Tell me how and where you play football and I’ll tell you how much you have to run

The aim of this study was to describe the team accumulated physical response per minute considering only the effective playing time (EPT) attending to different contextual and strategic variables in the Spanish Football First Division (LaLiga Santander). A sample of 2,959 performances was included in the analysis, considering a 4-year period of analysis (from 2016–17 to 2019–20). The physical variables were: total distance covered with (DTminPOS) and without (DTminNOpos) possession of the ball, and distance covered at > 21 km·h^-1 with possession (DT21minPOS) and without (DT21minNOpos). Two contextual variables, i.e. Place (Home/Away) and Score (Lost/Draw/Win), and two strategic variables, i.e. level of effective playing time (LevelETP) and level of possession of the ball (LevelPOS), were analysed. The teams ran more without possession of the ball than with possession; nevertheless, the teams that had less possession of the ball had higher values in the distance covered at > 21 km·h^-1 with possession of the ball and vice versa. Furthermore, the strategic variables also had influence on the physical response (DT and DT21) of the teams,LevelETP and LevelPOS, although with interactive effects: longer playing time, less accumulated distance, and greater possession, greater accumulated distance in the defensive phase, both per min. The findings of this study may offer important practical implications to practitioners in order to assess physical performances of the players in matches, because it is crucial to integrate in the analysis the different contextual and strategic variables where the match has taken place to assess performances of the teams.     

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Authors of papers published in Rockefeller University Press journals (The Journal of Cell Biology, The Journal of Experimental Medicine, or The Journal of General Physiology) now retain copyright to their published work. This permits authors to reuse their own work in any way, as long as they attribute it to the original publication. Third parties may use our published materials under a Creative Commons license, six months after publication.     

You wrote it; you own it!

Authors of papers published in Rockefeller University Press journals (The Journal of Cell Biology, The Journal of Experimental Medicine, or The Journal of General Physiology) now retain copyright to their published work. This permits authors to reuse their own work in any way, as long as they attribute it to the original publication. Third parties may use our published materials under a Creative Commons license, six months after publication.     

Host‐associated genomic differentiation in congeneric butterflies: now you see it,now you do not

Ecotypic variation among populations may become associated with widespread genomic differentiation, but theory predicts that this should happen only under particular conditions of gene flow, selection and population size. In closely related species, we might expect the strength of host‐associated genomic differentiation (HAD) to be correlated with the degree of phenotypic differentiation in host‐adaptive traits. Using microsatellite and Amplified Fragment Length Polymorphism (AFLP) markers, and controlling for isolation by distance between populations, we sought HAD in two congeneric species of butterflies with different degrees of host plant specialization. Prior work on Euphydryas editha had shown strong interpopulation differentiation in host‐adapted traits, resulting in incipient reproductive isolation among host‐associated ecotypes. We show here that Euphydryas aurinia had much weaker host‐associated phenotypic differentiation. Contrary to our expectations, we detected HAD in Euphydryas aurinia, but not in E. editha. Even within an E. aurinia population that fed on both hosts, we found weak but significant sympatric HAD that persisted in samples taken 9 years apart. The finding of significantly stronger HAD in the system with less phenotypic differentiation may seem paradoxical. Our findings can be explained by multiple factors, ranging from differences in dispersal or effective population size, to spatial variation in genomic or phenotypic traits and to structure induced by past histories of host‐adapted populations. Other infrequently measured factors, such as differences in recombination rates, may also play a role. Our result adds to recent work as a further caution against assumptions of simple relationships between genomic and adaptive phenotypic differentiation.