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  • Author: Hermann Zbinden-Foncea x
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Hermann Zbinden-Foncea, Luc J. C. van Loon, Jean-Marc Raymackers, Marc Francaux and Louise Deldicque

Mitogen-activated protein kinase (MAPK) pathways are activated in skeletal muscle during endurance exercise, but the upstream molecular events are incompletely resolved. As an increase in plasma nonesterified fatty acids (NEFA) is a common feature of long-lasting exercise, the authors tested the hypothesis that NEFA contribute to the activation of MAPK during endurance exercise. Acipimox was used before and during endurance exercise to prevent the elevation of plasma NEFA levels in healthy subjects and patients with diabetes. In 2 separate studies, healthy subjects cycled for 2 hr and patients with diabetes for 1 hr at 50% Wmax. In control conditions, plasma NEFA concentrations increased from 0.35 to 0.90 mM during exercise in healthy subjects and from 0.55 to 0.70 mM in patients with diabetes (p < .05). Phosphorylation states of extracellularly regulated kinase 1 and 2 (ERK1/2), p38, and c-Jun NH2-terminal kinases (JNK) were significantly increased after exercise in the vastus lateralis in both groups. Acipimox blocked the increase in plasma NEFA concentrations and almost completely repressed any rise in ERK1/2 and p38 but not in JNK. In conclusion, the data support a role for plasma NEFA in the activation of p38 and ERK1/2 in skeletal-muscle tissue of healthy and diabetic subjects during endurance exercise. Further investigation will be required to determine the molecular link between NEFA and MAPK activation during exercise in human skeletal muscle.

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Hermann Zbinden-Foncea, Isabel Rada, Jesus Gomez, Marco Kokaly, Trent Stellingwerff, Louise Deldicque and Luis Peñailillo

Purpose: To examine the effects of a moderate dose of caffeine in elite male volleyball players on countermovement-jump (CMJ) performance, as well as temporal concentric- and eccentric-phase effects. Methods: Ten elite male volleyball players took part in 2 experimental days via a randomized crossover trial 1 wk apart in which they ingested either 5 mg/kg of caffeine or a placebo in double-blind fashion. Heart rate and blood pressure were measured at rest and 60 min postingestion. Afterward, subjects also performed 3 CMJ trials 60 min postingestion, of which the average was used for further analysis. They filled out a questionnaire on possible side effects 24 h posttrial. Results: Caffeine intake, compared with placebo, increased CMJ peak concentric force (6.5% ± 6.4%; P = .01), peak power (16.2% ± 8.3%; P < .01), flight time (5.3% ± 3.4%; P < .01), velocity at peak power (10.6% ± 8.0%; P < .01), peak displacement (10.8% ± 6.5%; P < .01), peak velocity (12.6% ± 7.4%; P < .01), peak acceleration (13.5% ± 8.5%; P < .01), and the force developed at peak power (6.0% ± 4.0%; P < .01) and reduced the time between peak power and peak force (16.7% ± 21.6%, P = .04). Caffeine increased diastolic blood pressure by 13.0% ± 8.9% (P < .05), whereas no adverse side effects were found. Conclusions: The ingestion of 5 mg/kg of anhydrous caffeine improves overall CMJ performance without inducing side effects.

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Mauricio Castro-Sepulveda, Jorge Cancino, Rodrigo Fernández-Verdejo, Cristian Pérez-Luco, Sebastian Jannas-Vela, Rodrigo Ramirez-Campillo, Juan Del Coso and Hermann Zbinden-Foncea

During exercise, the human body maintains optimal body temperature through thermoregulatory sweating, which implies the loss of water, sodium (Na+), and other electrolytes. Sweat rate and sweat Na+ concentration show high interindividual variability, even in individuals exercising under similar conditions. Testosterone and cortisol may regulate sweat Na+ loss by modifying the expression/activity of the cystic fibrosis transmembrane conductance regulator. This has not been tested. As a first approximation, the authors aimed to determine whether basal serum concentrations of testosterone or cortisol, or the testosterone/cortisol ratio relate to sweat Na+ loss during exercise. A total of 22 male elite soccer players participated in the study. Testosterone and cortisol were measured in blood samples before exercise (basal). Sweat samples were collected during a training session, and sweat Na+ concentration was determined. The basal serum concentrations of testosterone and cortisol and their ratio were (mean [SD]) 13.6 (3.3) pg/ml, 228.9 (41.4) ng/ml, and 0.06 (0.02), respectively. During exercise, the rate of Na+ loss was related to cortisol (r = .43; p < .05) and to the testosterone/cortisol ratio (r = −.46; p < .01), independently of the sweating rate. The results suggest that cortisol and the testosterone/cortisol ratio may influence Na+ loss during exercise. It is unknown whether this regulation depends on the cystic fibrosis transmembrane conductance regulator.