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Original research

Effects of sodium phosphate and caffeine ingestion on repeated-sprint ability in male athletes Benjamin J. Kopec, Brian T. Dawson, Christopher Buck, Karen E. Wallman ∗ School of Sport Science, Exercise and Health, The University of Western Australia, Australia

a r t i c l e

i n f o

Article history: Received 13 August 2014 Received in revised form 6 March 2015 Accepted 8 April 2015 Available online xxx Keywords: Dietary supplements Aerobic exercise Sports performance Team-sports

a b s t r a c t Objectives: To assess the effects of sodium phosphate (SP) and caffeine supplementation on repeatedsprint performance. Design: Randomized, double-blind, Latin-square design. Methods: Eleven team-sport males participated in four trials: (1) SP (50 mg kg−1 of free fat-mass daily for six days) and caffeine (6 mg kg−1 ingested 1 h before exercise); SP + C, (2) SP and placebo (for caffeine), (3) caffeine and placebo (for SP) and (4) placebo (for SP and caffeine). After loading, participants performed a simulated team-game circuit (STGC) consisting of 2 × 30 min halves, with 6 × 20-m repeated-sprint sets performed at the start, half-time and end of the STGC. Results: There were no interaction effects between trials for first-sprint (FS), best-sprint (BS) or totalsprint (TS) times (p > 0.05). However, SP resulted in the fastest times for all sprints, as supported by moderate to large effect sizes (ES; d = 0.51–0.83) and ‘likely’ to ‘very likely’ chances of benefit, compared with placebo. Compared with caffeine, SP resulted in ‘possible’ to ‘likely’ chances of benefit for FS, BS and TS for numerous sets and a ‘possible’ chance of benefit compared with SP + C for BS (set 2). Compared with placebo, SP + C resulted in moderate ES (d = 0.50–0.62) and ‘possible’ to ‘likely’ benefit for numerous sprints, while caffeine resulted in a moderate ES (d = 0.63; FS: set 3) and ‘likely’ chances of benefit for a number of sets. Conclusions: While not significant, ES and qualitative analysis results suggest that SP supplementation may improve repeated-sprint performance when compared with placebo. © 2015 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.

1. Introduction Caffeine and sodium phosphate represent two nutritional aids shown to improve exercise performance. While caffeine can improve endurance performance,1–3 its effect on repeated-sprint ability (RSA) is inconclusive. For example, sprint times during 5 sets of 6 × 20-m sprints were significantly faster after caffeine (6 mg kg−1 ),4,5 while no benefit was found for 2 × 60-s cycling bouts separated by 3 min6 or 10 × 20-m running sprints departing every 10 s.7 These results however, may have been due to excessive accumulation of metabolic waste products due to using sustained sprint efforts and/or short recovery periods.8 To date, the most common mechanism proposed to explain caffeine’s ergogenic effect is adenosine receptor antagonism, which may have a stimulatory effect on the central nervous system that reduces feelings of exertion and pain, as well as promoting heightened alertness and

∗ Corresponding author. E-mail address: [email protected] (K.E. Wallman).

increased neural firing rates that directly affect skeletal muscle.9 Notably, all of these proposed benefits of caffeine have been posited to improve repeated-sprint performance.4,5 Similar to caffeine, sodium phosphate (SP) can improve endurance performance10–12 and maximal oxygen uptake ˙ 2 max ) following 3.6–4 g or 50 mg kg−1 free fat mass (FFM) (VO doses ingested daily over a 3–6 day period,10,12,13 but its effect on RSA is unknown. Numerous mechanisms have been proposed to explain the ergogenic effects of SP supplementation. Briefly, these are increases in (a) 2,3-Diphosphoglycerate (DPG) in red blood cells, promoting oxygen unloading from haemoglobin to the tissues;14 (b) myocardial efficiency, which may increase stroke volume;12 (c) hydrogen ion buffering ability;14 (d) adenosine triphosphate (ATP) and phosphocreatine (PCr) resynthesis due to a larger energy (phosphate) pool;14 and (e) activation of rate-limiting constituents of the glycolytic and Krebs cycles.15 Of relevance, all these mechanisms may potentially result in improved RSA, but this has not yet been investigated. Nor has the combined effects of SP and caffeine on RSA. As the mechanisms proposed to improve exercise performance after SP or caffeine ingestion are different,

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it is possible that in combination these substances may result in greater improvement in exercise performance than when either supplement is ingested alone. For example, the combined effect of improved buffering, muscle energy (phosphate) pool, tissue unloading of oxygen and myocardial efficiency (from SP loading), plus increased neural firing rates that have positive effects on muscle activation and reduced sensations of effort and pain (from caffeine ingestion) may together result in faster repeated-sprint performance. Therefore, the aim of this study was to assess the effects of SP and caffeine, alone and combined (SP + C), on RSA performed before, midway and after a 60 min simulated team-game circuit (STGC). 2. Methods Eleven male, team-sport (Australian football, basketball, hockey, soccer) athletes (mean ± SD age 20 ± 2 y, height 181.7 ± 4.4 cm, body-mass 74.5 ± 8.2 kg, training/competition involvement per week of 372 ± 124 min) were recruited from local sporting clubs. All participants consumed 5%, the true effect was deemed unclear. When clear interpretation was possible, a qualitative descriptor was assigned to the following quantitative chances of benefit: 25–74%, benefit possible; 75–94%, benefit likely; 95–99%, benefit very likely; >99%, benefit almost certain.

a

b

0.10/40 (44/16) 0.05/32 (44/23) 0.16/47 (43/10) 0.16/47 (44/9) 0.02/35 (35/30) 0.32/70 (21/9) 0.13/48 (35/17) 0.12/47 (35/19) 0.13/44 (42/14) 0.42/83 (15/2) 0.38/74 (24/2) 0.34/73 (25/2) 0.30/73 (24/4) 0.62/90 (8/3) 0.42/80 (15/5) 0.45/83 (13/4) 0.44/79 (17/4) 0.76/92 (6/2) 0.74/93 (6/1) 0.74/93 (6/1) 0.29/67 (27/6) 0.32/74 (21/5) 0.37/72 (24/4) 0.37/79 (19/2) 1.050 1.096 1.145 3.304 ± ± ± ± 19.150 19.240 19.272 57.709 0.910 0.792 0.706 2.219 ± ± ± ± 19.052 19.191 19.116 57.249 ± ± ± ± 19.431 19.918 19.694 59.040

0.823 1.094 0.854 2.611

19.170 19.580 19.396 58.062 ± ± ± ±

0.952 1.031 0.752 2.608

0.19/55 (36/8) 0.25/65 (31/5) 0.22/57 (33/10) −0.07/24 (39/38) 0.16/52 (32/16) 0.07/36 (50/14) 0.13/45 (41/14) 0.45/85 (13/2) 0.34/76 (22/2) 0.23/58 (34/7) 0.50/86 (11/3) 0.48/89 (9/2) 0.42/79 (17/4) 0.83/95 (4/1) 0.79/94 (5/1) 0.29/65 (27/8) 0.36/76 (20/4) 0.48/86 (12/2) 3.109 ± 0.148 3.140 ± 0.174 3.119 ± 0.177 3.099 ± 0.149 3.167 ± 0.158 3.130 ± 0.132 3.142 ± 0.145 3.223 ± 0.156 3.198 ± 0.150

3.080 ± 0.153 3.101 ± 0.137 3.085 ± 0.134

0.26/65 (26/9) 0.14/45 (44/11) 0.28/70 (23/8) −0.02/34 (29/37) 0.19/55 (31/14) −0.12/21 (36/43) 0.25/62 (27/10) 0.34/75 (21/4) 0.21/60 (32/8) 0.23/64 (32/4) 0.50/87 (11/2) 0.39/85 (13/3) 0.51/87 (11/2) 0.69/91 (7/2) 0.72/92 (6/2) 0.25/59 (25/16) 0.33/71 (23/6) 0.63/89 (9/2) 3.132 ± 0.169 3.152 ± 0.174 3.164 ± 0.197 3.089 ± 0.162 3.130 ± 0.148 3.112 ± 0.178 3.129 ± 0.162 3.183 ± 0.160 3.144 ± 0.121 3.168 ± 0.145 3.234 ± 0.153 3.235 ± 0.165

SP vs SP + C CAFF

SP

SP + C

CAFF vs PLA

SP + C vs PLA

SP vs CAFF

SP + C vs CAFF SP vs PLA PLA

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First 20-m time (s) n = 11 Set 1 Set 2a n = 10 n = 10 Set 3 a Best 20-m time (s) Set 1 n = 11 Set 2 n = 10 Set 3 n = 10 Total sprint time (s) Set 1 n = 11 n = 10 Set 2 a n = 10 Set 3 a Overall

All results are presented as mean ± SD. Gymnasium ambient temperature and relative humidity during trials were 18 ± 3 ◦ C and 64.2 ± 5.9% (model QuestTemp 32; Quest Technologies, Oconomowoc, WI, USA) and not different between trials (p = 0.82; p = 0.22, respectively). Circuit times were also not different for laps 1, 30, 31 and 60 between trials (p = 0.59). Although no interaction effect (p = 0.88) existed for first 20-m sprint (FS) times, these were faster after SP for every set performed, with moderate ES and ‘likely’ chances of benefit found when compared with placebo for all sets (Table 1). Further, SP resulted in a ‘likely’ benefit for FS compared with caffeine for set 2. Additionally, FS times were faster after SP + C compared with placebo (moderate ES for set 2 and ‘possible’ to ‘likely’ benefit for all sets), while FS times were faster after caffeine compared with placebo for set 3 (moderate ES and a ‘likely’ chance of benefit). Although no interaction effect (p = 0.60) existed for best sprint (BS) times, these were fastest after SP for every set performed compared with placebo, with this supported by ‘very likely’ or ‘likely’ benefit for all sets and moderate to large ES for sets 2 and 3 (Table 1). Further, BS times were faster after SP compared with

Cohen’s d effect size/Percentage chance that effect is beneficial (trivial/detrimental)b

3. Results

Mean ± SD

Imports, Carlton, Australia) were measured after the warm-up and each RSA set. Participants completed training and food diaries 24 h before the first trial and then used these to replicate individual eating and activity patterns for all other trials. They were given a list of foods, beverages and pharmaceuticals containing caffeine, which they abstained from consuming for 24 h before each trial. On completing the study, dietary analysis of each participant’s self-reported caloric intake was undertaken (FoodWorks v 4.2.0, Xyris Software, Queensland, Australia). Resting venous blood samples (8.5 mL) were collected one week before each trial, with another sample taken before the warmup (at a standardized time of day) for determination of serum phosphate, 2,3-DPG and caffeine concentrations. Serum phosphate was measured using an Abbott Architect c16000 analyser, employing specified Abbott reagents (Abbott Laboratories, Abbott Park, IL 60065, USA). The CV for serum phosphate analysis was 2.0% at 2.95 mmol/L. Concentration of 2,3 DPG was measured using a Roche diagnostic kit (Cat. No. 148 334; Roche Diagnostics, Indianapolis, IN) on a Cobas Mira Plus chemistry analyser (Roche Diagnostics, Indianapolis, IN). The CV for 2,3-DPG analysis was 1.45% at a concentration of 2.38 mmol/L. Caffeine was quantified from EDTA-treated plasma via reverse-phase high performance liquid chromatography, where samples were introduced from an autosampler onto a reverse phase C18 column (Waters Corporation, Milford, MA). The CV for caffeine was 13.95% at a concentration of 7.83 mmol/L. Statistics Package for the Social Sciences Version 16.0 for Windows (SPSS, Inc., Chicago, IL) was used to perform two-way, repeated-measures ANOVAs for primary and secondary variables. Where appropriate, Bonferroni post hoc comparisons were then used to locate any differences. Statistical significance was set at p ≤ 0.05. Cohen’s d effect sizes (ES; ≤0.2, small; 0.5–0.79, moderate; ≥0.8, large) were also calculated,19 plus smallest worthwhile changes in performance scores between trials using methods outlined by Batterham and Hopkins.20 The smallest worthwhile value of change for a 20-m sprint has been calculated to be 0.8%.7 Where chances of benefit and harm were both calculated to be >5%, the true effect was deemed unclear. When clear interpretation was possible, a qualitative descriptor was assigned to the following quantitative chances of benefit: 25–74%, benefit possible; 75–94%, benefit likely; 95–99%, benefit very likely; >99%, benefit almost certain.

Table 1 Repeated sprint ability test scores (first sprint time, best sprint time, total sprint time and percent decrement) for the four conditions: placebo (PLA), caffeine (CAFF), sodium phosphate (SP) and combined sodium phosphate and caffeine (SP + C).

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Table 2 Heart rate (HR), ratings of perceived exertion (RPE) and blood lactate (La) values recorded during the repeated sprint ability (RSA) trials for the placebo (PLA), caffeine (CAFF), sodium phosphate (SP) and combined sodium phosphate and caffeine (SP + C) trials (n = 11). Mean ± SD

RSA La (mmol/L) Set 1 n = 11 Set 2 n = 10 Set 3 n = 10 HR (bpm) Set 1 n = 11 Set 2a n = 10 Set 3a n = 10 RPE Set 1 n = 11 Set 2a n = 10 Set 3a n = 10 a

PLA

CAFF

SP

SP + C

6.8 ± 2.2 6.4 ± 2.3 5.8 ± 3.3

6.6 ± 2.4 6.1 ± 3.2 6.6 ± 2.9

7.4 ± 3.0 6.8 ± 2.8 6.5 ± 2.2

7.0 ± 2.9 7.5 ± 4.6 6.2 ± 3.1

167 ± 13 172 ± 10 171 ± 9

171 ± 11 172 ± 9 172 ± 8

13 ± 1 16 ± 1 17 ± 1

14 ± 2 16 ± 1 17 ± 1

169 ± 9 174 ± 7 174 ± 9

168 ± 8 176 ± 5 174 ± 7

13 ± 2 16 ± 1 17 ± 1

14 ± 2 17 ± 1 17 ± 1

Significantly different from Set 1 values (p ≤ 0.05).

Table 3 Serum phosphate (n = 11), 2,3-DPG (n = 6) and caffeine (n = 6) concentrations recorded pre- and post-loading for the sodium phosphate (SP), caffeine (CAFF), sodium phosphate and caffeine (SP + C) and placebo (PLA) trials. SP Trial Phosphate (mmol/L) 1.31 ± Pre-loading 1.38 ± Post-loading 2,3-DPG (mmol/L) 2.03 ± Pre-loading 1.92 ± Post-loading Caffeine (mmol/L) Pre-loading 1.51 ± 1.41 ± Post-loading

Caffeine Trial

SP + C Trial

Placebo Trial

0.11 0.12

1.35 ± 0.19 1.44 ± 0.12

1.43 ± 0.13 1.43 ± 0.07

1.40 ± 0.22 1.39 ± 0.14

0.35 0.23

2.13 ± 0.43 1.93 ± 0.39

2.18 ± 0.24 2.06 ± 0.43

2.03 ± 0.34 1.90 ± 0.38

0.54 0.49

1.51 ± 0.83 2.66 ± 1.03

1.10 ± 0.35 2.66 ± 1.05

1.33 ± 0.81 1.83 ± 1.16

caffeine (‘likely’ benefits for sets 2 and 3) with a ‘possible’ benefit found when compared with SP + C (set 2). Additionally, caffeine resulted in ‘likely’ benefits compared with placebo for sets 2 and 3, while SP + C resulted in ‘likely’ benefits (sets 2 and 3) and a moderate ES (set 2) when compared with placebo. A significant main effect for time was found for BS times (p = 0.007), with these being slower in sets 2 and 3 compared with set 1. While there was no interaction between trials (p = 0.38) for total sprint (TS) times, these were faster following SP compared with placebo, for each set and for overall time. This was supported by moderate ES for sets 2, 3 and overall, as well as ‘likely’ benefit for all sets and overall (Table 1). Further, SP resulted in ‘likely’ benefits compared with caffeine (sets 2, 3 and overall). Additionally, caffeine resulted in ‘likely’ benefits compared with placebo (sets 2, 3 and overall), while SP + C resulted in a moderate ES (set 2) and ‘likely’ benefit for all sets and overall compared with placebo. A main effect for time was also found for TS times (p = 0.010), with these being slower in sets 2 and 3 compared with set 1. The only significant results found for HR and RPE during the trials were main effects for time (p < 0.001 for both); with both variables increasing from set 1 to sets 2 and 3 (Table 2). Furthermore, there were no significant effects found for blood lactate values (p > 0.05; Table 2), nor for serum phosphate (p = 0.44), 2,3DPG (p = 0.70) or caffeine (p = 0.11) concentrations recorded preand post-loading for the four trials (Table 3). No significant differences (p = 0.98) in 24 h dietary intake (food diaries) before the trials was found. Total kJ, protein, carbohydrate, fat and phosphorus intake in the 24 h before each trial was 13,536 ± 3219 kJ, 174 ± 29 g, 297 ± 69 g, 141 ± 68 g and 2496 ± 106 mg, respectively. No side effects were reported for any trial.

4. Discussion This study assessed the effects of SP, SP + C and caffeine on RSA performed before, midway and after a 60 min STGC in male, teamsport athletes. While results were not significant, SP resulted in ‘likely’ to ‘very likely’ chances of benefit for all sprints measured compared with placebo, with numerous sprints associated with moderate to large ES. Additionally, a number of sprints assessed after SP + C were associated with moderate ES and ‘possible’ to ‘likely’ chances of benefit compared with placebo. Minimal benefit was found for caffeine compared with placebo. Furthermore, faster sprint times after SP compared with caffeine, were supported by ‘possible’ to ‘likely’ benefits for numerous sprints, while results for SP and SP + C were similar, apart for a possible benefit of SP on BS (set 2). Overall, these results suggest that SP has the potential to improve RSA in male, team-sport athletes when fresh (set 1) and while fatiguing (sets 2 and 3), compared with caffeine or placebo, with some benefit also found for SP + C. Notably, the first RSA set, where total sprint time ranged between 19.05 ± 0.91–19.43 ± 0.82 s, would have initially relied more heavily on the phosphocreatine (PCr) energy system, with a greater emphasis on anaerobic (and aerobic) glycolysis as sprinting continued.21 Importantly, mechanisms proposed to provide ergogenic benefit following SP supplementation relate to both anaerobic and aerobic metabolism, as detailed below. Improved initial and later RSA performance following SP supplementation seen here may have been due to increased extracellular phosphate availability, which Kreider et al.12 consider to be a primary mechanism for benefit of SP loading on exercise performance. Increased extracellular phosphate availability is proposed to result in a greater diffusion of phosphate intracellularly, which may allow for a more rapid and efficient restoration of ATP and PCr, enhanced anaerobic and aerobic metabolism and improved exercise performance.12,22 Furthermore, increased extracellular phosphate availability was initially thought to be reflected by increases in serum phosphate levels post-loading.12 However, serum phosphate concentrations measured after SP loading have returned varying results in respect to a faster 40-km cycle time˙ 2 max values trial (no change in concentrations)12 and improved VO (significantly higher levels12 and no change in concentrations23 ) compared with placebo. Consequently, it has been suggested that serum phosphate concentration may not be an accurate measure for assessing the effects of SP loading on intracellular phosphate concentrations.12,23 In our study, no significant change in serum phosphate concentrations following SP loading existed, despite improvement in RSA for the SP and SP + C trials, highlighting that this measure may not be indicative of SP loading effects in the body. Furthermore, enhanced buffering capacity after SP supplementation is another mechanism that may have improved RSA here. Notably, other studies have reported a shift in the anaerobic thresh˙ 2 max old to higher workloads during a cycling time-trial12 and VO test.13 Some support for this mechanism is provided here by improved RSA following SP loading that was not associated with significantly higher blood lactate concentrations compared with the other trials. Improved myocardial efficiency and increased 2,3-DPG concentrations may have also played some role here in improving RSA following SP loading, particularly during the later RSA sets where aerobic metabolism would have likely increased.21 Improved myocardial efficiency after SP loading was initially described by Kreider et al.12 who reported significantly increased myocardial contractility, stroke volume and cardiac output during endurance exercise, which ultimately should provide more oxygen to the working muscles. These findings were directly related to improved mean power output (17%) during a 40-km cycle time-trial and

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˙ 2 max after SP loading (Kreider et al.12 ). Fura 9% increase in VO ther, Czuba et al.13 reported a significant decrease in maximal HR (2.7%) during a graded exercise test after SP supplementation compared with placebo, concluding this was possibly due to enhanced myocardial contractility, causing an increased stroke volume. Of relevance, the faster RSA found in the current study after SP ingestion was not associated with increases in HR, suggesting a possible involvement of myocardial efficiency here. However, as improved exercise performance after SP loading has also been associated with higher HR values12 , simple HR measures may not be a good indicator for this mechanism. Increased 2,3-DPG concentrations after SP supplementation has also been associated with improved aero˙ 2 max ,13,23,24 with bic metabolism, as evidenced by increases in VO Czuba et al.13 reporting a moderate correlation between these two measures (r = 0.47, p = 0.01). However, improvement in exercise performance after SP supplementation has also not always been associated with changes in 2,3-DPG concentration,12–14 with no significant differences found for this measure here. Lastly, this study found only minimal benefit of caffeine on RSA. As noted earlier, caffeine’s effect on RSA has been equivocal. Further, while caffeine concentrations measured from venous blood samples were higher post-loading compared with pre-loading values in the caffeine and SP + C trials, these values were not significantly different from each other. Interestingly, the caffeine dose used in the current study was the same as that used in two other studies that reported benefit of caffeine on RSA.4,5 Unfortunately, these studies did not measure serum caffeine concentrations as done here, thereby precluding comparison of these values between studies. Possibly, the prolonged nature of the repeated-sprinting protocol used here may have resulted in a build-up of metabolic waste products that may have minimized any benefit of caffeine on RSA. Of relevance, there were no significant differences in RPE values between trials for any of the RSA sets; sense of effort is commonly reported to be reduced following caffeine ingestion.9 Further research is needed here. 5. Conclusion While results were not significant, there is some evidence to suggest that SP supplementation, and to a lesser extent SP + C, may improve RSA in male team-sports athletes when fresh and/or fatigued, compared with placebo, with minimal benefit associated with caffeine. These results are important to coaches and athletes who wish to improve repeated-sprint ability during a team-sport game. 6. Practical applications • Sodium phosphate loading may improve RSA in team-sport games in male athletes. • Caffeine and SP loading combined does not result in better RSA than SP supplementation alone. • Caffeine supplementation has minimal benefit to RSA during a STGC.

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Acknowledgements No external financial support was received for this study. References 1. Bell DG, McLellan TM. Exercise endurance 1, 3, and 6 h after caffeine ingestion in caffeine users and nonusers. J Appl Physiol 2002; 93:1227–1234. 2. Cox GR, Desbrow B, Montgomery PG et al. Effect of different protocols of caffeine intake on metabolism and endurance performance. J Appl Physiol 2002; 93:990–999. 3. Spriet LL, MacLean DA, Dyck DJ et al. Caffeine ingestion and muscle metabolism during prolonged exercise in humans. Am J Physiol 1992; 262(6): E891–E898. 4. Carr A, Dawson B, Schneiker K et al. Effect of caffeine supplementation on repeated sprint running performance. J Sports Med Phys Fit 2008; 48: 472–478. 5. Pontifex KJ, Wallman KE, Dawson BT et al. Effects of caffeine on repeated sprint ability, reactive agility time, sleep and next day performance. J Sports Med Phys Fit 2010; 50(4):455–464. 6. Crowe MJ, Leicht AS, Spinks WL. Physiological and cognitive responses to caffeine during repeated, high-intensity exercise. Int J Sport Nutr Exerc Metab 2006; 16(5):528–544. 7. Paton C, Hopkins WG, Vollebregt L. Little effect of caffeine ingestion on repeated sprints in team-sport athletes. Med Sci Sports Exerc 2001; 33(5):822–825. 8. Schneiker KT, Bishop D, Dawson B et al. Effects of caffeine on prolonged intermittent-sprint ability in team-sport athletes. Med Sci Sports Exerc 2006; 38(3):578–585. 9. Fredholm B, Battig K, Holmen J et al. Actions of caffeine in the brain with special reference to factors that contribute to its widespread use. Pharmacol Rev 1999; 51:83–132. 10. Brewer CP, Dawson B, Wallman KE et al. Effect of repeated sodium phosphate loading on cycling time-trial performance and VO2 peak . Int J Sport Nutr Exerc Metab 2013; 23:187–194. 11. Folland JP, Stern R, Brickley G. Sodium phosphate loading improves laboratory cycling time-trial performance in trained cyclists. J Sci Med Sport 2008; 11:464–468. 12. Kreider RB, Miller GW, Schenck D et al. Effects of phosphate loading on metabolic and myocardial responses to maximal and endurance exercise. Int J Sport Nutr 1992; 2(1):20–47. 13. Czuba M, Zajac A, Poprzecki S et al. Effects of sodium phosphate loading on aerobic power and capacity in off road cyclists. J Sports Sci Med 2009; 8: 591–599. 14. Czuba M, Zajac A, Poprzecki S et al. The influence of sodium phosphate supplementation on VO2 max , serum 2,3-diphosphoglycerate level and heart rate in off-road cyclists. J Hum Kinet 2008; 19:149–164. 15. Brain MC, Card RT. Effect of inorganic phosphate on red cell metabolism: in vitro and in vivo studies. Adv Exp Med Biol 1972; 28:145–154. 16. Sim AY, Dawson BT, Guelfi KJ et al. Effects of static stretching in warm-up on repeated sprint performance. J Strength Cond Res 2009; 23(7):2155–2162. 17. Bishop D, Spencer M, Duffield R et al. The validity of a repeated sprint ability test. J Sci Med Sport 2001; 4:19–29. 18. Borg G. Psychophysical bases of perceived exertion. Med Sci Sports Exerc 1982; 14(5):377–381. 19. Cohen J. Statistical power analysis for the behavioural sciences, 2nd ed. Hillsdale, NJ, Lawrence Erlbaum Associates Inc, 1988. 20. Batterham AM, Hopkins WG. Making meaningful inferences about magnitudes. Sportscience 2005; 9:6–13. 21. Gaitanos GC, Williams C, Boobis LH et al. Human muscle metabolism during intermittent maximal exercise. J Appl Physiol 1993; 75:712–719. 22. Kreider RB, Miller GW, Williams MH et al. Effects of phosphate loading on oxygen uptake, ventilatory anaerobic threshold and run performance. Med Sci Sports Exerc 1990; 22(2):250–256. 23. Stewart I, McNaughton L, Davies P. Phosphate loading and the effects on VO2 max in trained cyclists. Res Q Exerc Sport 1990; 61(1):80–84. 24. Cade R, Conte M, Zauner C et al. Effects of phosphate loading on 2,3diphosphoglycerate and maximal oxygen uptake. Med Sci Sports Exerc 1984; 16:263–268.

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Effects of sodium phosphate and caffeine ingestion on repeated-sprint ability in male athletes.

To assess the effects of sodium phosphate (SP) and caffeine supplementation on repeated-sprint performance...
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