Oral ATP Supplement: effects on performance and repeat sprint ability

Article Review: Oral Adenosine-5′-triphosphate (ATP) Administration Increases Postexercise ATP Levels, Muscle Excitability, and Athletic Performance Following a Repeated Sprint Bout.  (see below for full citation)

Introduction: Adenosine-5’ -triphosphate (ATP) is best known for its role as an intracellular fuel source.  Small amounts of ATP are stored in the muscle and can rapidly be converted into energy by the enzyme ATPase.  Another rapid and short-lived source of stored energy is creatine phosphate.  When ATP is depleted, creatine kinase can resynthesize ATP from ADP using creatine phosphate.  Sustained ATP production comes from glycolysis and aerobic respiration, which covert carbohydrates and fatty acids into energy. In addition to its use as an energy source, ATP also has a vast impact on extracellular functions.  These functions include skeletal muscle calcium permeability, the blocking of chloride efflux, and vasodilation.  The importance of ATP as an energy source and extracellular influence has led to its investigation in athletic performance.  Low dose (150 mg) ATP supplementation for 15 days failed to improve bench press strength or measures of power.  However, the supplementation group was able to perform more overall volume during their working sets.  Higher dosed (400-800mg) ATP studies have resulted in greater benefits.  These benefits include increases in peak torque, maximal strength, vertical jump power, lean body mass, and post exercise blood flow.

Initially, the bioavailability of oral ATP was thought to be poor.  Supplementation failed to increase plasma levels of ATP indicating a lack of systematic bioavailability.  Closer examination of ATP supplementation found increased portal vein ATP concentration and nucleoside uptake by erythrocytes.  Even greater scrutiny revealed increased ATP synthesis by erythrocytes, independent of systemic ATP levels.  These findings suggest an indirect mechanism of oral ATP: influencing the capacity for erythrocytes to produce ATP without elevating systemic levels of ATP.    This increased capacity for ATP production is believed to cause the improvements noted in athletic performance, especially in high intensity sporting movements.   Therefore, the goal of this study was to examine ATP supplementation and its effects on power output and mental performance during and following repeated sprints.  In addition to performance benefits, a secondary goal of this study is to test whether ATP supplementation prevents drops in post workout ATP and its associated metabolites.

Purpose:  The purpose of this study was to investigate whether ATP supplementation prevents decrements in post workout ATP and its metabolites and increases physical and mental performance during repeated sprints.

Subject Description:  Forty-two (n=42) males between the ages of 18 and 30 were selected for this study.  Selection required individuals having resistance trained at least 3 times per week for the past 6 months and have a minimum of a year of experience.  Individuals were instructed to avoid resistance training for at least 72 hours pre-testing.  A dietician screening was used to ensure a consistent diet of 15-20% protein, 45-55% carbohydrates, and 25-30% fats was followed.  Other inclusion criteria included not taking performance enhancing supplements, non-smoker, not taking amino acid supplements, not using anabolic/catabolic hormones, and not on medications which would influence the study.

Procedures and methods:  The study was a double-blind randomized control trial.  Individuals either received ATP (400 mg, disodium salt) or placebo (400 mg, rice flour) for 14 days.  Prior to the supplementation, baseline sprint measurements were performed.  On day 15, individuals again received either ATP or placebo 30 minutes prior to sprint testing.  The sprint testing used a Wingate Ergomedic, allowing the weight to drop at 175 revolutions per minute, with a rest of 45 seconds between bouts.  Ten 6-second sprints were performed.  Individuals were familiarized with the sprint protocol 3 times prior to initiation of the baseline measurement.  During the test, the individual was instructed to cycle as fast as possible for 6 seconds with a resistance set to 7.5% body mass.  Power was recorded by a computer connected to the standard cycle ergometer using the Monark Anaerobic software.  The intraclass correlation of peak power (PPO) was r=0.96.  Muscle activation was measured using Delsys wireless electromyography sensors placed on the vastus lateralis.  Activation was measured during each sprint.  The root mean square was normalized to the first sprint and assigned the value 100%.  Muscle excitability was defined as the ratio of power output to muscle activation.  Greater power output to activation assumed greater muscle excitability.

Blood samples were taken at baseline, day 15 in a fasted stated and immediately and 30 minutes post exercise.  Blood was drawn from the antecubital vein.  Whole blood was evaluated by adding 7% trichloroacetic acid (stops metabolic activity) and then liquid chromatography was used to measure ATP and its metabolites.

Reaction time testing was performed immediately before the Wingate testing on pre and post follow-up evaluations. This testing was performed using a Dynavision apparatus, which is specifically designed to measure visual scanning and attention, reactions and coordination, and cognitive skill.   Reaction time specifically involves the individuals having to rapidly strike an illuminated key 30 cm away.  The ICC of the response time was r=.89.

Vertical jump peak power was assessed using a Tendo unit.  Three jumps were performed prior to Wingate testing at pre and post follow up evaluations.  The average of the results was used.  The ICC of the vertical jump peak power was r=0.97.

Results:  No significant differences were found in ATP or any of its metabolites at any time frame (p>0.05).  Analysis of covariance noted absolute changes in the supplementation group for ATP, ADP, and AMP (p<0.05).  The absolute changes for the sum of ATP-ADP-AMP was 171.8 +/- 54.5 in the supplementation verses -72.5 +/- 88.0 in the placebo.  For ATP-ADP 179.2 +/-0.7 in the ATP group verses-58.4 +/-53.0 in the placebo.  For ATP-AMP, 24.3 +/- 10.4 in the ATP group verses -30.0 +/- 14.8  in the placebo (p < 0.04, no units changes were absolute).

Both groups suffered similar decrements in peak power (placebo Pre-Post: 41.2-36.8% and ATP: 41.0-28%).  CIdiff revealed significant improvements in PPO pre to post with ATP at bout 8 (mean 102.6 W, 95% CIdiff, 21.6 to 183.5 W; bout 10: mean 90.8 W, 95% CIdiff, 9.8 to 171.8 W.

Muscle excitability was significantly increased with ATP supplementation.  Increases in ME were noted in early bouts (bout 2, +21.5%, p<0.02) and ATP prevent a decline in later bouts.  In the placebo, a significant drop in ME was noted (bouts 8, 9, 10: -30.5, -28.3, and -27.9%, p < 0.02).

No significant findings for vertical jump power or reaction time were noted.

Discussion:  It appears short-term ATP supplementation can combat fatigue associated declines in muscle performance and enhance muscle excitability.  This study demonstrated oral ATP supplementation prevented loss of peak power under fatigued situations near the end of exhaustive repeat sprint testing.   However, ATP failed to induce improvements in peak power during the early stages of sprint testing.  These results are in contrast with findings of creatine, which also influences ATP production and improves performance during both resting and fatigued states.  The authors note it is possible the supplementation period was too short.

These findings are important for individuals participating in sports which require brief maximal sprints interspersed with rest breaks such as soccer, football, and hockey.  Another interesting finding of this study is the enhancement of muscle excitability by ATP.  This enhancement is believed to be a peripheral mechanism, and possibly attributable to improvements in blood flow.  Vertical jump and reaction time appear unaffected by short term ATP usage.  For the vertical jump, this is in contrast to longer term studies.  The most likely reasoning for this is the short study period and lack of training intervention.  Failure of improvements in reaction time indicates ATP simply may not be effective at improving this endpoint.  Lastly, this study demonstrated ATP can help sustain ATP levels in the blood following intense exercise.  This finding again applies to sports where intense activity is interspersed with rest periods.  In conclusion, it appears acute oral ATP supplementation can help prevent decrements in blood levels of ATP and performance associated with intense exercise while simultaneously increasing muscle excitability.

My Thoughts:  Overall, I found this article interesting because I deal with a lot of strength/power athletes.  With this type of population you are always trying to find a possible edge to increase performance.  Creatine has long been a staple in strength/power athletes due to its ability to improve performance under rested and fatigued states.  Oral ATP supplementation appears to also be a viable option (not WADA banned) to help improve repeat performance.  Although these results don’t exactly wow you, ATP may be something that is more effective with a training intervention.   Longer term studies have shown larger increases in performance.  This may be due to completing more weight or training volume due to less fatigue.  For future research, I would like to see actual strength/power athletes supplemented with this over the course of 12 weeks and followed up with event specific performance.  This would help take any guess work out of applying lab values (peak power) and give us actual numbers on performance increases.

Purpura, M., Rathmacher, J. A., Sharp, M. H., Lowery, R. P., Shields, K. A., Partl, J. M., … Jäger, R. (2017). Oral Adenosine-5′-triphosphate (ATP) Administration Increases Postexercise ATP Levels, Muscle Excitability, and Athletic Performance Following a Repeated Sprint Bout. Journal of the American College of Nutrition36(3), 177-183. doi:10.1080/07315724.2016.1246989

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