Jesús F. Escanero

Aggregation of human polymorphonuclear leukocytes by endothelin: role of platelet-activating factor

The mechanisms by which endothelin-1 (ET-1) acts on polymorphonuclear leukocytes (PMN) are insufficiently known. In this study, we assessed the hypotheses that ET-1 is a PMN-aggregating agent, and that platelet-activating factor (PAF) is the principal mediator of ET-1-induced PMN aggregation. ET-1 induced dose-related PMN aggregation, which started 1 min after ET-1 exposure. Two different specific PAF receptor antagonists blocked the effect of ET-1 on PMN aggregation. In addition, ET-1 induced a significant increase in the production of PAF by PMN after 2 to 5 min of ET-1 incubation. ET-1 induced PAF release from PMN rather than accumulation. This PAF production was dependent on intra- and extracellular Ca2+. In this regard, the PAF receptor antagonists significantly blunted the ET-1-induced peak in cytosolic free Ca2+ ([Ca2+]i). Our results, therefore, indicate that ET-1 is effective in causing aggregation of human PMN and that its action appears to be mediated by PAF production via a Ca(2+)-dependent mechanism.

Comparison of nine theoretic models estimating the mechanical power output in cycling.

Objective: To assess which of the equations used to estimate mechanical power output for a wide aerobic range of exercise intensities gives the closest value to that measured with the SRM training system. Methods: Thirty four triathletes and endurance cyclists of both sexes (mean (SD) age 24 (5) years, height 176.3 (6.6) cm, weight 69.4 (7.6) kg and Vo2max 61.5 (5.9) ml/kg/min) performed three incremental tests, one in the laboratory and two in the velodrome. The mean mechanical power output measured with the SRM training system in the velodrome tests corresponding to each stage of the tests was compared with the values theoretically estimated using the nine most referenced equations in literature (Whitt (Ergonomics 1971;14:419–24); Di Prampero et al (J Appl Physiol 1979;47:201–6); Whitt and Wilson (Bicycling science. Cambridge: MIT Press, 1982); Kyle (Racing with the sun. Philadelphia: Society of Automotive Engineers, 1991:43–50); Menard (First International Congress on Science and Cycling Skills, Malaga, 1992); Olds et al (J Appl Physiol 1995;78:1596–611; J Appl Physiol 1993;75:730–7); Broker (USOC Sport Science and Technology Report 1–24, 1994); Candau et al (Med Sci Sports Exerc 1999;31:1441–7)). This comparison was made using the mean squared error of prediction, the systematic error and the random error. Results: The equations of Candau et al, Di Prampero et al, Olds et al (J Appl Physiol 1993;75:730–7) and Whitt gave a moderate mean squared error of prediction (12.7%, 21.6%, 13.2% and 16.5%, respectively) and a low random error (0.5%, 0.6%, 0.7% and 0.8%, respectively). Conclusions: The equations of Candau et al and Di Prampero et al give the best estimate of mechanical power output when compared with measurements obtained with the SRM training system.

Variants of the Solute Carrier SLC16A1 Gene (MCT1) Associated With Metabolic Responses During a Long-Graded Test in Road Cyclists

Abstract González-Haro, C, Soria, M, Vicente, J, Fanlo, AJ, Sinués, B, and Escanero, JF. Variants of the solute carrier SLC16A1 gene (MCT1) associated with metabolic responses during a long-graded test in road cyclists. J Strength Cond Res 29(12): 3494–3505, 2015—Variants of the solute carrier SLC16A1 gene have been associated with alterations in MCT1 expression, because of a lactate (La−) transport deficiency across the cell membrane and a blood La− accumulation. The aim of this study was to associate the allelic and genotypic frequencies of 1470T>A, 2917(1414) C>T, and IVS3-17A>C variants relative to the blood La− kinetics and metabolic responses to a progressive effort until exhaustion. Twenty-five well-trained road cyclists performed a long-graded laboratory test: 10 minutes at 2.0 W·kg−1, first step at 2.5 W·kg−1 with increments of 0.5 W·kg−1 every 10 minutes until exhaustion. Blood La−, nonesterified fatty acids (NEFAS), and glucose levels were measured; fat and carbohydrate oxidation rates were estimated through stoichiometric equations. Three variants of SLC16A1 gene were determined for each subject, which were divided in two groups: wt (wild type)/mt (mutated type) and mt/mt genotype group versus wt/wt genotype group. Metabolic responses were compared between both groups with an unpaired Students t-test; Friedman and Wilcoxon tests were performed for nonparametric data. The statistical significance was set at p ⩽ 0.05. For 1470TA polymorphism, no significant blood La− differences were found between groups. 2197(1414)C>T allele carriers and IVS3-17A>C carriers showed significantly higher blood La− levels, lower blood NEFAS, and glucose levels at submaximal intensities. These findings open a new perspective to investigate SLC16A1 variants (1470TA and IVS3-17A>C) on La− deficiency transport and its regulation/interaction with other metabolic pathways. Future studies would be needed to clarify whether 1470T>A, 2917(1414)C>T, and IVS3-17A>C allelic/genotypic distribution benefit performance in endurance athletes.

Submaximal exercise intensities do not provoke variations in plasma magnesium concentration in well-trained euhydrated endurance athletes with no magnesium deficiency.

The purpose of this study was to assess the effect of exercise intensity during an incremental exercise test on plasma Mg concentration in well-trained euhydrated athletes. Twenty-seven well-trained endurance athletes carried out a cycloergometer test: after a warm-up of 10 min at 2.0 W·kg(-1), the workload increased by 0.5 W·kg(-1) every 10 min until exhaustion. Oxygen uptake (VO(2)), blood lactate concentration ([La(-)](b)), catecholamines, and plasma Mg were measured at rest, at the end of each stage and at 3, 5 and 7 minutes post-exercise. Urine specific gravity (U(SG)) was analyzed before and after the test, and subjects drank water ad libitum. Fat oxidation rate (FAT(oxr)), carbohydrate oxidation rate (CHO(oxr)), energy expenditure from fat (EE(FAT)), energy expenditure from carbohydrate (EE(CHO)), and total EE (EE(TOTAL)) were estimated using stoichiometric equations. Plasma Mg concentration at each relative exercise intensity (W·kg(-1)) were compared by means of repeated-measures ANOVA. Pearsons correlations were performed to assess the relationship between variables. The significance level was set at p<0.05. No significant differences were found in U(SG) between before and after the test (1.014±0.004 vs 1.014±0.004 g·cm(-3)). Nor were significant differences found in plasma Mg as a function of the different exercise intensities. Further, no significant correlations were detected between Mg and metabolic variables. In conclusion, acute exercise at a range of submaximal intensities in euhydrated well-trained endurance athletes does not affect plasma Mg concentration, suggesting that the plasma volume plays an important role in Mg homeostasis during exercise.

Variations in serum magnesium and hormonal levels during incremental exercise

In this study, we examined the relationship between plasma magnesium levels and hormonal variations during an incremental exercise test until exhaustion in 27, well-trained, male endurance athletes. After a warm-up of 10 min at 2 W/kg, the test began at an initial workload of 2.5 W/kg and continued with increments of 0.5 W/kg every 10 min until exhaustion. Plasma magnesium, catecholamine, insulin, glucagon, parathyroid hormone (PTH), calcitonin, aldosterone and cortisol levels were determined at rest, at the end of each stage and three, five and seven minutes post-exercise. With the incremental exercise test, no variations in plasma magnesium levels were found, while plasma adrenaline, noradrenaline, PTH, glucagon and cortisol levels increased significantly. Over the course of the exercise, plasma levels of insulin decreased significantly, but those of calcitonin remained steady. During the recovery period, catecholamines and insulin returned to basal levels. These findings indicate that the magnesium status of euhydrated endurance athletes during incremental exercise testing may be the result of the interrelation between several hormonal variations.