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The molecular mechanisms underlying the response to exercise and inactivity are not fully understood. We propose an innovative approach to profile the skeletal muscle transcriptome to exercise and inactivity using 66 published datasets. Data collected from human studies of aerobic and resistance exercise, including acute and chronic exercise training, were integrated using meta-analysis methods ( www.metamex.eu ). Here we use gene ontology and pathway analyses to reveal selective pathways activated by inactivity, aerobic versus resistance and acute versus chronic exercise training. We identify NR4A3 as one of the most exercise- and inactivity-responsive genes, and establish a role for this nuclear receptor in mediating the metabolic responses to exercise-like stimuli in vitro. The meta-analysis (MetaMEx) also highlights the differential response to exercise in individuals with metabolic impairments. MetaMEx provides the most extensive dataset of skeletal muscle transcriptional responses to different modes of exercise and an online interface to readily interrogate the database. The pathways that underlie the effects of exercise on metabolism remain incompletely described. Here, the authors perform a meta-analysis of transcriptomic data from 66 published datasets of human skeletal muscle. They identify pathways selectively activated by inactivity, aerobic or resistance exercise, and characterize NR4A3 as one of the genes responsive to inactivity.

Background To determine the validity of the lactate threshold (LT) and maximal oxygen uptake () determined during graded exercise test (GXT) of different durations and using different LT calculations. Trained male cyclists (n = 17) completed five GXTs of varying stage length (1, 3, 4, 7 and 10 min) to establish the LT, and a series of 30-min constant power bouts to establish the maximal lactate steady state (MLSS). was assessed during each GXT and a subsequent verification exhaustive bout (VEB), and 14 different LTs were calculated from four of the GXTs (3, 4, 7 and 10 min)—yielding a total 56 LTs. Agreement was assessed between the highest measured during each GXT () as well as between each LT and MLSS. and LT data were analysed using mean difference (MD) and intraclass correlation (ICC). Results The value from GXT1 was 61.0 ± 5.3 mL.kg-1.min-1 and the peak power 420 ± 55 W (mean ± SD). The power at the MLSS was 264 ± 39 W. from GXT3, 4, 7, 10 underestimated by ~1–5 mL.kg-1.min-1. Many of the traditional LT methods were not valid and a newly developed Modified Dmax method derived from GXT4 provided the most valid estimate of the MLSS (MD = 1.1 W; ICC = 0.96). Conclusion The data highlight how GXT protocol design and data analysis influence the determination of both and LT. It is also apparent that and LT cannot be determined in a single GXT, even with the inclusion of a VEB.

Mitochondrial defects are implicated in multiple diseases and aging. Exercise training is an accessible, inexpensive therapeutic intervention that can improve mitochondrial bioenergetics and quality of life. By combining multiple omics techniques with biochemical and in silico normalisation, we removed the bias arising from the training-induced increase in mitochondrial content to unearth an intricate and previously undemonstrated network of differentially prioritised mitochondrial adaptations. We show that changes in hundreds of transcripts, proteins, and lipids are not stoichiometrically linked to the overall increase in mitochondrial content. Our findings suggest enhancing electron flow to oxidative phosphorylation (OXPHOS) is more important to improve ATP generation than increasing the abundance of the OXPHOS machinery, and do not support the hypothesis that training-induced supercomplex formation enhances mitochondrial bioenergetics. Our study provides an analytical approach allowing unbiased and in-depth investigations of training-induced mitochondrial adaptations, challenging our current understanding, and calling for careful reinterpretation of previous findings. Exercise training can be therapeutic but how mitochondria respond remains unclear. Here, the authors use multiple omics techniques to reveal a complex network of non-stoichiometric mitochondrial adaptations that are prioritized or deprioritised during different phases of exercise training.

Analyses of mitochondrial adaptations in human skeletal muscle have mostly used whole-muscle samples, where results may be confounded by the presence of a mixture of type I and II muscle fibres. Using our adapted mass spectrometry-based proteomics workflow, we provide insights into fibre-specific mitochondrial differences in the human skeletal muscle of men before and after training. Our findings challenge previous conclusions regarding the extent of fibre-type-specific remodelling of the mitochondrial proteome and suggest that most baseline differences in mitochondrial protein abundances between fibre types reported by us, and others, might be due to differences in total mitochondrial content or a consequence of adaptations to habitual physical activity (or inactivity). Most training-induced changes in different mitochondrial functional groups, in both fibre types, were no longer significant in our study when normalised to changes in markers of mitochondrial content. Exercise alters the mitochondrial proteome, but little is known about changes in different fibre types. Here, the authors provide insight into fibre-specific mitochondrial differences before and after training using proteomics in human skeletal muscle.

Autophagy is a key intracellular mechanism by which cells degrade old or dysfunctional proteins and organelles. In skeletal muscle, evidence suggests that exercise increases autophagosome content and autophagy flux. However, the exercise-induced response seems to differ between rodents and humans, and little is known about how different exercise prescription parameters may affect these results. The present study utilised skeletal muscle samples obtained from four different experimental studies using rats and humans. Here, we show that, following exercise, in the soleus muscle of Wistar rats, there is an increase in LC3B-I protein levels immediately after exercise (+109%), and a subsequent increase in LC3B-II protein levels 3 h into the recovery (+97%), despite no change in Map1lc3b mRNA levels. Conversely, in human skeletal muscle, there is an immediate exercise-induced decrease in LC3B-II protein levels (−24%), independent of whether exercise is performed below or above the maximal lactate steady state, which returns to baseline 3.5 h following recovery, while no change in LC3B-I protein levels or MAP1LC3B mRNA levels is observed. SQSTM1/p62 protein and mRNA levels did not change in either rats or humans following exercise. By employing an ex vivo autophagy flux assay previously used in rodents we demonstrate that the exercise-induced decrease in LC3B-II protein levels in humans does not reflect a decreased autophagy flux. Instead, effect size analyses suggest a modest-to-large increase in autophagy flux following exercise that lasts up to 24 h. Our findings suggest that exercise-induced changes in autophagosome content markers differ between rodents and humans, and that exercise-induced decreases in LC3B-II protein levels do not reflect autophagy flux level.

There are epidemiological associations between obesity and type 2 diabetes, cardiovascular disease and Alzheimer’s disease. The role of amyloid beta 42 (Aβ 42 ) in these diverse chronic diseases is obscure. Here we show that adipose tissue releases Aβ 42 , which is increased from adipose tissue of male mice with obesity and is associated with higher plasma Aβ 42 . Increasing circulating Aβ 42 levels in male mice without obesity has no effect on systemic glucose homeostasis but has obesity-like effects on the heart, including reduced cardiac glucose clearance and impaired cardiac function. The closely related Aβ 40 isoform does not have these same effects on the heart. Administration of an Aβ-neutralising antibody prevents obesity-induced cardiac dysfunction and hypertrophy. Furthermore, Aβ-neutralising antibody administration in established obesity prevents further deterioration of cardiac function. Multi-contrast transcriptomic analyses reveal that Aβ 42 impacts pathways of mitochondrial metabolism and exposure of cardiomyocytes to Aβ 42 inhibits mitochondrial complex I. These data reveal a role for systemic Aβ 42 in the development of cardiac disease in obesity and suggest that therapeutics designed for Alzheimer’s disease could be effective in combating obesity-induced heart failure. Epidemiological evidence has identified associations among obesity, Alzheimer’s disease, and cardiovascular disease. Here, the authors report that adipose tissue releases amyloid beta 42 (Aβ42) and that antagonizing Aβ42 protects cardiac function in obesity murine models.

To compare the effect of 4-week unknown vs known loads strength training intervention on power output performance and throwing velocity in junior team handball players. Twenty-eight junior team-handball players (17.2 ± 0.6 years, 1.79 ± 0.07 m, 75.6 ± 9.4 kg)were divided into two groups (unknown loads: UL; known loads: KL). Both groups performed two sessions weekly consisting of four sets of six repetitions of the bench press throw exercise, using the 30%, 50% and 70% of subjects' individual 1 repetition maximum (1RM). In each set, two repetitions with each load were performed, but the order of the loads was randomised. In the KL group, researchers told the subjects the load to mobilise prior each repetition, while in the UL group, researchers did not provide any information. Maximal dynamic strength (1RM bench press), power output (with 30, 50 and 70% of 1RM) and throwing velocity (7 m standing throw and 9 m jumping throw) were assessed pre- and post-training intervention. Both UL and KL group improved similarly their 1RM bench press as well as mean and peak power with all loads. There were significant improvements in power developed in all the early time intervals measured (150 ms) with the three loads (30, 50, 70% 1RM) in the UL group, while KL only improved with 30% 1RM (all the time intervals) and with 70% 1RM (at certain time intervals). Only the UL group improved throwing velocity in both standing (4.7%) and jumping (5.3%) throw (p > 0.05). The use of unknown loads has led to greater gains in power output in the early time intervals as well as to increases in throwing velocity compared with known loads. Therefore unknown loads are of significant practical use to increase both strength and in-field performance in a short period of training.

Este trabajo, pretende analizar y describir la importancia que desempeñan los factores afectivos (emociones, creencias y actitudes) en el aprendizaje de las matemáticas. Se presentan los resultados de un estudio realizado con 384 alumnos del tercer ciclo de Educación Primaria, con edades comprendidas entre los 10 y 12 años para evaluar los aspectos afectivos hacia la materia en relación con el rendimiento académico. Entre las seis dimensiones que contempla el cuestionario, el autoconcepto matemático, las creencias acerca de su destreza matemática y las atribuciones de causalidad sobre dicha materia presentan mayores niveles de significatividad con las calificaciones. El estudio muestra que estos factores y el rendimiento académico están correlacionados acentuando la necesidad de otorgar un papel más destacado a los componentes afectivos para mejorar la calidad de la matemática.

Monitoring fatigue and performance is important for adjusting training loads in soccer. Therefore, knowing the status of the player when applying a training stimulus is key to optimizing the players’ development. This study aims to evaluate the interaction between internal and external load, during training and matches, in an elite youth soccer team. Methods: seventeen youth players of the highest Spanish category were monitored with GPS devices during training and matches, as well as recording their nocturnal heart rate variability (HRV). We employed a linear mixed model to assess the physical demands between training and matches, and to compare the HRV variables. Results: a higher total distance (+2993.35–5746.56 m; ES = 1.4), distance at high intensity (+641.24–1907 m; ES = 1.5), sprint distance (+350.46–795.05 m; ES = 2.1), number of sprints (+18.38–41.58; ES = 1.9), and number of repeated sprints (+5.91–15.30; ES = 1.7) (all p < 0.001), but not in the number of accelerations, were reported during the matches when compared to the training sessions during the 11 weeks. The analysis of the HRV variables showed no significant differences between the accumulated values during a training week, providing similar results pre-match or post-match (p > 0.05). The LF/HFRATIO showed a negative influence on the total distance ran, distance at high intensity, distance in sprint, number of sprints, and repeated sprint. RRMEAN was positively related to the sprint number. Conclusion: the results of the present study suggest that nocturnal HRV variables are not different between pre-match and post-match. Furthermore, it suggests that LF/HFRATIO and RRMEAN during pre-match can determine the external load that the player will be able to complete during the match.

To determine the validity of the lactate threshold (LT) and maximal oxygen uptake ( ) determined during graded exercise test (GXT) of different durations and using different LT calculations. Trained male cyclists (n = 17) completed five GXTs of varying stage length (1, 3, 4, 7 and 10 min) to establish the LT, and a series of 30-min constant power bouts to establish the maximal lactate steady state (MLSS). was assessed during each GXT and a subsequent verification exhaustive bout (VEB), and 14 different LTs were calculated from four of the GXTs (3, 4, 7 and 10 min)-yielding a total 56 LTs. Agreement was assessed between the highest measured during each GXT ( ) as well as between each LT and MLSS. and LT data were analysed using mean difference (MD) and intraclass correlation (ICC). The value from GXT1 was 61.0 ± 5.3 mL.kg-1.min-1 and the peak power 420 ± 55 W (mean ± SD). The power at the MLSS was 264 ± 39 W. from GXT3, 4, 7, 10 underestimated by ~1-5 mL.kg-1.min-1. Many of the traditional LT methods were not valid and a newly developed Modified Dmax method derived from GXT4 provided the most valid estimate of the MLSS (MD = 1.1 W; ICC = 0.96). The data highlight how GXT protocol design and data analysis influence the determination of both and LT. It is also apparent that and LT cannot be determined in a single GXT, even with the inclusion of a VEB.