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Gary J. Walker, Phillipa Caudwell, Natalie Dixon, and Nicolette C. Bishop

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.

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Elizabeth L. Abbey and Janet Walberg Rankin

Maintenance of repeated-sprint performance is a goal during team-sport competition such as soccer. Quercetin has been shown to be an adenosine-receptor antagonist and may reduce oxidative stress via inhibition of the enzyme xanthine oxidase (XO). The purpose of the study was to determine the effect of quercetin consumption on performance of repeated sprints and, secondarily, the XO and inflammatory-marker response induced by repeated-sprint exercise. Fifteen recreationally active, young adult men completed 2 repeated-sprint tests (RST), 12 × 30-m maximal-effort sprints (S1–S12), each after 1 wk supplementation with a placebo, a 6% carbohydrate commercial sports drink, or that drink with 500 mg of quercetin-3-glucoside, consumed twice a day (1,000 mg/d). Blood samples were collected before supplementation (B0), at baseline before each RST (B1), immediately after RST (B2), and 1 hr after RST (B3). Mean sprint time increased progressively and was significantly higher by S9 for both treatments (5.9%); however, there were no significant differences between treatments. Percent fatigue decrement (%FD) for placebo (3.8% ± 2.3%) was significantly less than with quercetin (5.1% ± 2.7%). Changes in blood XO, IL-6, and uric acid from B1 to B2 were +47%, +77%, and +25%, respectively, with no difference by treatment. In conclusion, repeated-sprint performance was not improved by quercetin supplementation and was worse than with placebo when expressed as %FD. Quercetin did not attenuate indicators of XO activity or IL-6, a marker of the inflammatory response after sprint exercise.

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Neil D. Clarke, Darren L. Richardson, James Thie, and Richard Taylor

nonselectively blocks adenosine receptors and competitively inhibits the action of adenosine, which during exercise can lower pain perception, increase neuro-excitability, and sustain motor unit firing. 2 Therefore, adenosine receptor antagonism is the leading hypothesis as to how caffeine could have an

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Vitor de Salles Painelli, Emerson L. Teixeira, Bruno Tardone, Marina Moreno, Jonatas Morandini, Victória H. Larrain, and Flávio O. Pires

It is consensually agreed that caffeine potentiates performance through its effects on the central nervous system, as caffeine antagonizes the A 1 and A 2A adenosine receptors ( Fredholm et al., 1999 ), reducing the inhibition on neuronal synapsis. Moreover, perceptual responses to exercise, such

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Mark Glaister and Conor Gissane

through the antagonism of adenosine receptors, leading to increases in neurotransmitter release, motor unit firing rates, and pain suppression. 4 However, the ubiquitous nature of adenosine receptors, coupled with their ability to produce differential responses depending on the site of action and the

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Neil D. Clarke and Darren L. Richardson

possibly affected by a number of factors such as training status, genotype, and habitual caffeine use ( Pickering & Grgic, 2019a ). Caffeine’s primary ergogenic mechanisms are considered to arise from the antagonism of adenosine receptors leading to an increase in neurotransmitter release, motor unit

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Mark Glaister, Colin Towey, Owen Jeffries, Daniel Muniz-Pumares, Paul Foley, and Gillian McInnes

exercise. 1 Although early research supported a glycogen-sparing mode of action, the key mechanism by which caffeine is now believed to enhance athletic performance is by the antagonism of adenosine receptors. 1 , 2 Given the abundance of adenosine receptors and their ability to elicit multiple responses

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Mayur K. Ranchordas, George King, Mitchell Russell, Anthony Lynn, and Mark Russell

 al., 2012 ; Foskett et al., 2009 ). Caffeine acts as an adenosine receptor antagonist, thus reducing the perception of effort at a given intensity and increasing central drive ( Davis et al., 2003 ). Traditionally, caffeine has been provided in a capsule or beverage form approximately one hour prior to

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Hermann Zbinden-Foncea, Isabel Rada, Jesus Gomez, Marco Kokaly, Trent Stellingwerff, Louise Deldicque, and Luis Peñailillo

could be an important component. Graham and Spriet 9 suggested an antagonistic role of caffeine on adenosine receptors. The binding of caffeine to adenosine receptors seems to delay fatigue by counteracting the inhibitory action of adenosine on neuronal excitability and release of excitatory

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Filip Sabol, Jozo Grgic, and Pavle Mikulic

become less effective in those who habitually ingest larger quantities of caffeine. Caffeine is an adenosine receptor antagonist, and when ingested, it binds to adenosine receptors. 13 In animal models, studies report that chronic caffeine intake increases adenosine receptor concentration and this