Research on the ergogenic effects of caffeine has primarily examined aerobic performance and consistently shown ergogenic benefits (10,15,22,24,34). Traditionally, the Randle Effect (enhanced fat mobilization and metabolism and consequent glycogen sparing) is the proposed mechanism (10,13,15,24). Consequently, a strong argument can be made that caffeine would not affect anaerobic exercise, because glycogen sparing in this paradigm is frivolous. However, recent studies have challenged the Randle Effect, showing that caffeine does not affect glycogen via this mechanism (6,15,18,20,22). Additionally, numerous studies show that caffeine provides an ergogenic benefit in anaerobic performance (2,4,12,15,17,33). In one study, caffeine ingestion (5 mg·kg−1) was shown to increase blood lactate concentration and mean power output in high-intensity cycling (12). Conversely, Greer et al. (19) found no effect of 6 mg·kg−1 of caffeine on power output during four 30-second Wingate exercise tests, although it yielded increases in lactate and catecholamine concentrations. Specific to resistance training, Beck et al. (4) and Green et al. (17) found caffeine to moderately enhance resistance training performance, but their results differed with respect to specific muscle groups. Although research has been equivocal, the ergogenic benefits of caffeine ingestion before anaerobic performance support the hypothesis that the ergogenic mechanism of caffeine is something other than glycogen sparing.
Other proposed mechanisms include a tendency to influence myosin-actin interaction, raise catecholamine levels, and decrease pain perception (1,7,11,15,18,20,24,34). Medicinally, caffeine is combined with other pain-relieving substances to enhance their analgesic effect (15,23-26,31). If pain is a limiting psychological factor, the hypoalgesic effect of caffeine provides a potential mechanism for its ergogenic effect that may elicit ergogenic advantages in both aerobic and anaerobic performance.
Hence, one purpose of this study was to examine the effects of caffeine ingestion on muscular endurance and pain perception during light resistance training bouts to exhaustion. It was hypothesized that caffeine ingestion before exercise would increase repetitions to failure through a decrease in pain perception and blunted rating of perceived exertion (RPE) (10,11,17,26).
Furthermore, it would be interesting to compare the pain-relieving and ergogenic effects of caffeine with those of another common pain reliever, such as aspirin. In 1997, Cook et al. (8) found that a large dose of aspirin (20 mg·kg−1) taken 1 hour before exercise had no effect on leg muscle pain ratings after ramped maximal cycle ergometry to volitional exhaustion, whereas 6 mg·kg−1 of caffeine effectively attenuated muscle pain. By comparing the effects of caffeine directly to another pain reliever in a within-subjects trial, it may help elucidate a more precise mechanism for caffeine's ergogenic benefits.
In summary, caffeine's ergogenic effects on aerobic performance have been well established, but the Randle Effect has been questioned as a mechanism for caffeine's effect. Subsequent studies have shown that caffeine did have ergogenic effects on short-duration, high-intensity exercises including effects on performance and perceived pain intensity (PPI) (4,15,17,18,20). This investigation examined the independent effects of caffeine as well as aspirin on light resistance training performance, RPE, and pain perception.
Experimental Approach to the Problem
The study was a within-subjects, double-blind design. Treatment trials (caffeine, placebo, aspirin) were counterbalanced to account for ordering effects. Participants were required to refrain from caffeine, alcohol, and exercise for 24 hours before testing and to report for testing at least 3 hours postprandially. Once all required material was completed, each participant completed four lab sessions at the same time of day on the same day of the week. Participants continued with their normal training regimens throughout the study (except for 24 hours before each trial, when training was prohibited). Participants were instructed to maintain the same routines and eat the same meals before testing on the day of each testing session.
To begin the initial testing session, each participant's age (years) was recorded, and height (cm) and weight (kg) were measured. Body fat percentage was estimated using Lange skinfold calipers (Cambridge, Md) and a three-site method (men: chest, abdomen, thigh) (29). Participants performed leg extensions (LE) and seated arm curls (AC) in this study because they are popular exercises for athletes and recreational weight trainers. They were also chosen to make it easier for the participants to isolate their PPI to the specific muscles being used. The LE exercises were performed on a plate-loaded LE resistance training machine (Strive, Canonsburg, Pa). Each subject was instructed to sit with his back flat against the backrest and to hold tightly to the handles designated on the machine. The backrest was adjusted so that the mechanical axis of the machine was aligned with the anatomic axes of the knees. The participant's legs were placed against the shin pads attached to the bottom of the lever arm of the device, and the height of the pads was adjusted to comfortably fit the participant's shins (4). The AC exercises were performed on a Hammer Strength seated AC bench (Life Fitness, Schiller Park, Ill) with IGX free weights (Iron Grip Barbell Company, Santa Anna, Calif). The seat height was adjusted so that the participant was not leaning over the pad, but so his armpit rested comfortably on the pad. The initial lift-off of the spotter was not counted in the total repetitions for each set. The positioning of each participant was consistent among all testing sessions.
The resistance load used in this study was the participant's 12-repetition maximum (RM) for each exercise. This number of repetitions is at the upper end of the range of repetitions (8-12) recommended for hypertrophy by the American College of Sports Medicine and the National Strength and Conditioning Association (28,35). This study also hypothesized that pain could limit the number of repetitions lifted when lifting this load to failure. To obtain a 12-RM, the participant first estimated his 12-RM for LE and AC. The participant then lifted a 12-repetition warm-up set at 50% of this resistance. Then, the participant lifted his estimated 12-RM as many times as possible. Although a 12-RM was desired for this study, an 11- or 13-RM was also accepted. If he could not lift the weight 11 times, or if he lifted it 14 times, then weight was adjusted to acquire an approximate 12-RM on the next set. This 12-RM acquisition was performed first for LE and then for AC. Furthermore, participants were also introduced to Cook's Pain Intensity Scale (8,9) and Borg's RPE scale (5) in this session. The following three sessions were the treatment trials where each participant ingested either a dose of caffeine (6-6.4 mg·kg−1 body weight), aspirin (10-10.4 mg·kg−1 body weight), or a dextrose placebo with 500 ml of water 1 hour before testing. This dosage of caffeine was chosen because it has shown to elicit the maximum ergogenic effect per milligram of caffeine while still remaining within the legal limits of the International Olympic Committee (15-17,19). Additionally, research shows that moderate caffeine intake before exercise does not increase dehydration risk (3,30). Each substance was contained in identical pills prepared at a local pharmacy. Dextrose served as a diluent to top off each supplement. After the initial testing session, the treatment dosage was assigned to each participant according to his weight, and the treatments given to each participant were counterbalanced. Participants arrived at the treatment testing sessions 1 hour after ingestion of the appropriate supplement and performed the LE and AC exercises.
College-aged male volunteers (n = 15) served as participants using a nonprobability, convenient participant sampling (mean ± SD, age: 22.0 ± 1.3 years; height: 182.0 ± 7.1 cm; body weight: 78.6 ± 9.6 kg; body fat percentage: 14.0 ± 3.2%). Only men were examined because of potential complications that women introduce regarding pain perception and supplement ingestion (15) as well as potential discrepancies attributable to menstrual cycle timing that would complicate a consistent representation of a participant's pain tolerance. Overweight individuals and smokers were also excluded because smoking and an abnormal body weight affect caffeine metabolism (15). To minimize adverse reactions to caffeine, participants had to report a moderate daily caffeine intake (~100-400 mg) and be free of symptoms (self-reported) of caffeine hypersensitivity (3,14,21). To prevent inconsistent familiarization and acclimatization, all participants were required to have been resistance training two to four times per week for at least 8 weeks. All subjects completed an informed consent, a Physical Activity Readiness Questionnaire, and, on the basis of known risk factors, were classified as low risk with regard to qualifications listed in the American College of Sports Medicine health risk stratification (35). All procedures were approved by the local institutional review board before beginning data collection.
Participants arrived at the weight room and donned a Cardiosport (Deer Park, NY) heart rate (HR) monitor, and resting HR was taken after about 2 minutes of seated rest. Each participant then performed a 12-repetition warm-up set of LE at 50% of his 12-RM. The participant was then asked to lift his 12-RM until failure for four sets with 3 minutes of rest between each set and 5 minutes of rest between exercises (LE and AC). Verbal encouragement was consistently given to each participant throughout every set. Heart rate and PPI were also recorded before and after each set. Heart rate, PPI, and RPE were recorded, in that order, within 10 seconds after completing each set. Finally, HR, PPI, and RPE were recorded 5 minutes after the completion of the exercise. This same procedure was then followed for AC. On completion of both exercises, a questionnaire was given to the participant to determine different symptoms that the participant may have experienced as a result of consuming the supplements. All trials (placebo, aspirin, and caffeine) were conducted in the same manner, except for the specific supplement ingested. Figure 1 is a general timeline that summarizes these procedures.
Performance data (repetitions, RPE, PPI, and HR) and subjective responses were analyzed for each variable using 3 (trial) × 4 (set) repeated-measures analysis of variance (ANOVA) with a least significant difference post hoc procedure using SPSS 14.0 software. A Bonferroni post hoc was performed on the first set of each exercise. Separate ANOVAs were used for AC and LE exercise sessions. An a priori alpha was set at p ≤ 0.05. Using this level of significance and a power or 0.8, power analysis before data collection indicated a need for 15 participants. The intraclass correlation coefficients for LE repetitions, HR, PPI, and RPE were R = 0.89, R = 0.96, R = 0.95, and R = 0.93, respectively; those for AC repetitions, HR, PPI, and RPE were R = 0.94, R = 0.94, R = 0.96, and R = 0.93, respectively, with no significant (p > 0.05) mean differences between test and retest values for any measurements.
There was a significant increase (p < 0.05) in total repetitions with caffeine compared with placebo and aspirin in LE. Figure 2 shows that repetitions in LE set 1 were also significantly higher for caffeine than for aspirin or placebo. In addition to increased repetitions, caffeine also produced a significantly higher HR than aspirin and placebo (main effect). Figure 3 reveals that there is not a significant difference in RPE between caffeine and placebo despite an increased number of repetitions lifted. The RPE for aspirin was also significantly higher than for caffeine (main effect). Figure 4 shows that aspirin ingestion yielded a significantly higher PPI (vs. placebo) in the first set of LE. For the purposes of discussion, participants experiencing meaningful (greater than effect sizes) performance enhancements were labeled responders, with others considered nonresponders. In LE, 47% of participants' performance exceeded the predetermined effect size (≥ 5 repetitions) for total repetitions, with 53% exceeding the effect size (≥ 2 repetitions) for repetitions in set 1 with caffeine (vs. placebo).
In AC, Figure 5 shows that caffeine ingestion produced an increase approaching significance (p = 0.051) in repetitions (vs. placebo). The only significant change (p < 0.05) in AC was a significantly greater HR (caffeine vs. placebo and aspirin). In AC, 53% (total repetitions) and 47% (set 1 repetitions) of participants exceeded effect sizes with caffeine (vs. placebo), with only 13% experiencing decrements in performance (total repetitions).
On the postsession survey, participants reported significantly higher (p < 0.05) feelings of restlessness, tremors, and stomach distress when taking the caffeine supplement (Figure 6).
Previously, studies on the ergogenic effects of caffeine supplementation on aerobic exercise performance have proposed that free fatty acid mobilization and consequent glycogen sparing was the mechanism for caffeine's ergogenic benefit (10,13,15,34). Because anaerobic exercise depends on ATP from sources other than fatty acids, little research has been done regarding the effects of caffeine on anaerobic performance. However, by examining other possible mechanisms for caffeine, some studies have found caffeine to enhance anaerobic performance (2,4,12,15,17,33). Two possible mechanisms that have been proposed are caffeine's ability to increase catecholamine levels and to reduce pain perception. This study investigated the effects of caffeine and aspirin on muscle pain, RPE, and performance of two light resistance training exercises.
The results demonstrate that caffeine supplementation before LE significantly improved (p < 0.05) total repetition and repetitions lifted in set 1 (vs. aspirin and placebo) while also increasing total repetitions of AC to a degree that approaches significance (p = 0.051; vs. placebo). We hypothesized that caffeine would attenuate fatigue and result in an increase in repetitions, particularly in the latter sets of the exercises as pain might be more exaggerated; however, although caffeine did produce an increase in repetitions, the repetition increase was only significant in the first set and not in the latter sets of the exercises. Because of the short duration of this exercise, fatty acids would not serve as the primary source of ATP, and glycogen sparing is not the likely mechanism for the increase in repetitions. As referenced in other studies, the mechanism for caffeine's ergogenic benefits could be attributable to an increase in catecholamine levels or a reduction in pain perception (1,7,11,15,17,18,20,34). Because catecholamine levels were not measured in this study, it cannot be confidently concluded that altered levels of these hormones accounted for current results. Furthermore, the increase in repetitions could be a result of a decrease in pain perception. Caffeine reduces pain perception by blocking pronociceptive adenosine receptors. Adenosine concentration increases in the muscle during moderate- or high-intensity exercise and binds to adenosine receptors on the sensory nerve endings that can result in pain signaling. By blocking these receptors, caffeine inhibits pain perception (24,25,31). According to the central governor theory, Noakes et al. (26) state that performance is limited by a psychological mechanism in which signals from the periphery cause the brain to stop the work. Under this theory, if caffeine reduced pain perception, then work should continue longer (11). Because caffeine only produced a significant difference for repetitions in the first set, this could mean that pain is an inhibiting factor in the beginning of exercise, whereas a physiological mechanism of fatigue limits performance to a greater degree in the latter sets. Another speculation is that because caffeine increased performance of every set and the last set of LE approached significance, then, perhaps because participants lifted to exhaustion in every set, there were not enough repetitions lifted in the latter sets to detect a significant difference. Although some of caffeine's ergogenic effects could have resulted from increased catecholamine levels, because pain and RPE were blunted with increased performance, it is likely that pain inhibition influenced the performance (Figures 2-4). It is also interesting to note that the performance enhancement of caffeine in this study is different from that found by Beck et al. (4) and Green et al. (17). Beck et al. found that approximately 201 mg of caffeine in a caffeine-containing supplement significantly enhanced bench press performance but not LE. Green et al. tested the effects of 6 mg·kg−1 caffeine on bench press and leg press and found that caffeine significantly increased performance only in the latter sets of the leg press exercises. Therefore, it seems that caffeine supplementation does enhance performance for different resistance training exercises, but the exact mechanism for this ergogenic effect has not been determined.
The individuals' responses to the caffeine supplementation are also interesting. Approximately half of the participants significantly increased the total number of repetitions lifted and repetitions lifted in set 1 (LE and AC) with caffeine supplementation (vs. placebo). The other half of the participants showed no response in repetitions to the caffeine supplementation, with the exception of two participants who significantly decreased their total number of repetitions lifted in AC after caffeine ingestion. Rough observations show that “responders” were not homogeneous with respect to height, weight, or daily caffeine intake. Future studies should compare the characteristics of individuals for which caffeine elicits ergogenic effects with those on which it has no effect. It is important to point out that analyzing group data may often result in less than impressive results. However, as with most ergogenic aids, individual responses vary greatly in the current study. Because of the interindividual variation in responses, it is important to consider individual responses when making conclusions about the effectiveness of an ergogenic aid. Relying solely on group results may mask the effects experienced by individuals, and it would be a gross oversimplification to conclude that an aid is overall ineffective (on the basis of group results) when a majority of participants do experience large gains.
The RPE measures in this study also produced interesting results. RPE estimations were similar within all sets between caffeine and placebo (Figure 3). This outcome would be expected if a similar number of repetitions were completed; however, with the absence of change in RPE with greater repetitions (LE-set 1), it can be concluded that RPE was blunted by the treatment (caffeine). These RPE values even remained similar while caffeine significantly increased HR. Similarly, a blunted RPE response has been observed by Doherty et al. (12) with caffeine and high-intensity cycling and by Green et al. (17) with resistance training.
Another subjective measure that provided an interesting perspective was PPI. The PPI values for caffeine and placebo were similar in set 1 of LE, and caffeine produced significantly more repetitions (Figure 4). As with RPE, caffeine ingestion produced significantly more repetitions but did not increase the subjective measure of PPI. Because of their subjective bases, these RPE and PPI results may support the central governor theory of Noakes et al. (26,27) and a central mechanism for caffeine, at least in the beginning of resistance training exercise. Although this study does not contain in-depth mechanistic analyses, it does provide evidence that caffeine improves performance (repetitions) and blunts subjective measures, because RPE and PPI failed to increase concurrently with work completed.
In this study, aspirin supplementation did not enhance performance during any of the resistance training sets. Repetitions lifted were similar for aspirin and placebo and were significantly less than those of caffeine (Figures 2 and 5). Furthermore, aspirin significantly increased RPE and PPI in LE (vs. placebo). Similar pain ratings for aspirin and placebo are consistent with the finding of Cook et al. (8) where 20 mg·kg−1 of aspirin did not affect PPI after three 1-minute cycling bouts. It is difficult to explain the responses that the participants had to the aspirin supplementation. Although, aspirin did not negatively affect performance (repetitions), it did have a negative effect on the subjective measures after the sets (RPE, PPI). Aspirin was included in this study to compare its pain-relieving effect with that of caffeine; however, caffeine produced significantly more repetitions while still producing a significantly lower PPI than aspirin. Future endeavors are warranted evaluating potential ergogenic properties of other pain relievers and adenosine antagonists.
Responses to the postsessions survey indicate that caffeine consumption altered various subjective feelings. Participants reported feeling significantly (p < 0.05) more restless, more feelings of tremors, and greater stomach distress (Figure 6) while taking caffeine. Although much less conclusive than plasma measures of caffeine, altered psychophysiological responses provide indirect support that the participants complied with the treatment requirements and that caffeine was absorbed. It is difficult to distinguish, but the increase in muscle tremors could be attributable to the caffeine or to the increase in the number of repetitions in the caffeine trials. Regarding the stomach distress, consuming a standardized snack with supplements in future studies may attenuate this negative side effect. Although they did incur this negative side effect, participants were still able to increase performance while taking the caffeine. More specifically, the three participants who reported the greatest amounts of stomach distress with caffeine compared with placebo still lifted significantly more repetitions with caffeine (vs. placebo). Compared with placebo, aspirin produced no significant changes in any of the subjective feelings on this survey (Figure 6). Although caffeine did produce some negative subjective measures, these effects were not great enough to inhibit its overall ergogenic effect.
In summary, this study presents evidence that caffeine provides an overall ergogenic effect on two resistance training exercises. Specifically, participants were able to lift significantly more repetitions during the first set of LEs and ACs and more total repetitions of LEs without negatively altering subjective feelings such as RPE and PPI. The results also highlight the importance of carefully considering individual responses. Compared with caffeine, aspirin did not provide any change in repetitions lifted and produced negative effects in subjective feelings, with a significant increase in RPE and PPI. The opposite effects of caffeine and aspirin on performance and these subjective measures during resistance training should help elucidate the mechanism of caffeine's ergogenic effect on performance.
More in-depth research is required, however, to determine the precise mechanisms of caffeine's ergogenic effects on resistance training. Because caffeine has been shown to enhance anaerobic performance, future studies should focus on illuminating the mechanisms for caffeine's ergogenic properties. Specifically, research should investigate the influence of adenosine on pain perception and the effects of caffeine on high-intensity and short-duration resistance training. Further investigations on the variability of caffeine's effects on participants with variable daily caffeine intakes and caffeine dependencies should also be performed to see how variable caffeine sensitivity alters the effects of caffeine on anaerobic performance.
The present study of college-aged men has indicated that acute caffeine ingestion before light resistance exercise resulted in a significant increase in LEs and an increase approaching significance in seated ACs. However, the current evidence shows that these benefits are limited to a large relative dose of a caffeine supplement, and similar benefits may not be seen with ingestion of coffee or other caffeinated beverages. Furthermore, this large dose of caffeine did have some overall unfavorable effects such as increased stomach distress and increased tremors. Aspirin did not provide any recorded supplemental benefit to resistance training. Recreational and competitive athletes who perform high-intensity anaerobic activities, such as resistance training, might find that acute ingestion of a large dose of caffeine 1 hour before activity may increase their performance. Performance and stomach responses seem to vary among individuals, however, and should be taken into consideration.
The supplements for this study were funded by a research grant from the Graduate Student Association of the University of Alabama. The results of the present study do not constitute endorsement of the product by the authors or the NSCA.
1. Allen, DG and Westerblad, H. The effects of caffeine on intracellular calcium, force and the rate of relaxation of mouse skeletal muscle. J Physiol
487: 331-342, 1995.
2. Anselme, F, Collomp, K, Mercier, B, Ahmaidi, S, and Prefaut, C. Caffeine increases maximal anaerobic power and blood lactate concentration. Eur J Appl Physiol Occup Physiol
65: 188-91, 1992.
3. Armstrong, LE, Casa, DJ, Maresh, CM, and Ganio, MS. Caffeine, fluid-electrolyte balance, temperature regulation, and exercise-heat tolerance. Exerc Sport Sci Rev
35: 135-140, 2007.
4. Beck, TW, Housh, TJ, Schmit, RJ, Johnson, GO, Housh, DJ, Coburn, JW, and Malek, MH. The acute effects of a caffeine-containing supplement on strength, muscular endurance
, and anaerobic capabilities. J Strength Cond Res
20: 506-510, 2006.
5. Borg, G. Subjective aspects of physical and mental load. Ergonomics
21: 215-220, 1978.
6. Chesley, A, Howlett, RA, Heigenhauser, GF, Hultman, E, and Spriet, LL. Regulation of muscle glycogenolytic flux during intense aerobic exercise after caffeine ingestion. Am J Physiol
275: R596-R603, 1998.
7. Collomp, K, Ahmaidi, S, Audran, M, Chanal, JL, and Prefaut, C. Effects of caffeine ingestion on performance and anaerobic metabolism during the Wingate Test. Int J Sports Med
12: 439-443, 1991.
8. Cook, DB, O'Connor, PJ, Eubanks, SA, Smith, JC, and Lee, M. Naturally occurring muscle pain during exercise: assessment and experimental evidence. Med Sci Sports Exerc
29: 999-1012, 1997.
9. Cook, DB, O'Connor, PJ, and Ray, CA. Muscle pain perception and sympathetic nerve activity to exercise during opioid modulation. Am J Physiol Regul Integr Comp Physiol
279: R1565-R1573, 2000.
10. Costill, DL, Dalsky, GP, and Fink, WJ. Effects of caffeine ingestion on metabolism and exercise performance. Med Sci Sports Exerc
10: 155-158, 1978.
11. Davis, JM, Zhao, Z, Stock, HS, Mehl, KA, Buggy, J, and Hand, GA. Central nervous system effects of caffeine and adenosine on fatigue. Am J Physiol
284: R399-R404, 2003.
12. Doherty, M, Smith, PM, Hughes, MG, and Davison, RC. Caffeine lowers perceptual response and increases power output during high-intensity cycling. J Sports Sci
22: 637-643, 2004.
13. Essig, D, Costill, DL, and Van Handel, PJ. Effects of caffeine ingestion on utilization of muscle glycogen and lipid during leg ergometer cycling. Int J Sports Med
1: 86-90, 1980.
14. Frary, CD, Johnson, RK, and Wang, MQ. Food sources and intakes of caffeine in the diets of persons in the United States. J Am Diet Assoc
105: 110-113, 2005.
15. Graham, TE. Caffeine and exercise: metabolism, endurance and performance. Sports Med
31: 785-807, 2001.
16. Graham, TE and Spriet, LL. Metabolic, catecholamine and exercise responses to a high caffeine dose during prolonged exercise. J Appl Physiol
78: 867-874, 1995.
17. Green, JM, Wickwire, PJ, McLester, JR, Gendle, S, Hudson, G, Pritchett, RC, and Laurent, CM. Effects of caffeine in repetitions to failure and ratings of perceived exertion during resistance training. Int J Sport Physiol Perf
2: 250-259, 2007.
18. Greer, F, Friars, D, and Graham, TE. Comparison of caffeine and theophylline ingestion: exercise metabolism and endurance. J Appl Physiol
89: 1837-1844, 2000.
19. Greer, F, McLean, C, and Graham, TE. Caffeine, performance, and metabolism during repeated Wingate exercise tests. J Appl Physiol
85: 1502-1508, 1998.
20. Jackman, M, Wendling, P, Friars, D, and Graham, TE. Metabolic, catecholamine and endurance responses to caffeine during intense exercise. J Appl Physiol
81: 1658-1653, 1996.
21. James, JE, Bruce, MS, Lader, MH, and Scott, NR. Self-report reliability and symptomology of habitual caffeine consumption. Br J Clin Pharmacol
27: 507-514, 1989.
22. Kovacs, EMR, Stegen, JHCH, and Brouns, F. Effect of caffeinated drinks on substrate metabolism, caffeine excretion, and performance. J Appl Physiol
85: 709-715, 1998.
23. Laska, EM, Sunshine, A, Mueller, F, Elvers, WB, Siegal, C, and Rubin, A. Caffeine as an analgesic adjuvant. JAMA
251: 1711-1718, 1984.
24. Motl, RW, O'Connor, PJ, and Dishman, RK. Effect of caffeine on perceptions of leg muscle pain during moderate intensity cycling exercise. J Pain
4: 316-321, 2003.
25. Myers, DE, Shaikh, Z, and Zullo, TG. Hypoalgesic effect of caffeine in experimental ischemic muscle contraction pain. Headache
37: 654-658, 1997.
26. Noakes, TD, Gibson, ASC, and Lambert, EV. From catastrophe to complexity: a novel model of integrative central neural regulation of effort and fatigue during exercise in humans. Br J Sports Med
38: 511-514, 2004.
27. Noakes, TD, Gibson, ASC, and Lambert, EV. From catastrophe to complexity: a novel model of integrative central neural regulation of effort and fatigue during exercise in humans: summary and conclusions. Br J Sports Med
39: 120-124, 2005.
28. Pearson, D, Faigenbaum, A, Conley, M, and Kraemer, WJ. The National Strength and Conditioning Association's basic guidelines for the resistance training of athletes. Strength Cond J
22: 14-27, 2000.
29. Pollock, ML, Schmidt, DH, and Jackson, AS. Measurement of cardiorespiratory fitness and body composition in the clinical setting. Clin Ther
6: 12-27, 1980.
30. Sawka, MN, Burke, LM, Eichner, ER, Maughan, RJ, Montain, SJ, and Stachenfeld, NS. American college of sports medicine position stand. Exercise and fluid replacement. Med Sci Sports Exerc
39: 377-390, 2007.
31. Sawynok, J. Adenosine receptor activation and nociception. Eur J Pharmacol
317: 1-11, 1998.
32. Spriet, LL and Gibala, MJ. Nutritional strategies to influence adaptations to training. J Sports Sci
22: 127-141, 2004.
33. Stuart, GR, Hopkins, WG, Cook, C, and Cairns, SP. Multiple effects of caffeine on simulated high-intensity team-sport performance. Med Sci Sports Exerc
37: 1998-2005, 2005.
34. Van Soeren, MH and Graham, TE. Effect of caffeine on metabolism, exercise endurance, and catecholamine responses after withdrawal. J Appl Physiol
85: 1493-1501, 1998.
35. Whaley, MH. American College of Sports Medicine, Guidelines for Exercise Testing and Prescription
(6th ed.). Baltimore: Williams and Wilkins, 2006.