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The dose–response relationship between pseudoephedrine ingestion and exercise performance
Abstract   Peer reviewed

The dose–response relationship between pseudoephedrine ingestion and exercise performance

K R Pritchard-Peschek, David G Jenkins, M Osborne, Gary J Slater and D Taaffe
Journal of Science and Medicine in Sport, Vol.13(Supplement 1), p.e8
Asics Conference of Science and Medicine in Sport: Hot topics in the tropics, 2010 (Port Douglas, Australia, 03-Nov-2010–06-Nov-2010)
2010
url
https://doi.org/10.1016/j.jsams.2010.10.478View
Published Version

Abstract

pseudoephedrine performance drug dosage
Introduction: Despite the re-addition of pseudoephedrine (PSE) to the World Anti-Doping Agency's (WADA) Prohibited List, there is evidence to suggest that many athletes will still take the drug (in training and competition) to improve their performance. This is despite uncertainty regarding its efficacy as an ergogenic aid. Performance improvements have been observed with PSE supplementation, however inconsistencies in the dose administered and exercise protocols used make it difficult to interpret its ergogenic effect. The purpose of the present study was to examine a possible dose-response between PSE and endurance exercise performance, whilst tracking changes in biochemical markers that could provide insight on the mechanisms responsible for improvements in performance. Methods: Ten highly trained male cyclists and triathletes (age 26.5 years, range 18–38, mass 75.1 kg, range 65–84, VO2max 70.6 ml kg min−1, range 61.7–81.0) underwent three performance trials in which they completed a 20 min variable-intensity warm up, followed by a cycling time trial (TT) in which a fixed amount of work (7 kJ kg−1 body mass (BM)) was completed in the shortest possible time. Sixty minutes before the start of exercise, subjects orally ingested either 2.3 mg kg−1 or 2.8 mg kg−1 BM of PSE or a placebo (PLA) in a randomized, crossover, double-blind manner. Venous blood was sampled at baseline, pre- and post-warm up and post-exercise for the analysis of pH plus lactate and glucose concentration, while plasma [PSE] was measured at baseline, pre-warm up and post-exercise. Results: Pseudoephedrine in doses of 2.8 mg kg−1 and 2.3 mg kg−1 BM did not significantly improve cycling TT performance compared to PLA (23:28.0 ± 2:07.4 min; 24:48.9 ± 2:13.0 min; 25:09.6 ± 2:18.6 min, respectively; p = 0.60). Plasma [PSE] increased from pre-warm up to post-exercise in both treatment conditions (630.2 ± 127.2 ng/mL; 834.0 ± 86.3 ng/mL 2.3 mg kg−1; p < 0.001 vs. 806.1 ± 204.1 ng/mL; 953.3 ± 146.9 ng/mL 2.8 mg kg−1; p < 0.001), with the 2.8 mg kg−1 dose eliciting the highest plasma [PSE] both pre-warm up and post-exercise (2.8 mg kg−1 > 2.3 mg kg−1 > PLA; p < 0.001). Conclusion: There was a large individual variation in plasma [PSE] observed among subjects, which may potentially have impacted upon cycling TT performance as there were also large individual variations observed in TT time. It is evident there are external factors influencing PSE's bioavailability, and these changes in PSE kinetics may be responsible for the observed variation in cycling performance in the present study.

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