Association of Training Characteristics with Critical Power in Competitive Recreational Cyclists and Triathletes

Endurance athletes often employ a training zone approach to classify their training intensity, where Zones 1, 2, and 3 (Z1-Z3) correspond to low, moderate, and high intensities. Research has shown that many elite athletes across a multitude of endurance sports employ polarized training distributions (TIDs), i.e., they spend a large percentage of their training in Z1 with much of the remainder in Z3 and little training in Z2. This appears to be beneficial for performance in these populations. The typical TIDs among recreationally competitive endurance athletes and their impact on performance are less well understood. PURPOSE: The purpose of this study was to examine the TIDs of recreationally competitive cyclists and triathletes and the impact of training characteristics on cycling performance. METHODS: Participants (n = 19, age = 31.7 ± 10.7 years; height = 176.6 ± 8.8 cm; weight = 70.8 ± 8.6 kg, relative CP = 4.3 ± 0.7 W/kg) submitted raw activity files, which they had previously uploaded to Strava, a popular workout tracking site. We used a workout analysis program (Golden Cheetah, V3.5) and R statistical language to analyze training and racing data. We determined each athlete’s highest critical power (CP) relative to body weight by first finding the highest maximum mean power (MMP) over 2, 5, and 10 minutes achieved over the course of a single week and then employing the linear power inverse of time CP model. We considered relative CP (W/kg) as our proxy for endurance performance, as it highly correlates with race performances. We then extracted values for estimated maximal aerobic power (MAP), training volume (training hours), training intensity (mean training power as a percent of MAP), training frequency (number of sessions), and training polarization (polarization index (PI) calculated from percent time in power Z1-3) for the 12 weeks leading up to the performance measure. We determined the association of the training characteristics on relative CP while controlling for participant age and fitness (MAP) by employing a linear regression. RESULTS: Only 4 of 23 participants employed a polarized training approach as defined by a PI \u3e 2.0. Athletes spent on average 71.0 ± 9.5% of their training time in Z1, 16.1% ± 6.1 in Z2, and 12.9% ± 7.3 in Z3. They completed 74.9 ± 22.9 sessions and amassed 110.3 ± 46.9 hours of training time over the 12 weeks leading up the performance measure. In this preliminary analysis of 19 participants, we were unable to detect a statistically significant effect of polarization on relative CP, when controlling for age, fitness, and all other training variables. Yet, polarization was the explanatory variable with the largest impact on relative CP, b (SE) = 0.25 (0.55), t = 0.457, p = 0.656. CONCLUSION: Most of the recreationally competitive cyclists and triathletes in our study did not employ a polarized TID, despite data from elite cohorts and laboratory studies showing its benefits. More research into the effect of TID on performance and health in recreationally competitive athletes is needed to confirm its benefits in this population

Attachment to God as a Function of Mortality Salience and Intrinsic Religiosity

The present study examined the association between intrinsic religiosity and attachment to God following mortality salience. Participants (N = 158) consisted of Christian individuals who were asked to complete the Religious Orientation Scale (Allport & Ross, 1967) as a measure of intrinsic religiosity, a word search puzzle to prime either death-related or neutral words, and the Attachment to God Inventory (Beck & McDonald, 2004). A moderated regression found a significant interaction between MS and intrinsic religiosity on avoidant but not anxious attachment to God. Specifically, following reminders of death, low intrinsic individuals were more avoidant toward God compared to high intrinsic individuals. These findings suggest that MS is associated with bolstering religious beliefs in order to cope with existential anxieties

Rare Copy Number Variants in \u3cem\u3eNRXN1\u3c/em\u3e and \u3cem\u3eCNTN6\u3c/em\u3e Increase Risk for Tourette Syndrome

Tourette syndrome (TS) is a model neuropsychiatric disorder thought to arise from abnormal development and/or maintenance of cortico-striato-thalamo-cortical circuits. TS is highly heritable, but its underlying genetic causes are still elusive, and no genome-wide significant loci have been discovered to date. We analyzed a European ancestry sample of 2,434 TS cases and 4,093 ancestry-matched controls for rare (\u3c 1% frequency) copy-number variants (CNVs) using SNP microarray data. We observed an enrichment of global CNV burden that was prominent for large (\u3e 1 Mb), singleton events (OR = 2.28, 95% CI [1.39–3.79], p = 1.2 × 10−3) and known, pathogenic CNVs (OR = 3.03 [1.85–5.07], p = 1.5 × 10−5). We also identified two individual, genome-wide significant loci, each conferring a substantial increase in TS risk (NRXN1 deletions, OR = 20.3, 95% CI [2.6–156.2]; CNTN6 duplications, OR = 10.1, 95% CI [2.3–45.4]). Approximately 1% of TS cases carry one of these CNVs, indicating that rare structural variation contributes significantly to the genetic architecture of TS

Generation of twenty four induced pluripotent stem cell lines from twenty four members of the Lothian 4 Birth Cohort 1936

Cognitive decline is among the most feared aspects of ageing. We have generated induced pluripotent stem cells (iPSCs) from 24 people from the Lothian Birth Cohort 1936, whose cognitive ability was tested in childhood and in older age. Peripheral blood mononuclear cells (PBMCs) were reprogrammed using non-integrating oriP/EBNA1 backbone plasmids expressing six iPSC reprogramming factors (OCT3/4 (POU5F1), SOX2, KLF4, L-Myc, shp53, Lin28, SV40LT). All lines demonstrated STR matched karyotype and pluripotency was validated by multiple methods. These iPSC lines are a valuable resource to study molecular mechanisms underlying individual differences in cognitive ageing and resilience to age-related neurodegenerative diseases

Parent-of-origin-specific allelic associations among 106 genomic loci for age at menarche.

Age at menarche is a marker of timing of puberty in females. It varies widely between individuals, is a heritable trait and is associated with risks for obesity, type 2 diabetes, cardiovascular disease, breast cancer and all-cause mortality. Studies of rare human disorders of puberty and animal models point to a complex hypothalamic-pituitary-hormonal regulation, but the mechanisms that determine pubertal timing and underlie its links to disease risk remain unclear. Here, using genome-wide and custom-genotyping arrays in up to 182,416 women of European descent from 57 studies, we found robust evidence (P < 5 × 10(-8)) for 123 signals at 106 genomic loci associated with age at menarche. Many loci were associated with other pubertal traits in both sexes, and there was substantial overlap with genes implicated in body mass index and various diseases, including rare disorders of puberty. Menarche signals were enriched in imprinted regions, with three loci (DLK1-WDR25, MKRN3-MAGEL2 and KCNK9) demonstrating parent-of-origin-specific associations concordant with known parental expression patterns. Pathway analyses implicated nuclear hormone receptors, particularly retinoic acid and γ-aminobutyric acid-B2 receptor signalling, among novel mechanisms that regulate pubertal timing in humans. Our findings suggest a genetic architecture involving at least hundreds of common variants in the coordinated timing of the pubertal transition

Comparing genotyping algorithms for Illumina's Infinium whole-genome SNP BeadChips

The Brassica napus 60K Illumina Infinium™ SNP array has had huge international uptake in the rapeseed community due to the revolutionary speed of acquisition and ease of analysis of this high-throughput genotyping data, particularly when coupled with the newly available reference genome sequence. However, further utilization of this valuable resource can be optimized by better understanding the promises and pitfalls of SNP arrays. We outline how best to analyze Brassica SNP marker array data for diverse applications, including linkage and association mapping, genetic diversity and genomic introgression studies. We present data on which SNPs are locus-specific in winter, semi-winter and spring B. napus germplasm pools, rather than amplifying both an A-genome and a C-genome locus or multiple loci. Common issues that arise when analyzing array data will be discussed, particularly those unique to SNP markers and how to deal with these for practical applications in Brassica breeding applications

Migration and Health: A Framework for 21st Century Policy-Making

In the introductory article to a six-part PLoS Medicine series on Migration & Health, series guest editors Cathy Zimmerman, Mazeda Hossain, and Ligia Kiss outline a migratory process framework that involves five phases: pre-departure, travel, destination, interception, and return

Synaptic processes and immune-related pathways implicated in Tourette syndrome

Tourette syndrome (TS) is a neuropsychiatric disorder of complex genetic architecture involving multiple interacting genes. Here, we sought to elucidate the pathways that underlie the neurobiology of the disorder through genome-wide analysis. We analyzed genome-wide genotypic data of 3581 individuals with TS and 7682 ancestry-matched controls and investigated associations of TS with sets of genes that are expressed in particular cell types and operate in specific neuronal and glial functions. We employed a self-contained, set-based association method (SBA) as well as a competitive gene set method (MAGMA) using individual-level genotype data to perform a comprehensive investigation of the biological background of TS. Our SBA analysis identified three significant gene sets after Bonferroni correction, implicating ligand-gated ion channel signaling, lymphocytic, and cell adhesion and transsynaptic signaling processes. MAGMA analysis further supported the involvement of the cell adhesion and trans-synaptic signaling gene set. The lymphocytic gene set was driven by variants in FLT3, raising an intriguing hypothesis for the involvement of a neuroinflammatory element in TS pathogenesis. The indications of involvement of ligand-gated ion channel signaling reinforce the role of GABA in TS, while the association of cell adhesion and trans-synaptic signaling gene set provides additional support for the role of adhesion molecules in neuropsychiatric disorders. This study reinforces previous findings but also provides new insights into the neurobiology of TS