In recent years, several studies have reported that rinsing the mouth with a carbohydrate (CHO) solution, without ingesting it, can improve exercise performance in endurance events lasting 1 h or less (5,6,15,20,22,29,31). Although not all studies have found such an ergogenic effect (2,37), their negative findings have been attributed to the preexercise nutritional status of the participants (2) or a lack of sensitivity of the methodology used to measure performance (37). With respect to the effect of CHO mouth rinsing on other aspects of exercise performance, some studies have found no effectof CHO mouth rinsing on sprint performance (7) or maximal strength (27). Others have provided evidence that CHO mouth rinsing does improve sprint performance and muscle force production (1,17). Indeed, Gant et al. (17) found that the presence of CHO in the mouth increased maximal voluntary force in the elbow flexors, and Beaven et al. (1) showed that a single 5-s glucose mouth rinse improved mean power output in the initial sprint of a series of 5 × 6-s sprints compared with a noncaloric placebo.
The ergogenic effect of CHO mouth rinsing has been explained by the presence of receptors in the oral cavity, which when stimulated by the presence of CHO send signals that activate reward or pleasure centers in the brain, thereby improving exercise performance by reducing the perception of effort of the exercise (5). This notion is supported by the work of Chambers et al. (6), who showed, using functional magnetic resonance imaging, that CHO mouth rinsing with both glucose and nonsweet maltodextrin resulted in the activation of brain areas generally associated with reward, including the anterior cingulate cortex and striatum. It is important to note that this ergogenic effect of CHO mouth rinsing seems to depend on the caloric content of CHO in the rinse solution rather than the perception of sweetness per se. Indeed, several studies have shown that the administration of nonsweet CHO [maltodextrin (5,6,15)] provides some ergogenic benefits, whereas noncaloric artificial sweeteners have no effect on performance (6).
The evidence that the stimulation of CHO receptors in the oral cavity has the capacity to improve both endurance and sprint exercise performance raises the obvious question of whether stimulation of other types of taste receptors by other classes of tastants may also affect exercise performance. Of interest, studies based on functional magnetic resonance imaging have shown that the brain areas activated in response to the bitter tastant, quinine, overlap to a great extent with those stimulated by CHO (33,38). Furthermore, quinine has been shown to evoke greater and longer lasting autonomic nervous system (ANS) responses compared with the other five prototypical tastants [sweet, sour, salty, bitter, and umami (30,32)]. This raises the intriguing possibility that a bitter-tasting mouth rinse may also enhance exercise performance.
In view of the recent findings that CHO mouth rinsing significantly improves sprint performance (1), the primary aim of this study was to investigate whether combining mouth rinsing with the ingestion of a bitter-tasting solution composed of quinine acutely improves mean and peak power during a 30-s maximal cycling sprint effort. Mouth rinsing and ingestion were combined to ensure the activation of bitter taste receptors throughout the oral cavity, including those at the back of the tongue. Because it is unclear how concentrated the quinine solution should be, it was also the purpose of this study to identify the quinine concentra tion resulting in both maximal bitterness perception and ANS activation, without causing side effects such as nausea, and to adopt this quinine concentration to test its effect on sprint performance.
Preliminary Study: Dose–Response Relationship between Quinine Concentration and Bitter Taste Perception and ANS Responses
Because no previous research has examined the effect of quinine ingestion on exercise performance, the concentration of quinine to be used in this study was determined in a preliminary study aimed at identifying the quinine concentration that results in the strongest taste and ANS responses [skin conductance (SC) and instantaneous heart rate (IHR)] without causing any feelings of nausea.
Eighteen healthy male volunteers provided written consent to participate in this study (mean ± SD; age = 26 ± 3 yr, body mass index = 24 ± 3 kg·m−2). All were nonsmokers, did not report any gustatory or olfactory disorders, and were not taking any medication or experiencing illnesses that might alter their sense of taste or smell. Ethical clearance was obtained from the Human Research Ethics Committee of The University of Western Australia.
Participants attended the laboratory for two sessions, each conducted at the same time of day. First, participants completed a 6-n-propylthiouracil (PROP)-tasting session to assess the sensitivity of the participants to the bitter chemical PROP. This is because marked interindividual variations have been reported in bitter-tasting sensitivity, with the ability to taste the bitter chemical PROP generally adopted to compare individuals (34). The next session examined the relationship between the concentration of quinine and bitter taste intensity, ANS responses, and nausea level. Participants were instructed to avoid eating or drinking anything other than water for 1 h before each testing session.
Upon arrival at the laboratory, participants had electrodes placed at various locations on their hand and chest to allow for the continuous measurement of SC and IHR, respectively (as detailed later). Participants then put on headphones (Monster Beats Solo; Beats Electronics, Santa Monica, CA, USA) through which brown noise was played at a standardized volume (Simplynoise.com) to minimize external auditory distractions that could interfere with baseline ANS signals. Participants were instructed to sit comfortably for 15 min to adapt to the experimental conditions before commencing the session.
Assessment of PROP-Tasting Status
The PROP-tasting status of each participant was assessed by measuring the perceived intensity of PROP compared with a reference salt solution using the three-solution test described by Tepper et al. (34). Participants were categorized as PROP nontasters, medium tasters, or supertasters.
Assessment of the Dose–Response Relationships between Quinine Intake and Both Taste and ANS Responses
To determine the dose–response relationships between quinine intake and both taste and ANS responses, each participant was required to rinse his mouth with and then ingest 25 mL of six solutions of increasing concentrations of quinine hydrochloride (Sigma-Aldrich, St. Louis, MO) and six solutions of a single NaCl concentration (Sigma-Aldrich). All solutions were prepared with doubly deionized water (Direct-Q 5 Ultrapure Water System, Millipore, MA). The concentrations of quinine were 0, 0.5, 1, 2, 3, and 4 mM. NaCl was presented in a standardized concentration of 0.1 M to serve as a dishabituator (14). Quinine was selected as the bitter tastant in this study because it is safe for human consumption [commonly found as the bittering agent in tonic water (13)] and is often used as a bitter tastant in tasting studies (21).
On the day of testing, all solutions were kept at room temperature (24°C) and placed on a table in front of the participant in identical plastic cups. At the onset of the test, participants first tasted one of the NaCl solutions then alternated quinine and NaCl solutions. Quinine solutions were presented in order of ascending concentration because the expected nausea associated with ingesting the highest concentration of quinine would have the potential to invalidate the assessment of subsequent solutions. Each solution was rinsed in the mouth for 10 s before being ingested. Immediately after quinine ingestion, participants gave subjective ratings of taste intensity and hedonic value using a general labeled magnitude scale (glMS) (19) with adjectives altered to specify either intensity or unpleasantness. Participants also gave ratings of nausea using a 100-mm visual analog scale bounded by the descriptors “no nausea” and “severe nausea.” In addition, ANS responses were recorded continuously during each session (as detailed in the next section). The administration of each consecutive solution (either quinine or NaCl) took place once SC and HR returned to baseline levels and were no longer fluctuating (approximately 2–3 min). In the rest period between solutions, participants rinsed their mouth with water ad libitum. Preliminary work was performed to ensure that the rest period between consecutive successive quinine exposures at a given concentration did not result in any significant differences in taste perception.
ANS responses to quinine were assessed indirectly by measuring SC and IHR. SC (μS) was measured using bipolar finger electrodes (MLT116F GSR; AD Instruments, Sydney, Australia) placed on the second phalanx of the index and third digit on the nondominant hand. The amplitude of each response was measured as well as the ohmic perturbation duration (OPD) index, which has been shown to reflect the emotional load of the stimulus (36).
IHR (bpm) was recorded from three silver electrodes placed in a precordial position. The electrode sites were first shaved, lightly abraded, and cleaned with alcohol wipes before placement of electrodes. The D2 derivation signal (interval between consecutive R waves) was processed and delivered in the form of instantaneous HR frequency. The IHR response was measured as the difference between the prestimulus level value and the maximum increase induced by the stimulus.
The SC electrodes were used with a galvanic skin response amplifier (FE116 GSR Amp; AD Instruments) interfaced with a PowerLab data acquisition system (PowerLab 2/20; AD Instruments). SC and IHR signals were amplified, filtered, and recorded throughout the sessions with a sampling frequency of 10 Hz using the PowerLab system and analyzed with LabChart 7 software (AD Instruments).
Data and Statistical Analysis
Psychophysical curves were graphed for mean ANS (SC, IHR, and OPD) and subjective (intensity, hedonic value, and nausea) responses across the range of solution concentrations. A one-way repeated-measures ANOVA was used to compare the responses between quinine concentrations followed by Fisher’s LSD post hoc tests, with differences accepted at P < 0.05 (Statistical Package for the Social Sciences for Windows, Version 17.0; SPSS Inc., Chicago, IL). Participants were then divided into groups based on their PROP-tasting status, with the ANS and subjective responses compared using a two-way mixed-model ANOVA with Fisher’s LSD post hoc tests. All values, unless otherwise stated, are expressed as mean ± SEM.
Main Study: Effect of Quinine Administration on Sprint Performance
Fourteen trained male cyclists (mean ± SD; age = 30.1 ± 5.4 yr, height = 1.84 ± 0.09 m, mass = 77.0 ± 11.7 kg, V˙O2peak = 61.9 ± 7.7 mL·kg−1·min−1; PROP-tasting status = 3 nontasters, 5 medium tasters, and 6 supertasters) were recruited for this study from cycling and triathlon clubs. Participants were fully informed of the testing procedures before their written consent was obtained. However, to minimize the possibility of a placebo effect, they were deceived about the true aims of the study and were instead informed that the purpose of the study was to determine the effect of different taste solutions on the metabolic responses to maximal exercise. After completing all trials, participants were personally debriefed as to the true aim of the study. The procedures were approved by the Human Research Ethics Committee of The University of Western Australia.
Each participant visited the laboratory on five separate occasions, each separated by 7 d and conducted at the same time of day for each participant. The initial visit involved the assessment of PROP-tasting status and V˙O2peak before familiarization with both the mouth rinsing procedure and the sprint protocol to be used in the subsequent experimental trials.
For the following four experimental trials, participants completed a 30-s maximal cycling sprint immediately after rinsing their mouth and ingesting a bitter quinine solution (QUI), plain water (WAT), a sweet aspartame solution (ASP), or a no-rinse control (CON) administered in a randomized counterbalanced order. The WAT and the ASP conditions served as placebos because neither water nor aspartame mouth rinsing is beneficial for maximal cycling sprint performance (7) or endurance exercise (6).
Before investigating the effect of quinine on sprint performance, individual differences in PROP taste perception were determined for each participant (methods as previously described). After the PROP-tasting test, participants completed a V˙O2peak test on an air-braked cycle ergometer (Evolution Pty. Ltd., Adelaide, Australia) using the protocol and equipment described in Gam et al., (16). After the V˙O2peak test, participants were given plain water to rinse and then ingest, after which they completed the sprint protocol to be used in the subsequent experimental trials to become accustomed to the experimental procedures. Before leaving the laboratory, participants were given a food and physical activity diary and were asked to record all food and drink intake and physical activity in the 24 h before each experimental trial. A copy of the diary from the first trial was returned to each participant, and they were asked to replicate the same diet and activity pattern in the 24 h before each trial (19). Compliance was confirmed upon arrival to the laboratory for each experimental trial by inspection of food diaries from the previous 24 h. Participants were also instructed to fast overnight before each trial and to avoid strenuous exercise, alcohol, and caffeine in the 24 h preceding each trial.
On arriving at the laboratory in the morning, participants had their body mass measured and were fitted with an HR monitor (Garmin Ltd., Olathe, Kansas). They then performed a 4-min light cycling warm-up at 40% of V˙O2peak, followed by a 2- to 3-s practice sprint start (Exertech EX-10 front access cycle ergometer; Repco Cycle Company, Huntingdale, Victoria). Seat height was standardized for each participant. After a 10-min rest, participants were given either 0.36 mL·kg−1 body mass of a 2-mM quinine HCl solution (QUI; Sigma-Aldrich), plain water (WAT), or a 0.05% w/v aspartame solution (ASP; Sigma-Aldrich) or were not given any mouth rinse at all (CON). A volume of 0.36 mL·kg−1 was chosen to account for differences in body size, with each participant receiving approximately 25–35 mL of solution per session. Participants were instructed to rinse their mouth for 10 s and then ingest the solution. The solution was ingested after rinsing to ensure that bitter receptors at the back of the tongue were activated because there is evidence that the strongest sensation of bitterness occurs in that area of the oral cavity (35).
Immediately after ingesting the solution, participants performed a 30-s maximal sprint effort, initiated in a standing position with the preferred foot starting at the 2 o’clock position. Exercise testing was performed immediately after ingesting the testing solution in order for our findings not to be confounded by any effect that the gastrointestinal absorption of the solution may have on exercise performance. The cycle ergometer was interfaced with a customized program (Cyclemax, School of Sport Science, Exercise and Health, The University of Western Australia) to allow for the measurement of mean power output for 0–30 s (Pmean), peak power output (Ppeak), and mean power output for 0–10 s (P0–10), 10–20 s (P10–20), and 20–30 s (P20–30) of the sprint. Fatigue index, which is the rate of power decline during the test, was also calculated as described by Coppin et al. (11). Participants were instructed to cycle in an all-out manner for 30 s without pacing themselves.
Before the commencement of the mouth rinse protocol and at 0 and 7 min postsprint, HR was recorded, and each participant provided subjective RPE (3) and nausea ratings. Nausea ratings were made using a 100-mm visual analog scale anchored with the descriptors “no nausea” and “extreme nausea” (26). Immediately after each rating of nausea levels were taken, a capillary blood sample (125 μL) was obtained from the fingertip (Clinitubes, Radiometer, Copenhagen) and analyzed immediately for blood lactate and glucose levels using a blood gas analyzer (ABL™ 725; Radiometer, Copenhagen, Denmark).
The effects of mouth rinse treatment on each performance variable were compared using two-way repeated-measures ANOVA followed by Fisher’s LSD post hoc tests, with differences accepted at P < 0.05 (Statistical Package for the Social Sciences for Windows, Version 17.0; SPSS Inc.). Cohen’s effect size (ES) statistics was also used to highlight any trends. A Pearson product–moment correlation was used to evaluate whether PROP-tasting ability (measured by summing the gLMS scores for the three PROP solutions for each participant) was related to improvement in sprint performance. All values, unless otherwise stated, are expressed as mean ± SEM.
Preliminary Study: Dose–Response Relationship between Quinine Concentration and Bitter Taste Intensity and ANS Responses
As the concentration of quinine increased, there were significant increases in the perception of taste intensity and hedonic value (P < 0.05; Fig. 1). Nausea ratings were not affected by quinine concentrations <4 mM but were higher at 4 mM compared with all other concentrations (P = 0.048; Fig. 1).
As the concentration of quinine increased, there were significant increases in the responses of SC, OPD, and IHR (P < 0.05; Fig. 2).
Effect of PROP-tasting status on the dose–response relationship between quinine concentration and bitter taste intensity and ANS responses.
Of the 18 participants, 5 were nontasters, 5 were medium tasters, and 8 were supertasters. When participants were grouped into nontasters, medium tasters, and supertasters, there were no significant differences between groups for any of the ANS variables examined here or for the subjective ratings of taste intensity and hedonic value (P > 0.05). However, PROP supertasters did differ from medium and nontasters in that they experienced significant nausea in response to the ingestion of a 4-mM quinine solution, whereas average nausea level was not affected by this concentration of quinine in both medium tasters and nontasters. This indicates that, except nausea level, sensitivity to PROP is not related to the ANS and perceptual responses to quinine. This is in agreement with other studies (12,21) who have found no correlation between PROP sensitivity and sensitivity to other bitter compounds, including quinine. On the basis of these findings and to ensure that no participant experienced nausea in response to quinine ingestion, a quinine concentration of 2 mM was adopted for testing the effect of quinine on sprint performance, despite being associated with submaximal taste and ANS responses compared with higher concentrations.
Main Study: Effect of Quinine Administration on Sprint Performance
Nutritional intake and environmental conditions.
There was no significant difference in either total energy intake (CON 10,464 ± 201; QUI 10,573 ± 234; WAT 10,556 ± 230; ASP 10,431 ± 231 kJ; P = 0.470) or CHO intake (CON 326 ± 24; QUI 325 ± 20; WAT 318 ± 21; ASP 334 ± 21 g; P = 0.500) for the 24 h before each experimental trial. Laboratory temperature and relative humidity were similar between trials (P > 0.05).
Mean and peak power.
There was a significant main effect of treatment on mean power output for the 30-s sprint (P = 0.007). Post hoc analysis revealed that mean power was higher in QUI compared with CON (P = 0.021), WAT (P < 0.001), and ASP (P = 0.018) (Table 1). These differences were supported by large ES (Table 1). There were no significant differences in mean power output between CON, WAT, and ASP conditions (P > 0.05).
The main effect of treatment on peak power approached significance (P = 0.052). Peak power was significantly higher in QUI compared with CON (P = 0.021, ES = 0.84) and WAT (P = 0.013, ES = 0.79) but did not differ significantly from ASP (P = 0.114, ES = 0.47) (Table 1). There were no significant differences in peak power between CON, WAT, and ASP (P > 0.05).
Mean power between 0–10, 10–20, and 20–30 s, fatigue index.
P0–10 was significantly higher in QUI compared with WAT (P = 0.01, ES = 0.84) but was not significantly different from CON (P = 0.08, ES = 0.52) or ASP (P = 0.19, ES = 0.48) (Table 1). P10–20 was significantly higher in QUI compared with CON (P = 0.02, ES = 0.73), WAT (P = 0.005, ES = 0.94), and ASP (P = 0.026, ES = 0.69) (Table 1). P20–30 was not significantly different between QUI, CON (P = 0.138, ES = 0.43), and WAT (P = 0.138, ES = 0.44) but approached significance in QUI compared with ASP (P = 0.059, ES = 0.67) (Table 1). There were no significant differences in P0–10, P10–20, or P20–30 between CON, WAT, and ASP conditions (P > 0.05). There were no effects of treatment on fatigue index (P = 0.646) between experimental conditions.
PROP-tasting and sprint performance.
Of the 14 participants, 3 were nontasters, 5 were medium tasters, and 6 were supertasters. No correlation was found between sensitivity to PROP and any of the improvements in mean power (r2 = 0.046, P = 0.877), peak power (r2 = 0.088, P = 0.765), P0–10 (r2 = 0.071, P = 0.810), P10–20 (r2 = 0.051, P = 0.862), or P20–30 (r2 = 0.069, P = 0.814). Furthermore, all participants were able to taste the QUI and the ASP solutions and described them with the appropriate descriptor (e.g., bitter, sweet).
HR and subjective ratings.
Within each trial, both HR and RPE increased significantly in response to the 30-s sprint (P < 0.05), before decreasing during the 7-min postsprint period. HR and RPE were similar at all time points between the four experimental treatments (P > 0.05; Fig. 3). Likewise, nausea ratings were similar between trials at all time points (P > 0.05; Fig. 3).
The blood lactate responses to the 30-s sprint were similar between trials (P > 0.05; Fig. 3), although this variable did change significantly within trials in response to exercise (P < 0.05; Fig. 3). There were also no differences in blood glucose concentration between trials (P > 0.05; Fig. 3).
There is evidence that CHO mouth rinsing improves endurance exercise performance as well as muscle force production and maximal sprint performance (1,5,6,15,17,20,22,29,31) via the stimulation of CHO taste bud receptors in the oral cavity. This raises the issue of whether the oral administration of non-CHO tastants may also affect exercise performance. This study shows for the first time that mouth rinsing with a bitter-tasting quinine solution followed by its ingestion immediately before a maximal 30-s cycling sprint can improve performance. A significant 2.4%–3.9% improvement in mean power output was observed with the administration of quinine compared with an aspartame solution, a water solution, and a no-rinse control condition. Peak power output was also significantly higher (3.5%–3.7%) with quinine compared with water and no-rinse conditions. There were no differences in any of the performance measures between aspartame, water, and no-rinse conditions, and there was no relationship between PROP-tasting status and the magnitude of the quinine-mediated improvement in performance.
Because the bitter taste of the quinine solution could not be masked, several precautions were taken to ensure that any ergogenic effect of quinine on sprint performance was not the result of a placebo effect. First, participants were deceived about the true purpose of the study. They were told that the aim of this study was to examine the effect of different solutions on the responses of several blood variables (i.e., blood glucose and blood lactate) to a maximal sprint. To further minimize the possibility of a placebo effect, two placebo treatments were administered, namely, a plain water solution and a sweet aspartame solution, both known not to enhance performance (6,7). Given the absence of significant differences in any of the performance or subjective measurements between water, aspartame, and no-rinse conditions, it is unlikely that a placebo effect occurred in response to quinine intake.
Consistent with the fact that this study followed a counterbalanced experimental design, there was no order effect of trial administration for any of the performance variables measured (P > 0.05), indicating that the familiarization trial was sufficient to negate any learning effects. In addition, the coefficient of variation between the familiarization sprint (which included a water rinse) and the water rinse experimental sprint was 2.13% and 2.20% for mean and peak power output, respectively, suggesting limited variability with the competitive cyclists and the performance test used in this study. The relative improvements in performance observed using quinine compared with the control conditions (3.9%) is high enough to be important for competitive athletes because Paton and Hopkins (28) have asserted that the smallest worthwhile enhancement in power output for competitive track cyclists in events lasting <60 s is approximately 0.5%–1%. Whether the performance in other sprint events lasting less than 30 s (e.g., 100 and 200 m track sprint) would also benefit from quinine administration remains to be determined.
The mechanisms underlying the ergogenic benefits of quinine administration on sprint performance remain to be elucidated. One possibility is that quinine improves sprinting performance in a way similar to that proposed for CHO mouth rinsing by altering the perception of effort, motivation, and/or arousal level of the participants during exercise, allowing them to exercise at a higher intensity (5,29). Evidence that this may be the case here is the observation that RPE did not differ between quinine and other conditions despite the higher mean and peak power in the quinine trial. Because glucose ingestion has been reported to facilitate corticomotor output to both fresh and fatigued muscles (17), quinine administration may also have this effect. The aforementioned proposed mechanisms are consistent with the findings that there is marked overlap between the brain regions (e.g., anterior cingulate cortex, nucleus accumbens) stimulated by CHO and quinine (33,38).
The unpleasantness associated with the strong bitter taste of quinine may also have played a role in its ergogenic effect. Exposure to unpleasant visual stimuli has been found to result in improved reaction times and increased muscle force production in an isometric wrist extension task (9,10) as well as increased corticomotor excitability (8,10) compared with viewing neutral and pleasant stimuli. Negative taste stimuli may act in a similar way, thus providing support for the “negative brain theory” (4) that the pattern of brain activation in response to a negative or unpleasant stimulus favors urgent processing and action (23). Whether the unpleasantness of the strong bitter taste of quinine contributes to its ergogenic effect on sprint performance remains to be determined.
It is important to note that although quinine was chosen as the bitter tastant in this study, thousands of structurally diverse compounds elicit bitter taste. Moreover, there are more than 25 mammalian bitter taste receptors [known as T2Rs (24)], and each responds to several different bitter compounds. Some of these receptors are very broadly tuned, recognizing bitter compounds with diverse structural elements, whereas others only recognize tastants with specific structures (25). Therefore, it is possible that different bitter tastants may or may not affect exercise performance in the same manner as quinine. In addition, the localization of the T2Rs along the upper gastrointestinal tract is another factor that may mediate the effect of bitter tastants on exercise performance. Although T2Rs are found in taste buds in all regions of the oral cavity, there is evidence that bitterness is sensed most strongly in the circumvallate papillae where the taste buds are located in a V-shaped line at the back of the tongue and are innervated by the glossopharyngeal nerve (35). Because bitter taste is typically associated with substances that are potentially toxic or harmful, the T2Rs in the circumvallate papillae may serve as the last line of defense against the ingestion of these substances (24), thus explaining the strongest sensation of bitterness. It is for this reason that the 10-s mouth rinse was combined with ingestion in this study to maximally activate as many bitter receptors in the oral cavity as possible, including those at the back of the tongue. It is unclear, however, whether mouth rinsing alone or ingestion alone without prolonged mouth rinsing with quinine would be sufficient to produce an ergogenic effect comparable to that attained here with combining mouth rinsing and ingestion of quinine.
Other factors likely to impact the effect of quinine on sprinting performance include the concentration and timing of quinine administration. A concentration of 2 mM was used in the current study because we showed that at this level quinine did not cause any nausea, irrespective of one’s PROP-tasting status. Given that stronger ANS responses were observed in response to higher quinine concentrations and that not all participants experienced nausea under these conditions, it is possible that ingesting quinine at more than 2 mM may further improve sprint performance in some individuals. The time elapsed between quinine administration and sprint performance is another factor that may affect the benefits of quinine. This notion is supported by the observation that the ANS responses to quinine last for no more than 80–120 s (30,32), thus suggesting that for quinine to be beneficial, exercise should be performed immediately after quinine intake.
In conclusion, this study shows for the first time that mouth rinsing and ingestion of a quinine solution immediately before a maximal 30-s sprint can improve mean and peak power output. These findings are likely to be meaningful for sprinters or power athletes involved in short duration events. The mechanisms underlying the effect of quinine remain to be elucidated, as well as the effect of quinine (or other bitter tastants) mouth rinsing and ingestion on different modes of exercise, including endurance and resistance exercise.
The authors would like to thank all the participants for their time and effort. No funding was received for this study.
There are no conflicts of interest for any of the authors.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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