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This study investigated the effect of a high and low dose of caffeine on antigen-stimulated natural killer (NK) cell (CD3⁻CD56⁺) activation after prolonged, strenuous cycling, as assessed by the early-activation molecule CD69. In a randomized crossover design, 12 healthy male endurance-trained cyclists cycled for 90 min at 70% VO_2peak 60 min after ingesting either 0 (PLA), 2 (2CAF), or 6 (6CAF) mg/kg body mass of caffeine. Whole blood was stimulated with Pediacel (5 in 1) vaccine. A high dose of caffeine (6CAF) increased the number of CD3⁻CD56⁺ cells in the circulation immediately postexercise compared with PLA (p < .05). For both 2CAF and 6CAF, the geometric mean fluorescence intensity (GMFI) of CD69⁺ expression on unstimulated CD3⁻CD56⁺ cells was significantly higher than with PLA (both p < .05). When cells were stimulated with antigen, the GMFI of CD69 expression remained significantly higher with 2CAF than with PLA 1 hr postexercise (p < .05). Although not achieving statistical significance, 6CAF also followed a similar trend when stimulated (p = .09). There were no differences in GMFI of CD69 expression between 2CAF and 6CAF. These results suggest that a high (6 mg/kg) dose of caffeine was associated with the recruitment of NK cells into the circulation and that both a high and low (2 mg/kg) dose of caffeine increased unstimulated and antigen-stimulated NK-cell activation 1 hr after high-intensity exercise. Furthermore, there does not appear to be a dose-dependent effect of caffeine on NK-cell activation 1 hr after prolonged intensive cycling.

The aim of this study was to carry out a systematic review and meta-analysis of the effects of caffeine supplementation on physiological responses to submaximal exercise. A total of 26 studies met the inclusion criteria of adopting double-blind, randomized crossover designs that included a sustained (5–30 min) fixed-intensity bout of submaximal exercise (constrained to 60–85% maximal rate of oxygen consumption) using a standard caffeine dose of 3–6 mg·kg⁻¹ administered 30–90 min prior to exercise. Meta-analyses were completed using a random-effects model, and data are presented as raw mean difference (D) with associated 95% confidence limits (CLs). Relative to placebo, caffeine led to significant increases in submaximal measures of minute ventilation (D = 3.36 L·min⁻¹; 95% CL, 1.63–5.08; P = .0001; n = 73), blood lactate (D = 0.69 mmol·L⁻¹; 95% CL, 0.46–0.93; P < .00001; n = 208), and blood glucose (D = 0.42 mmol·L⁻¹; 95% CL, 0.29–0.55; P < .00001; n = 129). In contrast, caffeine had a suppressive effect on ratings of perceived exertion (D = −0.8; 95% CL, −1.1 to −0.6; P < .00001; n = 147). Caffeine had no effect on measures of heart rate (P = .99; n = 207), respiratory exchange ratio (P = .18; n = 181), or oxygen consumption (P = .92; n = 203). The positive effects of caffeine supplementation on sustained high-intensity exercise performance are widely accepted, although the mechanisms to explain that response are currently unresolved. This meta-analysis has revealed clear effects of caffeine on various physiological responses during submaximal exercise, which may help explain its ergogenic action.

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% VO_2max 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.

This study investigated the effects of caffeine on repeated, anaerobic exercise using a double-blind, randomized, crossover design. Seventeen subjects (five female) underwent cognitive (reaction time, number recall) and blood (glucose, potassium, catecholamines, lactate) testing before and after consuming caffeine (6 mg/kg), placebo, or nothing (control). An exercise test (two 60 s maximal cycling bouts) was conducted 90 min after caffeine/placebo consumption. Plasma caffeine concentrations significantly increased after caffeine ingestion, however, there were no positive effects on cognitive or blood parameters except a significant decrease in plasma potassium concentrations at rest. Potentially negative effects of caffeine included significantly higher blood lactate compared to control and significantly slower time to peak power in exercise bout 2 compared to control and placebo. Caffeine had no significant effect on peak power, work output, RPE, or peak heart rate. In conclusion, caffeine had no ergogenic effect on repeated, maximal cycling bouts and may be detrimental to anaerobic performance.