0.05 for CD8+, CD8+CD45RA+ and CD8+CD45RO+). Migration of CD4+ cells and CD4+CD45RA+ cells was approximately 35% and approximately 30% higher, respectively, on CHO than PLA at 1 h post-exercise (interaction, P<0.05 for both) and was higher on CHO than PLA for all other subpopulations (P<0.05, main effect for trial). There was little effect of exercise or CHO on migration of these cells towards uninfected (control) cell supernatants or on the proportion of these cells within the peripheral blood mononuclear cell population. The findings of this study suggest that physical stress reduces T cell migration towards HRV-infected cell supernatants and that ingestion of CHO can lessen this effect.

Immunoendocrine response to cycling following ingestion of caffeine and carbohydrate.

PURPOSE: This study investigated the effect of caffeine consumed with and without carbohydrate (CHO) on immunoendocrine responses after exercise. METHODS: On four occasions, 12 recreational male cyclists cycled for 2 h at 65% V O2max. Sixty minutes before exercise, participants ingested 6 mg.kg(-1) body mass of caffeine (CAF) or placebo (PLA), then during exercise they consumed a 6% CHO or placebo (PLA) drink, providing CAF/CHO, PLA/CHO, CAF/PLA, and PLA/PLA conditions. RESULTS: f-MLP-stimulated neutrophil oxidative burst responses were significantly higher after exercise on CAF/CHO and PLA/CHO (both P<0.05) than PLA/PLA when expressed as a percentage of baseline value. The response on CAF/PLA tended to be higher than PLA/PLA at this point (P=0.056). No significant differences between CAF/CHO, PLA/CHO, and CAF/PLA were observed after exercise; however, only PLA/CHO showed no significant postexercise decline. Coingestion of CAF/CHO significantly attenuated epinephrine (P<0.05) and IL-6 (P<0.05) responses that occurred after ingestion of CAF alone (CAF/PLA) and significantly attenuated the transient alterations in circulating leukocyte (P<0.05) and neutrophil (P<0.01) counts. Plasma cortisol concentration was significantly lower on PLA/CHO than CAF/PLA and PLA/PLA after exercise (P<0.05). Perceived exertion during exercise was significantly lower on CAF/CHO than the other three trials (P<0.05). CONCLUSION: Taken together, this suggests that coingestion of caffeine and CHO has greater influence on immunoendocrine responses than neutrophil functional responses to prolonged exercise.

Connecting funds with quality outcomes in health care: a blueprint for a Clinical Practice Improvement Payment.

There are significant geographic variations in the quality of health care, often with substantial gaps between what is known to be achievable and what is actually achieved in practice. This is a global problem that has persisted for many years despite a variety of conventional quality improvement initiatives. Attention has therefore recently turned to realignment of funding with specified levels of desired quality of care as an alternative. This paper outlines one approach that will be introduced as a pilot in Queensland.

Effect of caffeine supplementation on the extracellular heat shock protein 72 response to exercise.

The stimulus for the release of 72-kDa heat shock protein (HSP72) during exercise in humans is currently unclear. Recent evidence in an animal model is suggestive of an involvement of catecholamines. The present study, therefore, investigated the effect of caffeine supplementation, a known stimulator of sympathetic activity, on the extracellular (e)HSP72 response to prolonged exercise. Ten healthy male endurance-trained cyclists were recruited (age: 21 +/- 1 yr, maximum O(2) uptake 61.1 +/- 1.7 ml x kg(-1) x min(-1), mean +/- SE). Each subject was randomly assigned to ingest either 6 mg/kg body mass of caffeine (Caff) or placebo (Pla) 60 min before one of two 90-min bouts of cycling at 74 +/- 1% maximum O(2) uptake. Trials were performed at least 7 days apart in a counterbalanced design. Venous blood samples were collected by venepuncture at pretreatment, preexercise, postexercise, and 1 h postexercise. Serum caffeine and plasma catecholamines were determined using a spectrophotometric assay and high-performance liquid chromatography, respectively. Plasma HSP72 and cortisol were determined by ELISA. Serum caffeine concentrations were significantly increased throughout Caff, while no increases were detected in Pla. Caffeine supplementation and exercise was associated with a greater eHSP72 response than exercise alone (postexercise Caff 8.6 +/- 1.3 ng/ml; Pla 5.9 +/- 0.9 ng/ml). This greater eHSP72 response was associated with a greater epinephrine response to exercise in Caff. There was a significant increase in norepinephrine and cortisol, with no intertrial differences. The present data suggest that, in humans, catecholamines may be an important mediator of the exercise-induced increase in eHSP72 concentration.

Salivary IgA responses to prolonged intensive exercise following caffeine ingestion.

PURPOSE: Prolonged, intensive exercise is associated with a reduction in concentration and secretion of salivary IgA (s-IgA). Saliva composition and secretion are under autonomic nervous system control, and caffeine ingestion, a widespread practice among athletes for its ergogenic properties, is associated with increased sympathetic nervous system activation. Therefore, this study investigated the influence of caffeine ingestion on s-IgA responses to prolonged, intensive exercise. METHODS: In a randomized crossover design, 11 endurance-trained males cycled for 90 min at 70% VO2peak on two occasions, having ingested 6 mg x kg(-1) body mass of caffeine (CAF) or placebo (PLA) 1 h before exercise. Whole, unstimulated saliva samples were collected before treatment (baseline), preexercise, after 45 min of exercise (midexercise), immediately postexercise, and 1 h postexercise. Venous blood samples were collected from a subset of six of these subjects at baseline, preexercise, postexercise, and 1 h postexercise. RESULTS: An initial pilot study found that caffeine ingestion had no effect on s-IgA concentration, secretion rate, or saliva flow rate at rest. Serum caffeine concentration was higher on CAF than PLA at preexercise, postexercise, and 1 h postexercise (P < 0.001). Plasma epinephrine concentration was higher on CAF than PLA at pre- and postexercise (P < 0.05). s-IgA concentration was higher on CAF than PLA at mid- and postexercise (P < 0.01), and s-IgA secretion rate was higher on CAF than PLA at midexercise only (P < 0.02). Caffeine ingestion did not affect saliva flow rate. Saliva alpha-amylase activity and secretion rate were higher on CAF than PLA (main effect for trial, P < 0.05). CONCLUSIONS: These findings suggest that caffeine ingestion before intensive exercise is associated with elevated s-IgA responses during exercise, which may be related to increases in sympathetic activation.

Lymphocyte responses to influenza and tetanus toxoid in vitro following intensive exercise and carbohydrate ingestion on consecutive days.

The effect of carbohydrate (CHO) ingestion on antigen- (rather than mitogen-) stimulated T-cell responses to prolonged, intensive exercise may give a more realistic insight into the effect of CHO on T-cell functional capacity and subsequent infection risk. This study investigated the effect of CHO ingestion during prolonged, intensive exercise on influenza- and tetanus toxoid-stimulated T-cell cytokine mRNA expression and proliferation. Mitogen- [phytohemagglutinin (PHA)] stimulated proliferation was assessed for comparison. Responses were assessed following exercise on consecutive mornings to determine any carryover effect. Fifteen male games players performed two exercise trials in a double-blind, randomized, crossover design. Each trial comprised 90 min of intensive, intermittent running on consecutive mornings, with either CHO (6.4% wt/vol) or placebo (PLA) beverage ingestion before, during, and after each bout of exercise. Postexercise CD3(+) cell counts were higher in PLA than CHO on both days (P < 0.05). Antigen-stimulated T-cell cytokine mRNA expression was unaffected by exercise or CHO ingestion. Before exercise on day 2, T-cell proliferative responses to PHA, influenza, and tetanus toxoid were higher in CHO than PLA by 99, 80, and 58%, respectively (P < 0.01 for PHA, P < 0.05 for influenza and tetanus toxoid). At 1 h postexercise on day 2, PHA-induced proliferation was 70% higher in CHO than PLA (P < 0.05), yet there were no differences between trials for antigen-induced proliferative responses. Therefore, mitogen-induced T-cell proliferation following strenuous exercise and CHO does not necessarily reflect responses to specific antigens and, consequently, may not provide a good model for the situation in vivo.

The effect of caffeine ingestion on human neutrophil oxidative burst responses following time-trial cycling.

Following fixed-duration exercise of submaximal intensity, caffeine ingestion is associated with an attenuation of the exercise-induced decline in N-formyl-methionyl-phenyl-alanine (f-MLP) stimulated neutrophil oxidative burst. However, the response following high-intensity exhaustive exercise is unknown. Nine endurance-trained male cyclists ingested 6 mg caffeine or placebo per kilogram of body mass 60 min before cycling for 90 min at 70% of maximal oxygen consumption (VO2max) and then performing a time-trial requiring an energy expenditure equivalent to 30 min cycling at 70% maximum power output. Time-trial performance was 4% faster in the caffeine than in the placebo trial (P = 0.043). Caffeine was associated with an increased plasma adrenaline concentration after 90 min of exercise (P = 0.046) and immediately after the time-trial (P = 0.02). Caffeine was also associated with an increased serum caffeine concentration (P < 0.01) after 90 min of exercise and immediately after the time-trial, as well as 1 h after the time-trial. However, the f-MLP-stimulated neutrophil oxidative burst response fell after exercise in both trials (P = 0.002). There was no effect of caffeine on circulating leukocyte or neutrophil counts, but the lymphocyte count was significantly lower on caffeine (20%) after the time-trial (P = 0.003). Our results suggest that high-intensity exhaustive exercise negates the attenuation of the exercise-induced decrease in neutrophil oxidative burst responses previously observed when caffeine is ingested before exercise of fixed duration and intensity. This may be associated with the greater increase in adrenaline concentration observed in the present study.

The effect of caffeine ingestion on neutrophil oxidative burst responses following prolonged cycling.

This study investigated the effect of caffeine ingestion on neutrophil oxidative burst responses to prolonged cycling. In a two part study, 19 endurance trained male cyclists (Part A--11; Part B--8) performed 90 min of exercise at 70% VO2max 1 h after ingesting 6 mg/kg body mass of caffeine (CAF) or placebo (PLA). CAF ingestion had no effect on the PMA-stimulated oxidative burst response (Part A), yet it attenuated the exercise-induced decline in f-MLP stimulated response that occurred with PLA (Part B). CAF ingestion significantly increased serum caffeine concentration and plasma adrenaline concentration following exercise. In addition, circulating lymphocyte count was increased following CAF ingestion whereas there was no effect on neutrophil number. Therefore, although CAF ingestion was associated with an increase in adrenaline, this was not associated with an expected decrease in neutrophil function. This suggests that in the present study, CAF ingestion influenced neutrophil function via alternative mechanisms.