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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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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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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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Matthew Ellis, Mark Noon, Tony Myers and Neil Clarke

Soccer has an intermittent activity profile and yields energy from aerobic and anaerobic pathways. 1 Caffeine is a popular ergogenic and can enhance intermittent, 2 endurance, 3 and resistance 4 performance. Caffeine nonselectively blocks both adenosine receptors and competitively inhibits the

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Nicholas J. Hanson, Sarah C. Martinez, Erik N. Byl, Rachel M. Maceri and Michael G. Miller

Caffeine is one of the most widely used drugs in the world. There is evidence of a central nervous system effect from caffeine ingestion, through inhibition of adenosine receptors. 1 By decreasing neurotransmitter release by adenosine, caffeine can act to indirectly increase the amount of

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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

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Mark Evans, Peter Tierney, Nicola Gray, Greg Hawe, Maria Macken and Brendan Egan

caffeine occurs in several species, including humans ( Fredholm et al., 1999 ). One week of caffeine administration increased the number of A1 and A2A adenosine receptors in rat cerebral cortical membranes by 25% ( Fredholm, 1982 ). Thus, a larger dose of caffeine would be needed to antagonize the same