Compared with other stimulant drugs that have been investigated for their potential to enhance performance, pseudoephedrine (PSE) has received relatively little attention from the scientific community. Nonetheless, in the pursuit of performance improvement, some athletes continue to use PSE despite its recent reintroduction to the World Anti-Doping Agency (WADA) prohibited substance list and its contradictory performance responses (22).
Of those studies (5,6,9,10,12–15,21,25) that have examined the influence of preexercise PSE intake on exercise performance, it appears that only doses equal to or higher than 180 mg have the potential to improve performance (12,15,21). However, even in response to PSE doses in excess of 180 mg, the findings have been inconsistent. One factor potentially responsible for these inconsistencies may be preexercise feeding. Food consumed in conjunction with PSE is likely to influence its absorption, slowing PSE uptake into the body and resulting in lower peak plasma concentrations, perhaps also extending its duration of action (28).
Preexercise feeding could partially explain differences in findings between research groups as only four studies (5,6,15,21) have included a preexercise meal in their exercise trials whereas six have not (9,10,12–14,25). Ingesting food before exercise is standard practice for most athletes, and the potential for a supplement to influence performance should arguably be examined after a preexercise meal. In general, the time to peak plasma PSE concentrations after PSE intake has been reported to be 30–60 min and its duration of action 4–6 h (27). However, Gillies et al. (13) showed that under fasted conditions, the time to peak plasma PSE concentration was approximately 120 min during exercise after the ingestion of a therapeutic dose (120 mg) of PSE. Similarly, Skinner (23) has shown delays in the time to peak concentration and also reduced serum caffeine concentrations during exercise after the ingestion of 6 and 9 mg·kg−1 body mass (BM) of caffeine when coingested with a high-CHO meal. This is in agreement with the recent findings of Carr et al. (8), who reported a delay in time to peak alkalosis and blood bicarbonate concentrations compared with other studies after the ingestion of 0.3 mg·kg−1 BM of sodium bicarbonate with food and fluid. Of the four PSE studies that used a preexercise meal, two (15,21) have shown an improvement in exercise performance whereas only one study (12) in the nonfed trials has shown a performance effect.
The significance of postexercise urinary PSE concentrations has increased recently because of the reintroduction of PSE to the 2010 WADA prohibited substance list (29) for use in competition. Recent research (3,4) has indicated that athletes are likely to consume PSE for performance enhancement regardless of its legal status. Thevis et al. (26) recently investigated the prevalence of adverse analytical findings (AAF) of PSE from doping control measures before and after lifting the ban on its use in 2004. The results show a substantial increase in the number of AAF identified from the period 1996–2003 (0.06%) compared with the period 2007–2008 (0.62%), when PSE use was “decontrolled” (26).
Currently, doping control measures involve the collection and analysis of postexercise urine samples for the determination of PSE concentration. At present, urinary PSE concentrations in excess of the current WADA threshold of 150 μg·mL−1 are considered to be an AAF, therefore constituting a positive test. However, given the results of the urinary excretion studies of Strano-Rossi et al. (24) and Gillies et al. (13), the justification for a single cutoff value for an AAF is debatable. Strano-Rossi et al. (24) reported high interindividual variability in urinary PSE concentrations among participants, which were not dependent on sex, weight, or absolute dose ingested after the ingestion of various doses of PSE (24). Some participants consistently recorded values above the previous WADA threshold of 25 μg·mL−1 after single and multiple therapeutic doses of PSE (60 and 120 mg), and also with higher doses of 180 mg in both single and multiple administrations over an extended period (every 7 d for 5 wk) (24). Similarly, Gillies et al. (13) showed that the ingestion of a therapeutic dose of PSE (120 mg) elicited large increases in urinary concentrations during exercise, with 8 of 10 urine samples containing PSE immediately after exercise and all 10 samples containing PSE 1 h postexercise; the urinary PSE concentrations of 45 ± 14 and 114 ± 27 μg·mL−1 (mean ± SD) were reported immediately after exercise and 1 h postexercise, respectively (13). An additional finding of the study by Gillies et al. (13) was the interindividual variation in urinary and plasma PSE concentrations with exercise and the subsequent differences in urinary excretion rate, which the authors suggest may have been due to differences in urinary pH and renal clearance between subjects (13). Although the results of these studies varied depending on the ingestion protocols, the consistent variation in urinary concentrations among participants suggests inherent differences in the metabolism and excretion rates of PSE between individuals.
Given that preexercise feeding may influence subsequent peak plasma PSE concentrations and the duration of its action, the primary aim of the present investigation was to examine the influence of preexercise food intake on plasma PSE concentrations and subsequent exercise performance. A secondary aim was to consider the influence of preexercise feeding on subsequent urinary PSE concentrations.
Ten trained male endurance cyclists participated in this study. Participants were required to have a V˙O2max of ≥60 mL·kg−1·min−1. Each athlete underwent medical screening involving the completion of a health history questionnaire and provided written informed consent before the commencement of testing. The study was approved by the Medical Research Ethics Committee of The University of Queensland.
Participants completed one maximal oxygen uptake (V˙O2max) test, one familiarization trial, and four performance time trials (TT) over a 6-wk period. One session was completed each week with a minimum of 7 d separating each exercise session. The V˙O2max test was completed first, followed by the familiarization trial. Participants then completed the following four performance trials: 1) preexercise meal + PSE (PSE F), 2) preexercise meal + placebo (PLA F), 3) no preexercise meal + PSE (PSE NF), and 4) no preexercise meal + placebo (PLA NF). Participants ingested either PSE or placebo (PLA) 90 min before the start of exercise, and those in the “fed” condition then consumed the preexercise meal. All exercise was performed on an electronically braked cycle ergometer (Excalibur Sport, Lode, Groningen, the Netherlands).
During the first laboratory session, all participants completed a progressive maximal ergometer test for the determination of V˙O2max. Using procedures that have been described previously (21), expired air during exercise was continuously sampled and analyzed for oxygen (O2) and carbon dioxide (CO2) concentrations (SOV S-3A11 and COV CD-3A; Applied Electrochemistry, Pittsburgh, PA). On their second visit to the laboratory and after a 15-min warm-up, participants undertook their first familiarization TT, in which a set amount of work (7 kJ·kg−1 BM) was completed in the shortest possible time.
Supplementation and dietary controls.
In each of the subsequent four TT, participants consumed either 2.8 mg·kg−1 BM of PSE (Sigma-Aldrich) or a calcium carbonate PLA in an equal number of gelatin capsules 90 min before the start of exercise. Gelatin capsules containing the PLA and PSE were indistinguishable from one another. Participants in the fed trials then consumed a standardized preexercise meal, which provided 1.5 g·kg−1 BM of CHO and consisted of one Powerbar™, 500 mL of Gatorade™, and toast (the number of slices dependent on BM) with jam. The type and the quantity of food consumed in the preexercise meal were recorded and replicated in subsequent fed trials. Each participant was provided with a sample meal plan to help them achieve a minimum intake of 7 g·kg−1 BM of CHO in the 24-h period before each performance trial, which was subsequently replicated. Exercise in the 24-h period before the four TT was restricted to low-intensity light exercise and recorded in a training diary for subsequent replication.
Participants reported to the laboratory between 0500 and 0800 h on the morning of each TT after an overnight fast, and BM was measured. A baseline venous blood sample (6 mL) was then collected for the analysis of plasma PSE and catecholamine concentration. Participants were then randomized into the fed or fasted condition and ingested either PSE (2.8 mg·kg−1 BM) or PLA in random order. Participants in the fed condition consumed the preexercise meal and rested until the start of exercise. At 30, 50, and 70 min postingestion, venous blood (0.5 mL) was sampled for the later analysis of PSE concentration. At 85 min postingestion, venous blood was drawn (6 mL), and the participants completed a brief questionnaire that sought responses to the presence/absence of side effects experienced as a result of supplement ingestion.
At 90 min postingestion, participants began a 15-min standardized warm-up followed by a 5-min rest. They then began the TT in which they were required to complete a set amount of work (7 kJ·kg−1 BM) in the shortest possible time. The reproducibility of this test protocol has been evaluated previously, with a coefficient of variation of 3.4% (18). Participants were notified of their progression at every 10% completed of the target workload, but no further encouragement or feedback relating to their performance was given. The time taken to complete the target workload and each 10% increment was recorded, along with mean power output and heart rate. Upon completion of the TT, the postexercise blood sample was drawn (6 mL). Participants provided three urine samples during each of the four TT. A baseline sample was collected as the first void upon waking and brought to the laboratory; a further two samples were collected pre–warm-up and postexercise. All urine samples were stored at −80°C for the later analysis of PSE concentration.
Venous blood (6 mL) was sampled from an antecubital vein into an ethylenediaminetetraacetic acid tube (BD Vacutainer, Plymouth, UK) at baseline, pre–warm-up, and postexercise and stored at −80°C for the later analysis of plasma PSE and catecholamine concentration (epinephrine [EP] and norepinephrine [NE]). Three 0.5-mL venous blood samples were extracted into heparinized 1 mL syringes at these three time points for hemoglobin and hematocrit, and the immediate analysis of blood concentrations of lactate ([La−]), glucose ([Glu]), and pH, using a blood gas (I-stat Corporation, Princeton, NJ) and glucose (Abbott Diabetes Care Ltd., Oxon, UK) analyzer. One 0.5-mL venous blood sample was collected into heparinized 1-mL syringes at 30, 50, and 70 min postingestion and stored at −80°C for the later analysis of plasma PSE concentration.
Plasma PSE was measured using a method developed by the Pathology Queensland Laboratory (Royal Brisbane and Women’s Hospital, Brisbane, Australia) for use on a liquid chromatography dual mass spectrometer. The average sample recovery based on the d3-PSE internal standard was 91% ± 4%, and the intra-assay coefficient of variation (duplicate samples) for PSE was 1.6%. The catecholamine concentrations were measured using high-performance liquid chromatography with electrochemical detection, using the methods described by Holmes et al. (16) with minor modifications. The extraction process was modified in that the final elution of the catecholamines from the alumina was conducted using 0.2 M acetic acid (100 μL). The eluates were then transferred to the vial inserts and vacuum dried (Speedvac, Savant Instruments, Holbrook, NY) and reconstituted with mobile phase (50 μL).
The urinary PSE extraction method was a modified version of the techniques previously described (7,20). The current method was modified further for analysis using high-performance liquid chromatography with UV diode array detection at 210 nm rather than liquid chromatography dual mass spectrometry. The mobile phase was modified to consist of 7.5% v/v acetonitrile in 0.05 mol·L−1 KH2PO4 buffer with pH 3.0 (1).
Data were analyzed using the Statistical Package for the Social Sciences (version 16.0; SPSS Inc., Chicago, IL). A one-way repeated-measures ANOVA was used to determine the differences in TT performance across the four conditions (PSE F, PSE NF, PLA F, and PLA NF). Two-way (treatment × time) repeated-measures ANOVA were used to assess differences in blood pH, concentrations of blood lactate, glucose and catecholamines, and plasma and urinary PSE at the various time points during exercise. Where appropriate, follow-up tests were performed using Fisher’s least significant difference test to locate the source of significant differences. Relationships between variables were determined by Pearson or Spearman correlation as appropriate, whereas the associated chances of a beneficial/trivial/harmful effect were calculated using a published spreadsheet (17) to determine whether any change in TT performance was meaningful to competitive success. Significance was set at P < 0.05, and all data are reported as mean ± SD, unless stated otherwise.
Pseudoephedrine in a dose of 2.8 mg·kg−1 BM ingested 90 min before exercise did not significantly improve cycling TT performance compared with PLA (P = 0.717). The chances that the true effect of PSE on cycling TT performance was practically beneficial/trivial/harmful were 73.0%/26.9%/0.1%, respectively. Individual TT results are shown in Figure 1.
Plasma PSE increased over time in both fed and nonfed conditions, from baseline to postexercise. The PSE nonfed condition elicited higher plasma PSE at 50 and 70 min and pre–warm-up and postexercise compared with the fed condition (P = 0.009). Furthermore, when individual preexercise plasma PSE data were correlated with TT performance, there was a significant relationship in the fed condition (r = 0.697; P = 0.025). The mean and individual plasma [PSE] data are shown in Figures 2 and 3, respectively.
In the PSE F trial, postexercise [EP] was significantly greater than baseline only (P < 0.001). Preexercise [NE] was significantly increased in the PLA F trial (P = 0.03), and [NE] postexercise was significantly lower in the PLA NF trial (P = 0.002) compared with all other treatment conditions. To further explore the potential of a metabolic effect of PSE and the influence of food, postexercise catecholamine concentrations were compared with postexercise [La−] in both PSE F and PSE NF trials. Catecholamine concentrations postexercise were highly correlated to postexercise [La−] in both PSE conditions ([NE] PSE F, r = 0.837, P = 0.009 vs [NE] PSE NF, r = 0.947, P < 0.001 vs [EP] PSE F, r = 0.784, P = 0.021 vs [EP] PSE NF, r = 0.749, P = 0.013).
Mean urinary PSE increased from baseline to postexercise in both fed and nonfed conditions (P < 0.001) when the highest urinary PSE were measured (486.4 ± 318.8 vs 476.4 ± 269.7 μg·mL−1, respectively). Of particular note, all 10 participants reported postexercise urinary PSE well in excess of the current WADA threshold of 150 μg·mL−1 after the ingestion of 2.8 mg·kg−1 BM of PSE (Fig. 4). Individuals were ranked according to their preexercise and postexercise urinary PSE in both conditions in an attempt to identify individual differences in PSE excretion; however, there was no correlation between the urinary PSE between fed and nonfed trials either preexercise (P = 0.60 and 0.088) or postexercise (P = 0.03 and 0.934). Similarly, when preexercise individual urinary PSE data were correlated with TT performance, there was no significant relationship in either fed (r = 0.394, P = 0.26) or fasted conditions (r = 0.25, P = 0.516).
Postexercise [La−] was significantly higher with PSE supplementation compared with PLA (P = 0.001), with the PLA NF trial being significantly lower than all other treatment conditions (8.1 ± 1.7 mmol·L−1 PLA NF vs 11.8 ± 2.3 mmol·L−1 PSE F; 10.4 ± 2.5 mmol·L−1 PSE NF; 8.6 ± 3.4 mmol·L−1 PLA F; P = 0.045). Conversely, postexercise [Glu] was significantly reduced with PSE ingestion compared with PLA (P = 0.029), as was the blood pH at pre–warm-up and postexercise in the PSE trials.
These present findings are consistent with those from previous studies that showed no improvement in cycling TT performance (∼30–180 min) in response to 2.3 and 2.8 mg·kg−1 BM (22) and 2.5 mg·kg−1 BM of PSE (6). However, the present performance data contrast to those from our previous work (21), which showed a 5% improvement in cycling TT performance with the ingestion of 180 mg of PSE. These two studies differed in participant number (n = 6 vs 10) and training status of the individuals (as evidenced by the higher V˙O2max values and homogeneity of the participant group in the present study). We believe that the lower variability of data in the present study was the primary reason for the difference in findings between our two investigations.
Although plasma PSE concentration increased over time from baseline to postexercise in both the fed and fasted conditions, the coingestion of a preexercise meal with PSE resulted in lower plasma concentrations at 50 and 70 min postingestion and preexercise and postexercise compared with the nonfed condition. These findings are in agreement with previous research investigating the influence of food on drug absorption, whereby food intake tends to delay the absorption of drugs (11,28). Indeed, recent research on caffeine supplementation during exercise (23) has found that serum caffeine concentration is reduced and the time to peak concentration delayed when 6 and 9 mg·kg−1 BM of caffeine is consumed with a high CHO meal. Carr et al. (8) also reported a delay in the time to peak alkalosis and blood bicarbonate concentration compared with other studies, after the consumption of 0.3 mg·kg−1 BM of sodium bicarbonate with food and fluid (8).
Peak concentrations of PSE have been reported to occur between 30 and 60 min after oral ingestion in pharmacokinetic studies (20,27); however, Gillies et al. (13) have shown that PSE peaks in the plasma at approximately 120 min postingestion during exercise under fasted conditions. Consistent with our previous work (22), plasma concentrations of PSE in the present study continued to rise from baseline to postexercise (∼150 min) in both fed and fasted conditions. Also in agreement with our previous findings are the considerable differences in plasma PSE and responses to the same PSE intake among participants. In addition, despite the variable concentrations of plasma PSE among individuals, there were no reported adverse effects in any of the performance trials preexercise, during exercise, or postexercise.
Pseudoephedrine was reintroduced by WADA to its prohibited substance list in 2010, and our data show that the ingestion of 2.8 mg·kg−1 BM, with and without preexercise feeding, resulted in postexercise PSE urinary concentrations well in excess of the current WADA threshold of 150 μg·mL−1 (29). Moreover, the considerable individual variability in urinary PSE concentration among the present participants brings the validity of the WADA threshold value into question. Indeed, Barroso et al. (2) have recently stated that high interindividual variability in urinary PSE excretion rates makes the establishment of a cutoff value near impossible (2). If there exists large variability among individuals in the metabolism and excretion of a substance, which may potentially be greater than the measurement accuracy depending on the measurement procedures, further consideration must be given to the determination and existence of a threshold value. Thus, athletes who ingest PSE at high doses during competition potentially place themselves at risk of a positive doping test, although the findings of Gillies et al. (13) suggest it is not possible to use the ingested dose to predict urinary PSE concentrations postexercise (13).
When the potential influence of PSE supplementation on plasma catecholamine concentration was examined, it was found that postexercise NE was higher in the PSE trial compared with PLA. Moreover, postexercise concentrations of both catecholamines were significantly related to postexercise lactate concentration, which suggests that PSE accelerated muscle glycogenolysis (19). However, previous research has not consistently shown a relationship between PSE supplementation and measures that suggest changes in metabolism. The presence of a metabolic response independent of an improvement in performance in the present study suggests that there are factors independent of muscle metabolism that potentially contributes to PSE’s ergogenic potential. It has been suggested that enhanced central nervous system stimulation after PSE ingestion may alter the perception of effort and mask feelings of fatigue (9,12,13,15,25); however, this is yet to be investigated in relation to exercise performance.
In conclusion, the present study indicates that although preexercise feeding significantly lowered plasma PSE concentrations, a preexercise supplementation of 2.8 mg·kg−1 BM of PSE did not improve TT performance of approximately 30 min. Moreover, the ingestion of 2.8 mg·kg−1 BM of PSE 90 min before exercise with or without food is sufficient to elicit urinary PSE concentrations in excess of the current threshold set by WADA of 150 μg·mL−1, which would ultimately result in an AAF for an athlete if used during competition.
Kellie R. Pritchard-Peschek received funding from the School of Human Movement Studies, The University of Queensland.
The authors acknowledge the technical support of the Pathology Queensland Laboratory at the Royal Brisbane and Women’s Hospital and a research grant from the School of Human Movement Studies for running this study.
For the remaining authors, no sources of funding or conflicts of interest were declared.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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