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Craig Pickering and Jozo Grgic

coffee may raise adenosine levels ( de Paulis et al., 2002 ). This increase in adenosine levels could subsequently counteract the ergogenic effects of caffeine on exercise performance. Specifically, after ingestion, caffeine binds to adenosine receptors, reduces perceived exertion, and ultimately

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Rachael C. Gliottoni, John R. Meyers, Sigurbjörn Á. Arngrímsson, Steven P. Broglio, and Robert W. Motl

This experiment examined the effect of a moderate dose of caffeine on quadriceps muscle pain during a bout of high-intensity cycling in low- versus high-caffeine-consuming males. College-age men who were low (≤100 mg/day; n = 12) or high (≥400 mg/day; n = 13) habitual caffeine consumers ingested caffeine (5 mg/kg body weight) or a placebo in a counterbalanced order and 1 hr later completed 30 min of cycle ergometry at 75–77% of peak oxygen consumption. Perceptions of quadriceps muscle pain, as well as oxygen consumption, heart rate, and work rate, were recorded during both bouts of exercise. Caffeine ingestion resulted in a statistically significant and moderate reduction in quadriceps muscle-pain-intensity ratings during the 30-min bout of high-intensity cycle ergometry compared with placebo ingestion in both low (d = −0.42) and high (d = −0.55) caffeine consumers. The results suggest that caffeine ingestion is associated with a moderate hypoalgesic effect during high-intensity cycling in college-age men who are low or high habitual caffeine consumers, but future work should consider better defining and differentiating pain and effort when examining the effects of caffeine during acute exercise.

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Rachael C. Gliottoni and Robert W. Motl

This experiment examined the effect of a moderate dose of caffeine on perceptions of leg-muscle pain during a bout of high-intensity cycling exercise and the role of anxiety sensitivity in the hypoalgesic effect of caffeine on muscle pain during exercise. Sixteen college-age women ingested caffeine (5 mg/kg body weight) or a placebo and 1 hr later completed 30 min of cycling on an ergometer at 80% of peak aerobic capacity. The conditions were completed in a counterbalanced order, and perceptions of leg-muscle pain were recorded during the bouts of exercise. Caffeine resulted in a large reduction in leg-muscle pain-intensity ratings compared with placebo (d = −0.95), and the reduction in leg-muscle pain-intensity ratings was larger in those with lower anxiety-sensitivity scores than those with higher anxiety-sensitivity scores (d = −1.28 based on a difference in difference scores). The results support that caffeine ingestion has a large effect on reducing leg-muscle pain during high-intensity exercise, and the effect is moderated by anxiety sensitivity.

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Todd A. Astorino, Michael N. Terzi, Daniel W. Roberson, and Timothy R. Burnett

Caffeine has been shown to reduce leg-muscle pain during submaximal cycle ergometry, as well as in response to eccentric exercise. However, less is known about its analgesic properties during non-steadystate, high-intensity exercise. The primary aim of this study was to examine the effect of 2 doses of caffeine on leg pain and rating of perceived exertion (RPE) during repeated bouts of high-intensity exercise. Fifteen active men (age 26.4 ± 3.9 yr) completed 2 bouts of 40 repetitions of “all-out” knee extension and flexion of the dominant leg at a contraction velocity equal to 180°/s. Before each trial, subjects abstained from caffeine intake and intense exercise for 48 hr. Over 3 days separated by 48 hr, subjects ingested 1 of 3 treatments (5 mg/kg or 2 mg/kg of anhydrous caffeine or placebo) in a randomized, single-blind, counterbalanced, crossover design. Leg-muscle pain and RPE were assessed during and after exercise using established categorical scales. Across all treatments, pain perception was significantly increased (p < .05) during exercise, as well as from Bout 1 to 2, yet there was no effect (p > .05) of caffeine on pain perception or RPE. Various measures of muscle function were improved (p < .05) with a 5-mg/kg caffeine dose vs. the other treatments. In the 5-mg/kg trial, it is plausible that subjects were able to perform better with similar levels of pain perception and exertion.

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Trent Stellingwerff, Ingvill Måkestad Bovim, and Jamie Whitfield

, it is imperative to understand how the various metabolic pathways interact in order to produce the required amounts of adenosine triphosphate (ATP). This understanding best informs potential nutritional interventions that may impact training adaptation and/or performance in a periodized manner. This

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Laís Monteiro Rodrigues Loureiro, Caio Eduardo Gonçalves Reis, and Teresa Helena Macedo da Costa

involved in the process of glycogen synthesis. Adenosine monophosphate-activated protein kinase (AMPK) is an enzyme responsible for the translocation of glucose transporter 4 (GLUT-4) to the cell membrane when activated by skeletal muscle contraction ( Mu et al., 2001 ; Stapleton et al., 1996 ). AMPK

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Louise M. Burke, Asker E. Jeukendrup, Andrew M. Jones, and Martin Mooses

the 10,000-m track race to >3.5 hr in the 50-km race walk) are considered “submaximal,” with mean energy requirements of ∼75–92% of maximal oxygen uptake ( V ˙ O 2 max ; Londeree, 1986 ). These are heavily dependent on aerobic resynthesis of adenosine triphosphate ( Coyle, 2007 ) and require adequate

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Ronald J. Maughan

Creatine phosphate allows high rates of adenosine triphosphate resynthesis to occur in muscle and therefore plays a vital role in the performance of high-intensity exercise. Recent studies have shown that feeding large amounts of creatine (typically 20 g per day for 5 days) increases muscle total creatine (and phosphocreatine) content. The extent of the increase that is normally observed is inversely related to the presupplementation level. Vegetarians, who have a very low dietary creatine intake, generally show the largest increases. Creatine supplementation has been shown to increase performance in situations where the availability of creatine phosphate is important; thus, performance is improved in very high-intensity exercise and especially where repeated sprints are performed with short recovery periods. Creatine supplementation is widely practiced by athletes in many sports and does not contravene current doping regulations. There are no reports of harmful side effects at the recommended dosage.

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Paul L. Greenhaff

Phosphocreatine (PCr) availability is likely to limit performance in brief, high-power exercise because the depletion of PCr results in an inability to maintain adenosine triphosphate (ATP) resynthesis at the rate required. It is now known that the daily ingestion of four 5-g doses of creatine for 5 days will significantly increase intramuscular creatine and PCr concentrations prior to exercise and will facilitate PCr resynthesis during recovery from exercise, particularly in those individuals with relatively low creatine concentrations prior to feeding. As a consequence of creatine ingestion, work output during repeated bouts of high-power exercise has been increased under a variety of experimental conditions. The reduced accumulation of ammonia and hypoxanthine in plasma and the attenuation of muscle ATP degradation after creatine feeding suggest that the ergogenic effect of creatine is achieved by better maintaining ATP turnover during contraction.

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Martin J. Gibala

The contribution of amino acid oxidation to total energy expenditure is negligible during short-term intense exercise and accounts for 3–6% of the total adenosine triphosphate supplied during prolonged exercise in humans. While not quantitatively important in terms of energy supply, the intermediary metabolism of several amino acids—notably glutamate, alanine, and the branched-chain amino acids—afreets other metabolites .including the intermediates within the tricarboxylic acid (TCA) cycle. Glutamate appears to be a key substrate for the rapid increase in muscle TCA cycle intermediates (TCAI) that occurs at the onset of moderate to intense exercise, due to a rightward shift of the reaction catalyzed by alanine aminotransferase (glutamate + pyruvate <-> alanine + 2-oxoglutarate). The pool of muscle TCAI declines during prolonged exercise, and this has been attributed to an increase in leucine oxidation that relies on one of the TCAI. However, this mechanism does not appear to be quantitatively important due of the relatively low maximal activity of branched-chain oxoacid dehydrogenase, the key enzyme involved. It has been suggested that an increase in TCAI is necessary to attain high rates of aerobic energy production and that a decline in TCAI may be a causative factor in local muscle fatigue. These topics remain controversial, but recent evidence suggests that changes in TCAI during exercise are unrelated to oxidative energy provision in skeletal muscle.