Scientists from the Department of Physiology of the University of Granada (UGR) have shown that caffeine (about 3 mg/kg, the equivalent of a strong coffee) ingested half an hour before aerobic exercise significantly increases the rate of fat-burning.
They also found that if the exercise is performed in the afternoon, the effects of the caffeine are more marked than in the morning.
In their study, published in the Journal of the International Society of Sports Nutrition, the researchers aimed to determine whether caffeine – one of the most commonly consumed ergogenic substances in the world to improve sports performance – actually does increase oxidation or “burning” of fat during exercise.
Despite the fact that its consumption in the form of supplements is very common, the scientific evidence for its beneficial claims is scarce.
“The recommendation to exercise on an empty stomach in the morning to increase fat oxidation is commonplace. However, this recommendation may be lacking a scientific basis, as it is unknown whether this increase is due to exercising in the morning or due to going without food for a longer period of time,” explains the lead author of this research, Francisco José Amaro-Gahete of the UGR’s Department of Physiology.
A total of 15 men (mean age, 32) participated in the research, completing an exercise test four times at seven-day intervals. Subjects ingested 3 mg/kg of caffeine or a placebo at 8am and 5pm (each subject completed the tests in all four conditions in a random order). T
he conditions prior to each exercise test (hours elapsed since last meal, physical exercise, or consumption of stimulant substances) were strictly standardized, and fat oxidation during exercise was calculated accordingly.
Maximum fat oxidation
“The results of our study showed that acute caffeine ingestion 30 minutes before performing an aerobic exercise test increased maximum fat oxidation during exercise regardless of the time of day,” explains Francisco J. Amaro. The existence of a diurnal variation in fat oxidation during exercise was confirmed, the values being higher in the afternoon than in the morning for equal hours of fasting.
These results also show that caffeine increases fat oxidation during morning exercise in a similar way to that observed without caffeine intake in the afternoon.
In summary, the findings of this study suggest that the combination of acute caffeine intake and aerobic exercise performed at moderate intensity in the afternoon provides the optimal scenario for people seeking to increase fat-burning during physical exercise.
Following critical evaluation of the available literature to date, The International Society of Sports Nutrition (ISSN) position regarding caffeine intake is as follows:
- Supplementation with caffeine has been shown to acutely enhance various aspects of exercise performance in many but not all studies. Small to moderate benefits of caffeine use include, but are not limited to: muscular endurance, movement velocity and muscular strength, sprinting, jumping, and throwing performance, as well as a wide range of aerobic and anaerobic sport-specific actions.
- Aerobic endurance appears to be the form of exercise with the most consistent moderate-to-large benefits from caffeine use, although the magnitude of its effects differs between individuals.
- Caffeine has consistently been shown to improve exercise performance when consumed in doses of 3–6 mg/kg body mass. Minimal effective doses of caffeine currently remain unclear but they may be as low as 2 mg/kg body mass. Very high doses of caffeine (e.g. 9 mg/kg) are associated with a high incidence of side-effects and do not seem to be required to elicit an ergogenic effect.
- The most commonly used timing of caffeine supplementation is 60 min pre-exercise. Optimal timing of caffeine ingestion likely depends on the source of caffeine. For example, as compared to caffeine capsules, caffeine chewing gums may require a shorter waiting time from consumption to the start of the exercise session.
- Caffeine appears to improve physical performance in both trained and untrained individuals.
- Inter-individual differences in sport and exercise performance as well as adverse effects on sleep or feelings of anxiety following caffeine ingestion may be attributed to genetic variation associated with caffeine metabolism, and physical and psychological response. Other factors such as habitual caffeine intake also may play a role in between-individual response variation.
- Caffeine has been shown to be ergogenic for cognitive function, including attention and vigilance, in most individuals.
- Caffeine may improve cognitive and physical performance in some individuals under conditions of sleep deprivation.
- The use of caffeine in conjunction with endurance exercise in the heat and at altitude is well supported when dosages range from 3 to 6 mg/kg and 4–6 mg/kg, respectively.
- Alternative sources of caffeine such as caffeinated chewing gum, mouth rinses, energy gels and chews have been shown to improve performance, primarily in aerobic exercise.
- Energy drinks and pre-workout supplements containing caffeine have been demonstrated to enhance both anaerobic and aerobic performance.
Caffeine is the world’s most widely consumed psychoactive substance and naturally occurs in dozens of plant species, including coffee, tea and cocoa. Caffeine is ingested most frequently in the form of a beverage such as coffee, soft drinks and tea, although the consumption of many functional beverages, such as energy drinks, has been on a steady rise in the past two decades . In Western countries, approximately 90% of adults consume caffeine on a regular basis, with dietary caffeine consumption of U.S. adult men and women estimated at approximately 200 mg/day in a 2009–2010 survey [2–4]. In young adults and exercising individuals, there has also been a rise in the consumption of other caffeine-containing products, including energy drinks [1, 3], ‘pre-workout supplements’, chewing gum, energy gels and chews, aerosols, and many other novel caffeinated food products . Caffeine-containing products have a range of doses per serving, from 1 mg in milk chocolate up to > 300 mg in some dietary supplements .
Caffeine and its effects on health have been a longstanding topic of interest, and caffeine continues to be a dietary compound of concern in public health, as indicated by extensive investigations [7–10]. At the same time, caffeine has become ubiquitous in the sporting world, where there is keen interest in better understanding the impact of caffeine on various types of exercise performance. Accordingly, caffeine has dominated the ergogenic aids and sport supplement research domain over the past several decades [11–13].
Caffeine in sport: a brief history
In the early days (1900s) of modern sport, concoctions of plant-based stimulants, including caffeine and other compounds such as cocaine, strychnine, ether, heroin and nitroglycerin, were developed secretly by trainers, athletes and coaches, in what appears to be evidence for early day ergogenic aids designed to provide a competitive advantage . The use of various pharmaceutical cocktails by endurance athletes continued until heroin and cocaine became restricted to prescriptions in the 1920s, and further when the International Olympic Committee (IOC) introduced anti-doping programs in the late 1960s .
Some of the earliest published studies on caffeine came from two psychologists and colleagues William Rivers and Harald Webber, at Cambridge University, who both had an interest in disentangling the psychological and physiological effects of substances like caffeine and alcohol. Rivers and Webber, using themselves as subjects, investigated the effects of caffeine on muscle fatigue. The remarkable well-designed studies carried out from 1906 to 1907 used double-blinded placebo-controlled trials and standardization for diet (i.e. caffeine, alcohol), and were described in a 1907 paper in the Journal of Physiology . Significant research on the effects of caffeine on exercise performance with more subjects, different sports, and exploring variables such as the effects between trained and untrained individuals, began and continued through the 1940s [14, 17]. However, it was the series of studies investigating the benefits of caffeine in endurance sports in the Human Performance Laboratory at Ball State University in the late 1970s, led by David Costill [18, 19] and others , that sparked a generation of research on the effects of caffeine in exercise metabolism and sports performance.
Along with naturally occurring sources, such as coffee, tea and cocoa, caffeine is also added to many foods, beverages and novelty products, such as jerky, peanut butter, and candy, in both synthetic (e.g. powder) and natural (e.g. guarana, kola nut) forms. Synthetic caffeine is also an ingredient in several over-the-counter and prescription medications, as it is often used in combination with analgesic and diuretic drugs to amplify their pharmacological potency .
Approximately 96% of caffeine consumption from beverages comes from coffee, soft drinks and tea . Additionally, there are varying levels of caffeine in the beans, leaves and fruit of more than 60 plants, resulting in great interest in herbal and other plant-based supplements [23–26]. Caffeine-containing energy drink consumption [27–31] and co-ingestion of caffeine with (e.g. “pre-workouts”), or in addition to, other supplements (e.g. caffeine + creatine) is also popular among exercising individuals [32–39]. To date, the preponderance of caffeine and exercise performance literature has utilized anhydrous caffeine (in a capsule) [40–46] for simpler dose standardization and pla
cebo creation. There is also a growing body of literature studying the effects of using alternate delivery methods of caffeine during exercise  such as coffee [18, 47–56], energy drinks, herbal formulas  and ‘pre-workout’ formulas, among others. A review of alternate caffeine forms may be found in the Alternative caffeine sources section and Tables 4, ,5,5, ,6,6, ,77 and and88.
Table 4 Investigations examining the effects of caffeinated chewing gum on caffeine absorption and exercise performance
|Kamimori et al. 2002 ||Healthy males (n = 84; 12 per group)||• 50 mg caffeine capsule• 50 mg caffeine gum• 100 mg caffeine capsule• 100 mg caffeine gum• 200 mg caffeine capsule• 200 mg caffeine gum• Placebo||Both 100 and 200 mg of caffeine in gum and capsule formualtions provide comparable amounts of caffeine to the systemic circulation.Mean Tmax for the gum groups ranged from 44.2 to 80.4 min as compared with 84.0–120.0 min for the capsule groups|
|Ryan et al. 2012 ||College-aged, physically active males (n = 8)||• 200 mg caffeinated gum• Placebo gum||⬌ cycling TTE|
|Ryan et al. 2013 ||Well-trained male cyclists (n = 8)||• 300 mg caffeine gum• Placebo gum||*↑ cycling TT performance when 300 mg caffeine chewing gum was administered 5 min pre-TT|
|Lane et al. 2014 ||Well-trained males (n = 12) and females (n = 12)||• 3 mg/kg caffeine gum 40 min prior + 1 mg/kg 10 min prior• Placebo gum• Beet root juice• Beet root juice w/ caffeine||*↑ cycling TT performance by 3–4%Note: participant’s sex was accounted for during testing (female: 29.35 km; male: 43.83 km)|
|Oberlin-Brown et al. 2016 ||Well-trained male cyclists (n = 11)||• 200 mg caffeine gum• 200 mg caffeine + CHO gum• CHO gum• Placebo gum||⬌ cycling TT performance|
|Paton et al. 2015 ||Well-trained male (n = 10) and female (n = 10) cyclists||• ~ 3–4 mg/kg caffeine gum• Placebo gum||~ 3–4 mg/kg enhanced both endurance (> 5 min) and sprint power output (< 30 s) by similar amounts (~ 4%) during the final 10 km of a 30-km race|
|Paton et al. 2010 ||Competitive male cyclists (n = 9)||• 3 mg/kg caffeine gum• Placebo gum||*↓ power output decline in 3rd & 4th sprints|
|Bellar et al. 2012 ||Collegiate shot-put athletes (n = 9)||• 100 mg caffeine gum• Placebo gum||*↑ shot-put performance|
|Ranchordas et al. 2018 ||Collegiate male soccer players (n = 10)||• 200 mg caffeine gum• Placebo gum||*↑ Yo-Yo Intermittent Recovery Test level 1 and countermovement jump|
|Venier et al. 2019 [67, 68]||Resistance-trained men (n = 19)||• 300 mg caffeine gum• Placebo gum||*↑ Jumping height*↑ Isokinetic strength and power*↑ Movement velocity in the bench press*↑ Whole-body power output|
Table 5 Investigations examining the effects of caffeine mouth rinsing (CMR) on exercise performance
|Doering et al. 2014 ||Well-trained cyclists (n = 10)||• 10 s rinse 35 mg caffeine/25 mL X 8• Placebo rinse||⬌ plasma caffeine levels⬌ cycling TT Performance|
|De Pauw et al. 2015 ||Healthy males (n = 10)||• 20 s- 25 mL Rinse 1.2% caffeine• 20 s- 25 mL Rinse 6.4% CHO• Placebo Rinse||*↑ stroop task performance|
|Pomportes et al. 2017 ||Physically active males (n = 16) and females (n = 6)||• 20 s- 25 mL rinse 67 mg caffeine• 20 s- 25 mL rinse 7.0% CHO• 20 s- 25 mL rinse 0.4 g guarana• Placebo rinse||⬌ variability or production durations⬌ errors made|
|Beaven et al. 2013 ||Recreationally active males (n = 12)||• 5 s- 25 mL rinse 1.2% caffeine• 5 s- 25 mL rinse 6% CHO• Placebo rinse||*↑ mean power in first sprint for caffeine and CHO rinsesNS ↑ maximal power in first two sprints|
|Beaven et al. 2013 ||Recreationally active males (n = 12)||• 5 s- 25 mL rinse 1.2% caffeine• 5 s- 25 mL rinse 6.0% CHO• 5 s- 25 mL rinse 1.2% caffeine+ 6.0% CHO||*↑ peak power in first sprint*↑ mean power in fifth sprint|
|Kizzi et al. 2016 ||Glycogen depleted, recreationally active males (n = 8)||• 10 s- 25 mL rinse 2.0% caffeine• Placebo rinse||⬌ mean and peak power in 4th and 5th sprint|
|Sinclair and Bottoms 2014 ||Healthy males (n = 12)||• 5 s- 25 mL rinse 0.032% caffeine• 5 s- 25 mL rinse 6.4% CHO• Placebo rinse||*↑ arm crank TT performance|
|Bottoms et al. 2014 ||Healthy males (n = 12)||• 5 s- 125 mL rinse w/ 32 mg of caffeine• 5 s – 6.4% CHO solution• Placebo rinse||*↑ distance cycled during the caffeine mouth rinse trial (16.2 ± 2.8 km) was significantly greater compared to placebo trial (14.9 ± 2.6 km).There was no difference between CHO and caffeine trials|
|Pataky et al. 2016 ||Recreationally trained male (n = 25) and female (n = 13) cyclists||• Placebo rinse + 6 mg/kg caffeine capsule• 25 mL rinse 300 mg caffeine + placebo capsule• 25 mL rinse 300 mg caffeine + 6 mg/kg caffeine capsule||*↑ 3 km cycling TT performance|
|Lesniak et al. 2016 ||Recreationally active females (n = 7)||• 5 s- 25 mL rinse 1.2% caffeine• 5 s- 25 mL rinse 6.0% CHO• 5 s- 25 mL rinse 1.2% caffeine+ 6% CHO||⬌ cycling TT performance|
|Dolan et al. 2017 ||College lacrosse players (n = 10)||• 5 s- 25 mL Rinse 1.2% caffeine• 5 s- 25 mL Rinse 6.0% CHO• 5 s- 25 mL Rinse 1.2% caffeine+ 6.0% CHO• Placebo rinse• No rinse||⬌ intermittent sport performance|
|Clarke et al. 2015 ||Recreationally resistance-trained males (n = 15)||• 5 s- 25 mL rinse 1.2% caffeine• 5 s- 25 mL rinse 6.0% CHO• 5 s- 25 mL rinse 1.2% caffeine+ 6.0% CHO• Placebo rinse||⬌ total weight lifted|
Bold text associated with reported trial outcomes; s = seconds, mL = milliliters, CHO = carbohydrate, TT time trial, * = significant difference, NS = non-significant difference, ↑ = improved performance, ↓ = decreased, ⬌ = no improvement/change, mg = milligrams
Table 6 – Investigations examining the effects of caffeine nasal sprays on exercise and cognitive performance
|De Pauw et al. 2017 ||Healthy males (n = 10)||• Nasal spray 15 mg/mL caffeine• Nasal spray 80 mg/mL glucose• Placebo nasal spray||*↑ activity of cingulate, insular, and sensory-motor cortices⬌ stroop task performance|
|De Pauw et al. 2017 ||Moderately trained males (n = 11)||• Nasal spray 15 mg/mL caffeine• Nasal spray 80 mg/mL glucose• Placebo nasal spray||⬌ plasma caffeine levels⬌ wingate performance⬌ 30 min cycling TT performance⬌ stroop task performance|
|Laizure et al. 2017 ||Healthy adults (n = 17)||• Inspired powder 100 mg/mL caffeine (AeroShot)• Oral solution 100 mg/248 mL caffeine||⬌ peak plasma caffeine levels⬌ bioavailability|
mg/mL = milligram per milliliter, TT = time trial, * = significant difference, ⬌ = no improvement/change, ↑ = increased, ↓ = decreased, min = minute
Table 7 Investigations examining the effects of caffeinated bars and gels on exercise performance
|Hogervorst et al. 2008 ||Well-trained male cyclists (n = 24)||• Bar with 100 mg caffeine and 45.0 g CHO• Bar with only 45.0 g CHO• 300 mL non-caloric beverage||*↑Stroop and Rapid Visual Information Processing tests after 140 min and time to exhaustion exercise trial at 75% VO2max|
|Cooper et al. 2014 ||Recreationally trained males (n = 12)||• Gel with 100 mg caffeine and 25.0 g CHO• Gel with 25 g CHO• Gel placebo||*↓ fatigue and RPE during 3rd sprint setNS: sprint performance|
|Scott et al. 2015 ||Male college athletes (n = 13)||• Gel with 21.6 g CHO and 100 mg caffeine• Gel with 21.6 g CHO||*↑ performance in 2000 m rowing task|
|Venier et al. 2019 [67, 68]||Resistance-trained men (n = 17)||• Gel with 88 g CHO and 300 mg caffeine• Gel with 88 g CHO||*↑ jumping height*↑ isokinetic strength and power*↑ movement velocity in the bench pressNS: whole-body power output|
Bold text associated with reported trial outcomes; mg = milligrams, g = grams, CHO = carbohydrate, * = significant, NS = non-significant difference, VST = visual sensitivity test, ↑ = improved performance, ↓ = decreased, m = meters, RPE = rating of perceived exertion, mL = milliliters
Table 8 – Energy drinks and pre-workout supplements
|Endurance Exercise Performance||Alford et al. 2001 ||Young adults (n = 36)||-250 mL Energy drink with 80 mg caffeine and 26 g CHO-Carbonated placebo-No drink||*↑ Aerobic Endurance||-26 g CHO|
|Candow et al. 2009 ||Young men (n = 9) and women (n = 8)||-CHO free energy drink with 2 mg/kg caffeine-Non-caffeinated version of energy drink||⬌ High-intensity Run Time to Exhaustion|
|Walsh et al. 2010 ||Recreationally active men (n = 9) and women (n = 6)||-26 g Pre-workout with unknown amount of caffeine (ingredients listed in column 5)-Placebo||*↑ Mod-intensity Run Time to Exhaustion||−2.05 g taurine, caffeine, and gluconolactone, 7.9 g L-leucine, L-isoleucine, L-valine, L-arginine and L-glutamine, 5 g of di-creatine citrate, and 2.5 g of βalanine|
|Ivy et al. 2009 ||Trained cyclists men (n = 6) and women (n = 6)||-Energy drink with 160 mg caffeine-Placebo||*↑ Cycle Time Trial Performance by 4.7%||-2.0 g taurine, 1.2 g glucuronolactone, 54 g carbohydrate, 40 mg niacin, 10 mg pantothenic acid, 10 mg vitamin B6, and 10 microg vitamin B12|
|Sanders et al. 2015 ||Healthy participants (n = 15)||−12 oz. Placebo (Squirt)− 8.4 oz. Red Bull®− 16 oz. Monster Energy®− 2 oz. 5-h ENERGY®||⬌ RPE on Treadmill at 70% VO2 max⬌ Oxygen Consumption at 70% VO2 max|
|Al-Fares et al. 2015 ||Healthy female students (n = 32)||-Energy drink with 160 mg caffeine-Placebo with similar CHO content||⬌ VO2 max||−2.0 g taurine, 1.2 g glucuronolactone, 54 g carbohydrate, 40 mg niacin, 10 mg pantothenic acid, 10 mg vitamin B6, and 10 μg vitamin B12|
|Prins et al. 2016 ||Recreation endurance male (n = 13) and female (n = 5) runners||-Energy drink with 160 mg caffeine-Placebo||*↑ 5 k Time Trial||−2.0 g taurine, 1.2 g glucuronolactone, 54 g carbohydrate, 40 mg niacin, 10 mg pantothenic acid, 10 mg vitamin B6, and 10 microg vitamin B12|
|Kinsinger et al. 2016 ||Recreational male athletes (n = 23)||−1.93 oz Energy shot with 100 mg caffeine− 1.93 oz. Placebo||⬌ RPE on Treadmill VO2 max Test⬌ Treadmill VO2 max||-1870 mg (taurine, glucuronic acid, malic acid, N-acetyl L-tyrosine, L-phenylalanine and citicoline)|
|Resistance/Sprint Performance||Forbes et al. 2007 ||Young men (n = 11) and women (n = 40||-Energy drink with 2 mg/kg caffeine-Non-caffeinated version of energy drink||*↑ Bench-Press Repetitions by 6%|
|Del Coso et al. 2012 ||Healthy men (n = 9) and women (n = 3)||-Energy drink with 1 mg/kg caffeine-Energy drink with 3 mg/kg caffeine-Non-caffeinated version of energy drink||*↑ Half-Squat Maximal Power by 7%*↑ Bench-Press Maximal Power by 7%|
|Gonzalez et al. 2011 ||Resistance-trained college males (n = 8)||−26 g Pre-workout with unknown amount of caffeine (ingredients listed in column 5)-Placebo||*↑ # of Bench-Press and Squat Repetitions at 80% 1RM by 11.8%*↑ Average Power Output for the Workout||-2.05 g taurine, caffeine, and gluconolactone, 7.9 g L-leucine, L-isoleucine, L-valine, L-arginine and L-glutamine, 5 g of di-creatine citrate, and 2.5 g of βalanine|
|Astorino et al. 2011 ||Collegiate female soccer players (n = 15)||-255 mL energy drink with 1.3 mg/kg caffeine + 1 g taurine-Placebo||⬌ Sprint-based Exercise Performance||-1 g taurine|
|Campbell et al. 2016 ||College men (n = 8) and women (n = 11)||-37 mL Energy shot with 2.4 mg/kg caffeine-37 mL Placebo||⬌ Vertical Jump⬌ YMCA Bench-PressNS↑ Curl-up Endurance|
|Eckerson et al. 2013 ||Resistance-trained men (n = 17)||−500 mL Energy drink with 160 mg caffeine + 2 g taurine− 500 mL Energy drink with 160 mg caffeine− 500 mL Placebo||⬌ 1RM Bench-Press Strength⬌ Total Volume Lifted||−2 g Taurine|
|Astley et al. 2018 ||Resistance-trained men (n = 15)||-Energy drink with 2.5 mg/kg caffeine-Non-caffeinated version of energy drink||*↑ Knee Extensions in Dominant Leg*↑ 80% 1RM Bench-Press Reps*↑ Isometric Grip Strength|
|Magrini et al. 2016 ||Healthy men (n = 23) and women (n = 8)||-4 oz Energy drink with 158 mg caffeine-4 oz. Placebo||⬌ Total Push-ups|
|Anaerobic Exercise Performance for Power||Forbes et al. 2007 ||Young men (n = 11) and women (n = 4)||-Energy drink with 2 mg/kg caffeine-Non-caffeinated version of energy drink||⬌ Wingate Peak Power⬌ Wingate Average Power|
|Campbell et al. 2010 ||Recreationally active young men (n = 9) and women (n = 6)||-Energy drink with 2.1 mg/kg caffeine-Non-caffeinated version of energy drink||⬌ Wingate Peak Power|
|Hoffman et al. 2009 ||Male strength/power athletes (n = 12)||-Energy drink with 1.8 mg/kg caffeine-Non-caffeinated version of energy drink||⬌ Wingate Power Performance|
|Alford et al. 2001 ||Young adults (n = 36)||−250 mL Energy drink with 80 mg caffeine and 26 g CHO-Carbonated placebo-No drink||*↑ Maximum Speed on Cycle Ergometer||-26 g CHO|
|Campbell et al. 2016 ||College men (n = 8) and women (n = 11)||-37 mL Energy shot with 2.4 mg/kg caffeine-37 mL Placebo||⬌ Repeated Sprint Speed|
|Mood/ Reaction Time/ Alertness||Alford et al. 2001 ||Young adults (n = 36)||-250 mL Energy drink with 80 mg caffeine and 26 g CHO-Carbonated placebo-No drink||*↑ Choice Reaction Time*↑ Concentration*↑ Memory||-26 g CHO|
|Walsh et al. 2010 ||Recreationally active men (n = 9) and women (n = 6)||-26 g Pre-workout with unknown amount of caffeine (ingredients listed in column 5)-Placebo||*↑ Focus and Energy in 1st 10 min of Exercise⬌ Energy, Fatigue, and Focus Immediately Post-exercise||-2.05 g taurine, caffeine, and gluconolactone, 7.9 g L-leucine, L-isoleucine, L-valine, L-arginine and L-glutamine, 5 g of di-creatine citrate, and 2.5 g of βalanine|
|Hoffman et al. 2009 ||Male strength/power athletes (n = 12)||–Energy drink with 1.8 mg/kg caffeine-Non-caffeinated version of energy drink||*↓ Reaction Time*↑ Feelings of Energy and FocusNS↑ Alertness|
|Seidl et al. 2000 ||Male (n = 4) and female (n = 6) graduate students||-Energy drink with 160 mg caffeine-Placebo||*↓ Reaction Time at Night⬌ Vitality Scores at Night[[when compared to the Placebo Group who saw a significant decline in vitality and response time]]||2.0 g taurine, 1.2 g glucuronolactone, 54 g carbohydrate, 40 mg niacin, 10 mg pantothenic acid, 10 mg vitamin B6, and 10 microg vitamin B12|
|Scholey et al. 2004 ||Healthy volunteers (n = 20)||-250 ml Energy drink with 75 mg caffeine-Non-caffeinated version of energy drink-Placebo||*↑ Secondary Memory*↑ Speed of Attention||−37.5 g glucose, ginseng, and Ginkgo biloba|
|Smit et al. 2004 ||Healthy volunteers (n = 271)||–Caffeine + CHO + Carbonation-Placebo with carbonation-Placebo without carbonation||⬌ Mood and Performance (during fatiguing and cognitively demanding tasks)||-CHO|
|Rao et al. 2005 ||Healthy volunteers (n = 40)||–Caffeine + CHO-Placebo||*↑ Event Related Potentials in ECGs*↑ Behavioral Performance in Accuracy and Speed of Performance||-CHO|
|Howard et al. 2010 ||College students (n = 80)||-Energy drink with 1.8 ml/kg caffeine**-Energy drink with 3.6 ml/kg caffeine-Energy drink with 5.4 ml/kg caffeine-Non-caffeinated version of energy drink-No drink||Compared with the placebo and no drink conditions, the energy drink doses decreased reaction times on the behavioral control task, increased subjective ratings of stimulation and decreased ratings of mental fatigue.Greatest improvements in reaction times and subjective measures were observed with the lowest dose (1/8 mg/kg).||Taurine, sucrose and glucose, B-group vitamins|
|Wesnes et al. 2016 ||Young volunteers (n = 24)||-250 mL Energy drink with 80 mg caffeine + 27 g glucose-250 mL Energy drink with 80 mg caffeine-250 mL Placebo||*↑ Working and Episodic Memory||-27 g Glucose|
Outcomes are bold group specific; * = significant difference, ⬌ = no change, ↑ = improved performance, ↓ = decrease, TT = time trial, RPA = rating of perceived exertion, NS = non-significant improvement, mg/kg = milligram per kilogram, g = grams, CHO = carbohydrate, min = minutes, VO2 = aerobic capacity, m = meters, ml = milliliters, RPE = rating of perceived exertion
Caffeine legality in sport
Anti-doping rules apply to most sports, especially in those where athletes are competing at national and international levels. The IOC continues to recognize that caffeine is frequently used by athletes because of its reported performance-enhancing or ergogenic effects . Caffeine was added to the list of banned substances by the IOC in 1984 and the World Anti-Doping Agency (WADA) in 2000. A doping offense was defined as having urinary caffeine concentrations exceeding a cut-off of 15 μg/ml. In 1985, the threshold was reduced to 12 μg/ml . The cut-off value was chosen to exclude typical amounts ingested as part of common dietary or social coffee drinking patterns, and to differentiate it from what was considered to be an aberrant use of caffeine for the purpose of sports performance enhancement .
The IOC and WADA removed the classification of caffeine as a “controlled” substance in 2004, leading to a renewed interest in the use of caffeine by athletes. However, caffeine is still monitored by WADA, and athletes are encouraged to maintain a urine caffeine concentration below the limit of 12 μg/ml urine which corresponds to 10 mg/kg body mass orally ingested over several hours, and which is more than triple the intake reported to enhance performance [112, 113]. Interestingly, caffeine is also categorized as a banned substance by the National Collegiate Athletic Association (NCAA), if urinary caffeine concentration exceeds 15 μg/ml, which is greater than the “monitored substance” level set for WADA , and also well above amounts that are deemed ergogenic.
A comparison of caffeine concentrations obtained during in-competition doping control from athletes in several sports federations pre− 2004 versus post-2004, indicated that average caffeine concentrations decreased in 2004 after removal from the prohibited substance list . Reports on over 20,000 urine samples collected and analyzed after official national and international competitions between 2004 and 2008, and again in 2015 using 7500 urine samples found overall prevalence of caffeine use across various sports to be about 74% in the 2004 to 2008 time period and roughly 76% in 2015. The highest use of caffeine was among endurance athletes in both studies [115, 116]. Urinary caffeine concentration significantly increased from 2004 to 2015 in athletics, aquatics, rowing, boxing, judo, football, and weightlifting; however, the sports with the highest urine caffeine concentration in 2015 were cycling, athletics, and rowing .
Caffeine or 1,3,7-trimethylxanthine, is an odorless white powder that is soluble in both water and lipids and has a bitter taste. It is rapidly absorbed from the gastrointestinal tract, mainly from the small intestine but also in the stomach . In saliva, caffeine concentration reaches 65–85% of plasma levels, and is often used to non-invasively monitor compliance for ingestion or abstinence of caffeine .
Caffeine is effectively distributed throughout the body by virtue of being sufficiently hydrophobic to allow easy passage through most, if not all biological membranes, including the blood-brain barrier . When caffeine is consumed it appears in the blood within minutes, with peak caffeine plasma concentrations after oral administration reported to occur at times (Tmax) ranging from 30 to 120 min [43, 120–122].
The absolute bioavailability of caffeine is very high and reaches near 100% as seen in studies reporting areas under the plasma concentration-time curves (AUC) . Once caffeine is absorbed, there appears to be no hepatic first-pass effect (i.e., the liver does not appear to remove caffeine as it passes from the gut to the general circulation), as evidenced by similar plasma concentration curves when administered by either oral or intravenous routes .
Caffeine absorption from food and beverages does not seem to be dependent on age, gender, genetics or disease, or the consumption of drugs, alcohol or nicotine. However, the rates of caffeine metabolism and breakdown appear to differ between individuals through both environmental and genetic influences [3, 124, 125].
Over 95% of caffeine is metabolized in the liver by the Cytochrome P450 1A2 (CYP1A2) enzyme, a member of the cytochrome P450 mixed-function oxidase system, which metabolizes and detoxifies xenobiotics in the body . CYP1A2 catalyzes the demethylation of caffeine into the primary metabolites paraxanthine (1,7-dimethylxanthine), theobromine (3,7-dimethylxanthine) and theophylline (1,3-dimethylxanthine), which account for approximately 84, 12, and 4%, of total caffeine elimination, respectively [127, 128].
These three caffeine metabolites undergo further demethylations and oxidation to urates in the liver with about 3–5% remaining in caffeine form when excreted in the urine [129, 130]. While the average half-life (t1/2) of caffeine is generally reported to be between 4 and 6 h, it varies between individuals and even may range from 1.5 to 10 h in adults . The wide range of variability in caffeine metabolism is due to several factors.
The rate of caffeine metabolism may be inhibited or decreased with pregnancy or use of hormonal contraceptives , increased or induced by heavy caffeine use  cigarette smoking  or modified in either direction by certain dietary factors  and/or variation in the CYP1A2 gene, which will be discussed later [125, 132–134].
Several studies have also shown that the form of caffeine or its vehicle for entry into the body can modify the pharmacokinetics [58, 81, 119, 122]. One small trial (n = 3) evaluated Tmax for a variety of beverages that all included 160 mg of caffeine but in different volumes of solution, and reported that Tmax occurs at 0.5, 0.5, and 2 h for coffee, tea and cola, respectively .
In another study involving seven participants, caffeine plasma concentrations peaked rapidly at 30 min for capsule form, whereas caffeine absorption from cola and chocolate was delayed and produced lower plasma concentrations that peaked at roughly 90–120 min after consumption. This study also did not control for volume of administered solution (capsules and chocolate ingested with 360 ml water and 800 ml cola) .
Liguori et al.  evaluated a 400 mg dose of caffeine in 13 subjects and reported salivary caffeine Tmax values of 42, 39 and 67 min, for coffee, sugar-free cola and caffeine capsules, respectively. However, fluid volume was again not standardized (coffee – 12 oz., sugar-free cola – 24 oz., capsules – volume of administered fluid not reported).
The impact of temperature or rate of ingestion of caffeine has also been investigated, amidst concerns that cold energy drinks might pose a danger when chugged quickly, compared to sipping hot coffee. One study  compared five conditions that included: slow ingestion (20 min) of hot coffee, and fast (2-min) or slow (20-min) ingestion for both cold coffee and energy drinks. Similar to other caffeine pharmacokinetic studies [122, 135], White et al.  reported that although the rate of consumption, temperature, and source (coffee vs. energy drink) may be associated with slight differences in pharmacokinetic activity, these differences are small.
Chewing gum formulations appear to alter pharmacokinetics, as much of the caffeine released from the gum through mastication can be absorbed via the buccal cavity, which is considered faster due to its extensive vascularization, especially for low molecular weight hydrophobic agents . Kamimori et al.  compared the rate of absorption and relative caffeine bioavailability from chewing gum compared to a capsule form of caffeine.
Although caffeine administered in the chewing gum formulation was absorbed at a significantly faster rate, the overall bioavailability was comparable to the capsuled 100 and 200 mg caffeine dose groups. These pharmacokinetic findings are useful for military and sport purposes, where there is a requirement for rapid and maintained stimulation over specific periods of time.
Chewing gum may also be advantageous due to reduced digestive requirements, where absorption of caffeine in other forms (capsule, coffee etc.) may be hindered by diminished splanchnic blood flow during moderate to intense exercise. Finally, there is a growing prevalence of caffeinated nasal and mouth aerosols administered directly in the mouth, under the tongue or inspired may affect the brain more quickly through several proposed mechanisms , although there are only a few studies to date to support this claim.
The administration of caffeine via aerosol into the oral cavity appears to produce a caffeine pharmacokinetic profile comparable to the administration of a caffeinated beverage . Nasal and mouth aerosols will be discussed further in another section.
Mechanism of Action (MOA)
Although the action of caffeine on the central nervous system (CNS) has been widely accepted as the primary mechanism by which caffeine alters performance, several mechanisms have been proposed to explain the ergogenic effects of caffeine, including increased myofibrillar calcium availability [138, 139], optimized exercise metabolism and substrate availability , as well as stimulation of the CNS [140–142].
One of the earlier proposed mechanisms associated with the ergogenic effects of caffeine stemmed from the observed adrenaline (epinephrine)-induced enhanced free-fatty acid (FFA) oxidation after caffeine ingestion and consequent glycogen sparing, resulting in improved endurance performance [18, 45, 143]. However, this substrate-availability hypothesis was challenged and eventually dismissed, where after several performance studies it became clear that the increased levels of FFAs appeared to be higher earlier in exercise when increased demand for fuel via fat oxidation would be expected [141, 144, 145].
Furthermore, this mechanism could not explain the ergogenic effects of caffeine in short duration, high-intensity exercise in which glycogen levels are not a limiting factor. Importantly, several studies employing a variety of exercise modalities and intensities failed to show a decrease in respiratory exchange ratio (RER) and/or changes in serum FFAs, which would be indicative of enhanced fat metabolism during exercise when only water was ingested [144, 146–148].
Ingestion of lower doses of caffeine (1–3 mg/kg of body mass), which do not result in significant physiological responses (i.e. RER, changes in blood lactate, glucose), also appear to deliver measurable ergogenic effects, offering strong support for the CNS as the origin of reported improvements [43, 149, 150]. As such, focus has shifted to the action of caffeine during exercise within the central and peripheral nervous systems, which could alter the rate of perceived exertion (RPE) [151–154], muscle pain [151, 155–157], and possibly the ability of skeletal muscle to generate force .
Caffeine does appear to have some direct effects on muscle which may contribute to its ergogenicity. The most likely pathway that caffeine may benefit muscle contraction is through calcium ion (Ca2+) mobilization, which facilitates force production by each motor unit [138, 139, 150, 158].
Fatigue caused by the gradual reduction of Ca2+ release may be attenuated after caffeine ingestion [139, 159]. Similarly, caffeine may work, in part, in the periphery through increased sodium/potassium (Na+/K+) pump activity to potentially enhance excitation-contraction coupling necessary for muscle contraction .
Caffeine appears to employ its effects at various locations in the body, but the most robust evidence suggests that the main target is the CNS, which is now widely accepted as the primary mechanism by which caffeine alters mental and physical performance . Caffeine is believed to exert its effects on the CNS via the antagonism of adenosine receptors, leading to increases in neurotransmitter release, motor unit firing rates, and pain suppression [151, 155–157, 161].
There are four distinct adenosine receptors, A1, A2A, A2B and A3, that have been cloned and characterized in several species . Of these subtypes, A1 and A2A, which are highly concentrated in the brain, appear to be the main targets of caffeine . Adenosine is involved in numerous processes and pathways, and plays a crucial role as a homeostatic regulator and neuromodulator in the nervous system .
The major known effects of adenosine are to decrease the concentration of many CNS neurotransmitters, including serotonin, dopamine, acetylcholine, norepinephrine and glutamate [163–165]. Caffeine, which has a similar molecular structure to adenosine, binds to adenosine receptors after ingestion and therefore increases the concentration of these neurotransmitters [163, 165]. This results in positive effects on mood, vigilance, focus, and alertness in most, but not all, individuals [166, 167].
Researchers have also characterized aspects of adenosine A2A receptor function related to cognitive processes  and motivation [169, 170]. In particular, several studies have focused on the functional significance of adenosine A2A receptors and the interactions between adenosine and dopamine receptors, in relation to aspects of behavioral activation and effort-related processes [168–171].
The serotonin receptor 2A (5-HT2A) has also been shown to modulate dopamine release, through mechanisms involving regulation of either dopamine synthesis or dopaminergic neuron firing rate [172, 173]. Alterations in 5-HTR2A receptors may therefore affect dopamine release and upregulation of dopamine receptors [174, 175]. A possible mechanism for caffeine’s ergogenicity may involve variability in 5-HTR2A receptor activity, which may modulate dopamine release and consequently impact alertness, pain and motivation and effort . 5-HTR2A receptors are encoded by the HTR2A gene, which serves as a primary target for serotonin signaling , and variations in the gene have been shown to affect 5-HTR2A receptor activity [177, 178]. This may therefore modulate dopamine activity, which may help to elucidate some of the relationships among neurotransmitters, genetic variation and caffeine response, and the subsequent impact on exercise performance.
Muscle pain has been shown to negatively affect motor unit recruitment and skeletal muscle force generation proportional to the subjective scores for pain intensity [179, 180]. In one study, progressively increased muscle pain intensity caused a gradual decrease in motor firing rates .
However, this decrease was not associated with a change in motor unit membrane properties demonstrating a central inhibitory motor control mechanism with effects correlated to nociceptive activity . Other studies also indicate that muscle force inhibition by muscle pain is centrally mediated . Accordingly, caffeine-mediated CNS mechanisms, such as dopamine release , are likely imputable for pain mitigation during high-intensity exercise [155–157, 181, 183–186]. Although there appears to be strong evidence supporting the analgesic effects of caffeine during intense exercise, others have found no effect [185, 187].
The attenuation of pain during exercise as a result of caffeine supplementation may also result in a decrease in the RPE during exercise. Two studies [183, 184] have reported that improvements in performance were accompanied by a decrease in pain perception as well as a decrease in RPE under caffeine conditions, but it is unclear which factor may have contributed to the ergogenic effect. Acute caffeine ingestion has been shown to alter RPE, where effort may be greater under caffeine conditions, yet it is not perceived as such [12, 152–154].
A meta-analysis  identified 21 studies using mostly healthy male subjects (74%) between the ages of 20 and 35 years and showed a 5.6% reduction in RPE during exercise following caffeine ingestion. An average improvement in performance of 11% was reported across all exercise modalities. This meta-analysis established that reductions in RPE explain up to 29% of the variance in the improvement in exercise performance .
Others have not found changes in RPE with caffeine use . A more recent study by Green et al.  also showed that when subjects were instructed to cycle at specific RPE (effort) levels under caffeine conditions, the higher perceived intensity did not necessarily result in greater work and improved performance in all subjects equally. The authors noted that individual responses to caffeine might explain their unexpected findings.
In the last decade, our understanding of CNS fatigue has improved. Historically, it is well- documented that “psychological factors” can affect exercise performance and that dysfunction at any step in the continuum from the brain to the peripheral contractile machinery will result in muscular fatigue [189, 190]. The role of the CNS and its ‘motor drive’ effect was nicely shown by Davis et al.  who examined the effect of caffeine injected directly into the brains of rats on their ability to run to exhaustion on a treadmill.
In this controlled study, rats were injected with either vehicle (placebo), caffeine, 5′-N-Ethylcarboxamido adenosine (NECA), an adenosine receptor agonist, or caffeine NECA together. Rats ran 80 min in the placebo trial, 120 min in the caffeine trial and only 25 min with NECA. When caffeine and NECA were given together, the effects appeared to cancel each other out, and run time was similar to placebo.
When the study was repeated with peripheral intraperitoneal (body cavity) injections instead of brain injections, there was no effect on run performance. The authors concluded that caffeine increased running time by delaying fatigue through CNS effects, in part by blocking adenosine receptors . Caffeine also appears to enhance cognitive performance more in fatigued than well-rested subjects [192–194]. This phenomenon is also apparent in exercise performance  both in the field  and in the lab [60, 63, 149].
The placebo effect
The placebo effect is a beneficial outcome that cannot be attributed to a treatment or intervention but is brought about by the belief that one has received a positive intervention. For example, an individual may ingest a capsule with sugar or flour (a small amount of non-active ingredient) but believes that he/she ingested caffeine and experiences improvements in performance because of this belief . The nocebo effect is directly opposite to this in that a negative outcome occurs following the administration of an intervention or lack of an intervention (e.g. knowingly ingesting a placebo) . For example, the nocebo may be a substance without medical effects, but which worsens the health status of the person taking it by the negative beliefs and expectations of the patient. Similarly, the nocebo may be a ‘caffeine placebo’, where an individual’s performance is worse based on the belief that they did not ingest caffeine.
Several studies have provided evidence for placebo effects associated with caffeine ingestion [199–201] or other “beneficial” interventions  during exercise. An example of this was reported in a study  where well-trained cyclists exhibited a linear dose–response relationship in experimental trials from baseline to a moderate (4.5 mg/kg) and high dose (9 mg/kg) of caffeine respectively. Athletes improved as the perceived caffeine doses increased; however, a placebo was used in all interventions. Similarly, Saunders et al.  found that correct identification of caffeine appears to improve cycling performance to a greater extent than the overall effect of caffeine, where participants who correctly identified placebo showed possible harmful effects on performance. Therefore, readers are encouraged to consider whether studies that have explored the effects of caffeine on exercise have examined and reported the efficacy of the blinding of the participants.
Caffeine and endurance exercise
Less than a 1% change in average speed is enough to affect medal rankings in intense Olympic endurance events lasting ~ 45 s to 8 min . In other events, such as the men’s individual road race, the difference between the top three medalists was < 0.01% . At the highest level of sports, competitors will be near their genetic potential, will have trained intensively, followed prudent recovery protocols, and will have exploited all strategies to improve their performance—the use of an ergogenic aid, when legal, safe and effective, is an alluring opportunity.
Caffeine has consistently been shown to improve endurance by 2–4% across dozens of studies using doses of 3–6 mg/kg body mass [13, 195, 205–207]. Accordingly, caffeine is one of the most prominent ergogenic aids and is used by athletes and active individuals in a wide variety of sports and activities involving aerobic endurance. Caffeine has been shown to benefit several endurance-type sports including cycling [60, 206, 208], running [91, 209, 210] cross-country skiing  and swimming .
Much of the caffeine-exercise body of literature has focused on endurance-type exercise, as this is the area in which caffeine supplementation appears to be more commonly used and likely beneficial in most, but not all, athletes [11–13]. For example, the caffeine concentration in over twenty thousand urine samples obtained for doping control from 2004 to 2008 was measured after official national and international competitions [110, 115]. The investigations concluded that roughly 74% of elite athletes used caffeine as an ergogenic aid prior to or during a sporting event, where endurance sports are the disciplines showing the highest urine caffeine excretion (and therefore prevalence) after competition [110, 115].
A recent meta-analysis reporting on 56 endurance time trials in athletes (79% cycling), found the percent difference between the caffeine and placebo group ranged from − 3.0 to 15.9% . This wide range in performance outcomes highlights the substantial inter-individual variability in the magnitude of caffeine’s effects as reported. These inter-individual differences might be due to the methodological differences between the studies, habitual caffeine intake of the participants, and/or partly due to variation in genes that are associated with caffeine metabolism and caffeine response .
A recent systematic review was carried out on randomised placebo-controlled studies investigating the effects of caffeine on endurance performance and a meta-analysis was conducted to determine the ergogenic effect of caffeine on endurance time-trial performance . Forty-six studies met the inclusion criteria and were included in the meta-analysis. This meta-analysis found that caffeine has a small but significant effect on endurance performance when taken in moderate doses (3–6 mg/kg) as well as an overall improvement following caffeine compared to placebo in mean power output of 2.9 ± 2.2% and a small effect size of 0.22 ± 0.15. Time-trial completion time showed improvements of 2.3 ± 2.6% with a small effect size of 0.28 ± 0.12. However, there was some variability in outcomes with responses to caffeine ingestion, with two studies reporting slower time-trial performance, and five studies reporting lower mean power output during the time–trial .
In summary, caffeine has been consistently shown to be effective as an ergogenic aid when taken in moderate doses (3–6 mg/kg), during endurance-type exercise and sport. Dozens of endurance studies are highlighted through this review is various sections, showing consistent yet wide-ranging magnitudes of benefit for endurance performance under caffeine conditions.
Caffeine and muscular endurance, strength and power
Strength and power development through resistance exercise is a significant component of conditioning programs for both fitness and competitive sport. The most frequently consumed dose of caffeine in studies using strength tasks with trained or untrained individuals usually ranges from 3 to 6 mg/kg body mass (with 2 mg to 11 mg representing the entire range), ingested in the form of pills or capsules 30 to 90 min before exercise.
In resistance exercise, strength is most commonly assessed using 1 repetition maximum (1RM) , or different isometric and isokinetic strength tests . Muscular endurance assesses the muscle’s ability to resist fatigue and is an important quality in many athletic endeavors (e.g., swimming, rowing). Muscular endurance may be tested with repetitions of squats, maximal push-ups, bench press exercises (load corresponding to 60–70% of 1RM) to momentary muscular failure, or by isometric exercises such as the plank or static squat [216, 217].
Although several studies exploring the effects of caffeine on strength performance have been published since the 2010 ISSN caffeine position stand , some uncertainty surrounding the benefits of caffeine in activities involving muscular endurance, strength and power remains.
Caffeine was shown to be ergogenic for muscular endurance in two meta-analyses reporting effect sizes ranging from 0.28 to 0.38 (percent change range: 6 to 7%) [158, 218]. However, others have shown that it enhances strength but not muscular endurance [219, 220], and when studies have examined multiple strength-muscular endurance tasks, there were benefits across the board [67, 221], none at all [98, 222], or even impairments in muscular endurance with caffeine use [222, 223]. Ingesting caffeine prior to a muscular endurance task is likely to delay muscular fatigue, but these effects are not consistent among all studies.
Three meta-analyses explored the acute effects of caffeine on strength, and all reported ergogenic effects [158, 224, 225]. However, the effects in these meta-analyses were small, ranging from 0.16 to 0.20 (percent change: 2 to 7%). Such small improvements in muscular strength likely have the greatest practical meaningfulness for athletes competing in strength-based sports, such as powerlifting and weightlifting (athletes which already seem to be among the highest users of caffeine ).
Power output is often measured during a single-bout sprinting task using the Wingate test, which generally consists of ‘all-out’ cycling for 30 s performed at specific external loads (e.g., 7.5% of body mass). Power output is also assessed during different protocols of intermittent-sprinting and repeated-sprints often with the Wingate cycling test as well as assessments during running  or swimming repeated sprints .
The data for repeated sprint and power performance using Wingate data has been mixed. In an older study, 10 male team-sport athletes performed 18, 4-s sprints with 2-min active recovery . Here, caffeine ingestion (6 mg/kg) enhanced mean power output and sprint work by 7 and 8.5%, respectively . A more recent study examining the effects of acute caffeine ingestion on upper and lower body Wingate performance in 22 males did not report significant findings when measuring lower body mean and peak power using the Wingate test .
An older study by Greer et al.  also failed to report caffeine benefits on power output during a 30-s high-intensity cycling bout using the Wingate test. One meta-analysis reported that caffeine ingestion enhances mean and peak power during the Wingate test , although the effect sizes of 0.18 (+ 3%) and 0.27 (+ 4%), respectively are modest.
In contrast, another meta-analysis that examined the effects of caffeine on muscle power as assessed with the Wingate test for three of the studies, and repeated sprints for a maximum of 10-s for the fourth, did not report benefits from ingestion of caffeine . An average caffeine dose of 6.5 mg/kg of body mass was used across the four studies with no improvements in muscle power under caffeine conditions (effect size = 0.17, p = 0.36) compared to placebo trials, although the data collected spanned only 5 years .
A study by Lee et al.  reported that caffeine ingestion enhanced sprint performance involving a 90-s rest interval (i.e., intermittent-sprinting) but did not benefit repeated-sprints with a 20-s rest interval. This might suggest that the rest interval between sprints may modulate the ergogenic effects of caffeine. Indeed, a recent meta-analysis that focused on the effects of caffeine on repeated-sprint performance reported that total work, best sprint, and last sprint performance was not affected by caffeine ingestion .
Several studies have also shown substantial variability in outcomes. For example, one study  found that only 13 of 20 cyclists improved their performance with ~ 3–4 mg/kg of caffeine, while the remaining participants either worsened or did not alter their performance. Similarly, Woolf et al.  found that 5 mg/kg of caffeine improved overall peak power performance on the Wingate Test in 18 elite or professional athletes. However, 4 (28%) of the participants did not improve their performance with caffeine.
Average power, minimum power, and power drop were not significantly different between treatments, but 72% of the participants obtained a greater peak power during the caffeine trial than during the placebo trial. There was also no overall improvement in average power or fatigue index, despite 13 (72%), and 9 (50%) of the participants, respectively, improving their performance. In summary, caffeine ingestion may be beneficial to enhance single and intermittent-sprint performance, while caffeine’s effects on repeated-sprint performance are inconsistent and require further research to draw stronger conclusions on the topic.
Ballistic movements (such as throws and jumps) are characterized by high motor unit firing rates, brief contraction times, and high rates of force development . Many studies have explored the effects of caffeine on jumping performance [225, 235]. The body of evidence has indicated that caffeine supplementation increases vertical jump height during single and repeated jumps; however, the magnitude of these effects is rather modest, with effect sizes ranging from 0.17 to 0.22 (2 to 4%) [225, 235].
Besides jumping, several studies have explored the effects of caffeine on throwing performance. These studies reported that: (a) caffeine ingestion enhanced maximal shot put throwing distance in a group of 9 nine inter-collegiate track and field athletes ; and (b) caffeine ingestion at a dose of 6 mg/kg of body mass administered 60 min pre-exercise increased maximal medicine ball throwing distance . Overall, the current body of evidence indicates that caffeine supplementation may be useful for acute improvements in ballistic exercise performance in the form of jumps and throws. However, more research is needed to explore the effects of caffeine on different throwing exercise tests, as this has been investigated only in a few studies.
Generally, the primary sports-related goal of strength and power-oriented resistance training programs is to move the force-velocity curve to the right, indicating an ability of the athlete to lift greater loads at higher velocities . Several studies have explored the effects of caffeine on movement velocity and power in resistance exercise using measurement tools such as linear position transducers .
These studies generally report that caffeine ingestion provides ergogenic effects of moderate to large magnitudes, with similar effects noted for both mean and peak velocity, and in upper and lower-body exercises [67, 221, 239]. Even though this area merits further research to fill gaps in the literature, the initial evidence supports caffeine as an effective ergogenic aid for enhancing velocity and power in resistance exercise.
reference link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7777221/
More information: Mauricio Ramírez-Maldonado et al, Caffeine increases maximal fat oxidation during a graded exercise test: is there a diurnal variation?, Journal of the International Society of Sports Nutrition (2021). DOI: 10.1186/s12970-020-00400-6