Increasing effort without noticing: A randomized controlled pilot study about the ergogenic placebo effect in endurance athletes and the role of supplement salience.

PURPOSE: Previous research shows that endurance performance can be enhanced by placebo ergogenic aids. This study investigates the ergogenic placebo response, which we define as an increase in objective and physiological effort without an increase in subjective effort, in competitive cyclists. The primary objective of this study is to explore the role of supplement salience in the ergogenic placebo response, while the secondary aim is to assess whether believing to have taken an inactive placebo supplement attenuates the desired ergogenic effect. METHODS: We employed a double-blind placebo-controlled study design and compared a high salience (pudding) to a low salience (capsules) ergogenic placebo supplement and to a no treatment control group. Thirty-four male athletes (30.0 ± 5.7 years) performed two self-regulated time trials on an isokinetic cycling ergometer, one without intervention serving as a baseline and one with intervention according to group assignment. At both time trials, power output (objective effort), blood lactate (physiological effort) and the rating of perceived exertion (subjective effort) were measured. RESULTS: Receiving a high salience supplement can increase physiological and objective effort without a proportional rise in subjective effort, suggesting a decoupling of perceived exertion and endurance performance. Low salience and control group both showed no such ergogenic placebo response. Athletes' belief concerning the true nature of the ergogenic aid (inactive placebo vs. ergogenic supplement) did not influence the ergogenic placebo response. CONCLUSION: High salience placebo ergogenic aids can elicit enhanced performance without the athlete noticing (exertion), and deception of athletes seems unnecessary as even believing to have received an inactive placebo supplement maintains the ergogenic placebo response.

Effects of extracellular orotic acid on acute contraction-induced adaptation patterns in C2C12 cells.

Dietary administration of orotic acid (OA), an intermediate in the pyrimidine biosynthetic pathway, is considered to provide a wide range of beneficial effects, including cardioprotection and exercise adaptation. Its mechanisms of action, when applied extracellularly, however, are barely understood. In this study, we evaluated potential effects of OA on skeletal muscle using an in vitro contraction model of electrically pulse-stimulated (EPS) C2C12 myotubes. By analyzing a subset of genes representing inflammatory, metabolic, and structural adaptation pathways, we could show that OA supplementation diminishes the EPS-provoked expression of inflammatory transcripts (interleukin 6, Il6; chemokine (C-X-C Motif) ligand 5, Cxcl5), and attenuated transcript levels of nuclear receptor subfamily 4 group A member 3 (Nr4A3), early growth response 1 (Egr1), activating transcription factor 3 (Atf3), and fast-oxidative MyHC-IIA isoform (Myh2). By contrast, OA had no suppressive effect on the pathogen-provoked inflammatory gene response in skeletal muscle cells, as demonstrated by stimulation of C2C12 myotubes with bacterial LPS. In addition, we observed a suppressive effect of OA on EPS-induced phosphorylation of AMP-activated protein kinase (AMPK), whereas EPS-triggered phosphorylation/activation of the mammalian target of rapamycin (mTOR) was not affected. Finally, we demonstrate that OA positively influences glycogen levels in EP-stimulated myotubes. Taken together, our results suggest that in skeletal muscle cells, OA modulates both the inflammatory and the metabolic reaction provoked by acute contraction. These results might have important clinical implications, specifically in cardiovascular and exercise medicine.

Vitamin E supplementation does not increase the vitamin C radical concentration at rest and after exhaustive exercise in healthy male subjects.

BACKGROUND: Extensive exercise may promote the formation of reactive oxygen species and subsequently contribute to tissue damage. A compound which can protect cells and tissues is vitamin E. The vitamin E radical, formed during the radical scavenging process, can be reduced by vitamin C resulting in a higher level of the vitamin C radical (semidehydroascorbate free radical). An increase of the vitamin C radical, however, is assumed to exert prooxidative effects. AIM OF THE STUDY: To elucidate whether supplementation of vitamin E and exhaustive exercise lead to an increase of the vitamin C radical in human plasma. METHODS: A placebo controlled, cross over study with 13 male volunteers was carried out. After an 8 day supplementation period with 500 I.U. D-alpha-tocopherol, the subjects performed two exhaustive treadmill runs. Blood samples were collected at rest, 0, 0.25, 1, 3, 24 and 48 h after exercise. Serum was separated and concentrations of D-alpha-tocopherol and ascorbic acid were determined by HPLC. Vitamin C radical levels in plasma were assessed by electron paramagnetic resonance (EPR). RESULTS: Vitamin E and C both showed a tendency to decrease between 3 h and 24 h after exercise. Vitamin C radical level remained stable during the whole period. Neither vitamin E supplementation nor exercise had any influence on the plasma concentration of the vitamin C radical. CONCLUSIONS: Vitamin E supplementation under conditions of mild oxidative stress does not result in an increased vitamin C radical concentration.