RESUMO
ABSTRACT Objective: Our objective was to perform a systematic review and meta-analysis of the research literature assessing the effect of caffeine on athletic performance. Methods: A total of 13 studies published between 2010 and 2015 were included in the meta-analysis of the effects of caffeine on maximum running distance (2 studies), time trial performance (7 studies), and muscle power (4 studies). The effect sizes were calculated as standardized differences in means (std in means). Meta-analysis was completed using a random effects model. Results: Caffeine supplementation did not increase maximum running distance (effect size= 0.37, p= 0.14) and muscle power (effect size= 0.17, p= 0.36). However, improvements were observed in the time trial performance (effect size= −0.40, p< 0.01). Subgroup analyses revealed that the improvement in time trial results may be related to the use of the 6 mg/kg of body weight of caffeine dose (effect size= −0.45, p= 0.01). Conclusion: Our meta-analysis showed that caffeine intake does not improve performance in maximum running distance and muscle power, but it seems to improve time trial performance. The effect of caffeine on time trial performance related to dose.
RESUMEN Objetivo: Realizar una revisión sistemática y meta-análisis de la literatura de investigación que evalúa el efecto de la cafeína en el rendimiento atlético. Método: Un total de 13 estudios publicados entre 2010 y 2015 fueron incluidos en el meta-análisis de los efectos de la cafeína sobre la distancia máxima de carrera (2 estudios), el tiempo de prueba (7 estudios) y la potencia muscular (4 estudios). Los tamaños del efecto se calcularon como diferencias estandarizadas en las medias (std en los medias), y el meta-análisis se completó utilizando un modelo de efectos aleatorios. Resultados: La suplementación con cafeína no aumentó la distancia máxima de funcionamiento (tamaño del efecto= 0.37, p= 0.14) ni la potencia muscular (tamaño del efecto= 0.17, p= 0.36). Sin embargo, se observaron mejoras en el rendimiento del ensayo con tiempo (tamaño del efecto= −0.40, p< 0,01). Los análisis de subgrupos revelaron que la mejora en los resultados de los ensayos a tiempo podía estar relacionada con el uso de la dosis de 6 mg/kg de peso corporal de cafeína (tamaño del efecto= −0.45, p = 0.01). Conclusiones: El meta-análisis demostró que la ingesta de cafeína no mejora el rendimiento en la distancia máxima de carrera ni la potencia muscular, pero parece mejorar el rendimiento de la prueba de tiempo. Este efecto potencial de la cafeína en el rendimiento de la prueba de tiempo estuvo relacionado con la dosis.
Assuntos
Humanos , Cafeína , Teste de Esforço , Desempenho Atlético , Ingestão de Líquidos , Fontes Geradoras de Energia/efeitos adversosRESUMO
For a long period lactate was considered as a dead-end product of glycolysis in many cells and its accumulation correlated with acidosis and cellular and tissue damage. At present, the role of lactate in several physiological processes has been investigated based on its properties as an energy source, a signalling molecule and as essential for tissue repair. It is noteworthy that lactate accumulation alters glycolytic flux independently from medium acidification, thereby this compound can regulate glucose metabolism within cells. PFK (6-phosphofructo-1-kinase) is the key regulatory glycolytic enzyme which is regulated by diverse molecules and signals. PFK activity is directly correlated with cellular glucose consumption. The present study shows the property of lactate to down-regulate PFK activity in a specific manner which is not dependent on acidification of the medium. Lactate reduces the affinity of the enzyme for its substrates, ATP and fructose 6-phosphate, as well as reducing the affinity for ATP at its allosteric inhibitory site at the enzyme. Moreover, we demonstrated that lactate inhibits PFK favouring the dissociation of enzyme active tetramers into less active dimers. This effect can be prevented by tetramer-stabilizing conditions such as the presence of fructose 2,6-bisphosphate, the binding of PFK to f-actin and phosphorylation of the enzyme by protein kinase A. In conclusion, our results support evidence that lactate regulates the glycolytic flux through modulating PFK due to its effects on the enzyme quaternary structure.