Project description:We sought to determine skeletal muscle genome-wide DNA methylation and transcriptome changes to one bout of lower-load (LL) versus higher-load (HL) resistance exercise. Previously trained college-aged males (n=11, age: 23±4 years old, training experience: 4 ± 3 years) performed LL or HL bouts to failure separated by one week. The HL bout (a.k.a., 80 Fail) consisted of four sets of back squats and four sets of leg extensions to failure using 80% of their estimated one-repetition maximum (i.e., est. 1-RM from 3-RM testing), whereas the LL bout (a.k.a., 30 Fail) consisted of this same paradigm using 30% of their est. 1-RM. Vastus lateralis muscle biopsies were collected before, 3 hours, and 6 hours after each exercise bout. DNA and RNA were batch-isolated from muscle and analyzed for genome-wide DNA methylation and mRNA expression using the 850k Illumina MethylationEPIC array and Clariom S mRNA microarray, respectively. Although the total number of repetitions performed were significantly greater during the 30 Fail versus 80 Fail bout (p<0.001), total training volume (sets x reps x load) was not significantly different between conditions (p=0.571). Interestingly, 30 Fail led to decreased methylation across various promoter regions, albeit the transcriptome-wide responses between bouts were largely similar. According to bioinformatics, both bouts altered post-exercise mRNA profiles related to inflammatory signaling (e.g., Toll receptor, CCKR, chemokine and cytokine signaling), apoptosis, gonadotropin-releasing hormone, and integrin signaling. Also notable, more robust DNA methylation events occurred 3 hours versus 6 hours post-exercise regardless of bout (239,951 versus 12,419 CpG sites significantly hyper- or hypomethylated at these respective time points, p<0.01). Moreover, the percentage of significantly altered mRNAs that also demonstrated significantly inversed methylation patterns across one or more CpG sites was appreciably higher at 3 hours versus 6 hours following exercise (~75% versus ~15%, respectively). In conclusion, our transcriptomic data suggest that the molecular signaling events during the early post-exercise period are largely similar between LL and HL bouts, and this may explain why similar longer-term phenotypes (e.g., myofiber hypertrophy) result from these two training modalities. Additionally, our methylome data indicate that the majority of DNA methylation changes following an acute bout of resistance exercise occur rapidly (~3 hours) following exercise in previously trained men.

Project description:We sought to determine the skeletal muscle genome-wide DNA methylation and mRNA respons-es to one bout of lower-load (LL) versus higher-load (HL) resistance exercise. Trained col-lege-aged males (n=11, 23±4 years old, 4±3 years self-reported training) performed LL or HL bouts to failure separated by one week. The HL bout (i.e., 80 Fail) consisted of four sets of back squats and four sets of leg extensions to failure using 80% of participants estimated one-repetition maximum (i.e., est. 1-RM). The LL bout (i.e., 30 Fail) implemented the same paradigm with 30% of est. 1-RM. Vastus lateralis muscle biopsies were collected before, 3 hours, and 6 hours after each bout. Muscle DNA and RNA were batch-isolated and analyzed using the 850k Illumina Methyl-ationEPIC array and Clariom S mRNA microarray, respectively. Performed repetitions were sig-nificantly greater during the 30 Fail versus 80 Fail (p<0.001), although total training volume (sets x reps x load) was not significantly different between bouts (p=0.571). Regardless of bout, more CpG site methylation changes were observed at 3- versus 6-hours post exercise (239,951 versus 12,419, respectively; p<0.01), and nuclear global ten-eleven translocation (TET) activity, but not global DNA methyltransferase activity, increased 3- and 6-hours following exercise regardless of bout. The percentage of genes significantly altered at the mRNA level that demonstrated opposite DNA methylation patterns was greater 3- versus 6-hours following exercise (~75% versus ~15%, respectively). Moreover, high percentages of genes that were up- or downregulated 6 hours fol-lowing exercise also demonstrated significantly inversed DNA methylation patterns across one or more CpG sites 3 hours following exercise (65% and 82%, respectively). While 30 Fail de-creased DNA methylation across various promoter regions versus 80 Fail, transcriptome-wide mRNA and bioinformatics indicated that gene expression signatures were largely similar be-tween bouts. Bioinformatics overlay of DNA methylation and mRNA expression data indicated that genes related to “Focal adhesion”, “MAPK signaling”, and “PI3K-Akt signaling” were sig-nificantly affected at the 3- and 6-hour time points, and again this was regardless of bout. In con-clusion, extensive molecular profiling suggests that post-exercise alterations in the skeletal muscle DNA methylome and mRNA transcriptome elicited by LL and HL training bouts to failure are largely similar, and this could be related to equal volumes performed between bouts.

Project description:We sought to determine the skeletal muscle genome-wide DNA methylation and mRNA responses to one bout of lower load (LL) versus higher load (HL) resistance exercise. Trained college-aged males (n = 11, 23 ± 4 years old, 4 ± 3 years self-reported training) performed LL or HL bouts to failure separated by one week. The HL bout (i.e., 80 Fail) consisted of four sets of back squats and four sets of leg extensions to failure using 80% of participants estimated one-repetition maximum (i.e., est. 1-RM). The LL bout (i.e., 30 Fail) implemented the same paradigm with 30% of est. 1-RM. Vastus lateralis muscle biopsies were collected before, 3 h, and 6 h after each bout. Muscle DNA and RNA were batch-isolated and analyzed using the 850k Illumina MethylationEPIC array and Clariom S mRNA microarray, respectively. Performed repetitions were significantly greater during the 30 Fail versus 80 Fail (p < 0.001), although total training volume (sets × reps × load) was not significantly different between bouts (p = 0.571). Regardless of bout, more CpG site methylation changes were observed at 3 h versus 6 h post exercise (239,951 versus 12,419, respectively; p < 0.01), and nuclear global ten-eleven translocation (TET) activity, but not global DNA methyltransferase activity, increased 3 h and 6 h following exercise regardless of bout. The percentage of genes significantly altered at the mRNA level that demonstrated opposite DNA methylation patterns was greater 3 h versus 6 h following exercise (~75% versus ~15%, respectively). Moreover, high percentages of genes that were up- or downregulated 6 h following exercise also demonstrated significantly inversed DNA methylation patterns across one or more CpG sites 3 h following exercise (65% and 82%, respectively). While 30 Fail decreased DNA methylation across various promoter regions versus 80 Fail, transcriptome-wide mRNA and bioinformatics indicated that gene expression signatures were largely similar between bouts. Bioinformatics overlay of DNA methylation and mRNA expression data indicated that genes related to "Focal adhesion," "MAPK signaling," and "PI3K-Akt signaling" were significantly affected at the 3 h and 6 h time points, and again this was regardless of bout. In conclusion, extensive molecular profiling suggests that post-exercise alterations in the skeletal muscle DNA methylome and mRNA transcriptome elicited by LL and HL training bouts to failure are largely similar, and this could be related to equal volumes performed between bouts.

Project description:BACKGROUND:There are animal data suggesting green tea can enhance blood flow. However, human data are lacking. Thus, the purpose of this study was to examine the acute effects of low and high doses of a green tea-based supplement (GBS) on brachial artery blood flow before and following a resistance exercise bout. METHODS:In this, double-blinded placebo-controlled trial, college-aged males (n = 18) who self-reported recreationally resistance training for the previous 6 ± 3 years were assigned to one of two studies including a low (300 mg serving) (n = 9) or high dose (600 mg serving) (n = 8; 1 drop) GBS study. During testing sessions, participants reported to the laboratory following an overnight fast and rested in a supine position for 15 min. Thereafter, baseline measurements for resting heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), brachial artery diameter (BAD) and blood flow (BBF) were obtained (PRE). Participants then consumed either their respective GBS dose or a similar placebo dose (microcrystalline cellulose) in a supine resting state. HR, SBP, DBP, BAD and BBF were measured 45 min after placebo or GBS ingestion (PRE2). Participants were then placed in a recumbent position and performed 4 sets of 10 arm curl repetitions using an 11 kg dumbbell. Participants returned to a supine position and HR, SBP, DBP, BAD and BBF were obtained within the first 3 min following exercise (POST), 15 min after exercise (15POST), and 45 min after exercise (45POST). Participants returned to the laboratory 24-48 h later to repeat the same protocol with either GBS or the placebo depending on randomization. Two-way (supplement x time) repeated measures ANOVAs were used to compare dependent variables between testing sessions for Study 1 (300 mg of GBS and placebo) and Study 2 (600 mg of GBS and placebo), and statistical significance was set at p < 0.05. No statistical comparisons were made between studies. RESULTS:As expected, exercise increased BAD and BBF compared to resting baseline measured irrespective of supplementation. In addition, BAD and BBF did not differ between GBS and placebo at any time point after exercise in Study 1. In study 2, however, 600 mg GBS increased baseline-normalized BBF at immediately post exercise compared to placebo (placebo = 211 ± 155% increase, GBS = 349 ± 156% increase; p = 0.012) but not BAD. CONCLUSIONS:These data suggest a higher dose of GBS can enhance localized blood flow acutely following a resistance exercise bout. However, the long-term implications of these data are unclear, and more well-powered studies are needed to validate efficacy and elucidate potential mechanisms.

Project description:New findingsWhat is the central question of this study? What are the effects of compression garments on recovery from unaccustomed damaging exercise and subsequent protective adaptations? What is the main finding and its importance? Compression did not influence recovery, but was associated with blunted protective adaptations for isokinetic performance, which were completely absent at high velocities. Based on these findings, the use of compression garments for recovery would not be recommended following unaccustomed exercise, particularly if the maintenance of high-velocity performance following exercise-induced muscle damage is desirable.AbstractWhilst compression garments (CG) may enhance recovery from exercise-induced muscle damage (EIMD), many recovery strategies can attenuate adaptative responses. Therefore, the effects of CG on recovery from EIMD, and the rapid protective adaptations known as the repeated bout effect (RBE) were investigated. Thirty-four non-resistance-trained males (18-45 years) randomly received class II medical-grade CG or placebo for 72 h following eccentrically-focused lower-body exercise, in a double-blind, randomised controlled trial. Indices of EIMD were assessed at baseline, 0, 24, 48 and 72 h post-exercise, before exercise and testing were repeated after 14 days. Results were analysed using a three-way (time × condition × bout) linear mixed-effects model. Exercise impaired isometric and isokinetic strength, with soreness and thigh circumference elevated for 72 h (P < 0.001). Compression did not enhance recovery (P > 0.05), despite small to moderate effect sizes (ES, reported alongside 90% confidence intervals) for isokinetic strength (ES from 0.2 [-0.41, 0.82] to 0.65 [0.03, 1.28]). All variables recovered faster after the repeated bout (P < 0.005). However, RBE for peak isokinetic force was impaired in CG at 60° s-1 (group × bout interaction: χ2 = 4.24, P = 0.0395; ES = -0.56 [-1.18, 0.07]) and completely absent at 120° s-1 (χ2 = 16.2, P < 0.001, ES = -0.96 [-1.61, -0.32]) and 180° s-1 (χ2 = 10.4, P = 0.001, ES = -0.72 [-1.35, -0.09]). Compression blunted RBE at higher isokinetic velocities without improving recovery in non-resistance-trained males, potentially contraindicating their use following unaccustomed exercise in this population.

Project description:Deleterious mutations occur frequently in eukaryotes, resulting in individuals carrying multiple alleles that decrease their fitness. At a population level, if unchecked, accumulation of this mutation load can ultimately lead to extinction. How selection counters the accumulation of mutation load, limiting declines in population fitness, is not well understood. Here, we use manipulative experiments in zebrafish (Danio rerio) to investigate the opportunities for selection on mutation load. Inducing high mutation load through mutagenesis, we applied one generation of within-family selection on locomotor performance and characterized both the direct response to this selection and the indirect response of reproductive success. Offspring of slow swimming parents exhibited age-dependent declines in swimming speed, whereas their cousins, with faster swimming parents, did not. This pattern mimics previously documented differences between high and low mutation load populations of zebrafish, suggesting that slow swimming siblings inherited (and transmitted) more mutations than their faster swimming siblings. Crosses among offspring of slow swimming fish had, on average, <75% of the reproductive success of crosses among offspring of fast swimming parents, or crosses of offspring of slow swimmers with offspring of fast swimmers. This evidence of mutationally correlated swimming speed and reproductive success reveals the potential for concordant selection on mutation load through different fitness components. There was no evidence that crosses within families (where parents potentially shared the same mutations inherited from their common ancestor) had lower reproductive success than crosses among families, suggesting that viability selection was not acting predominantly through lethal recessive homozygotes. Rather, patterns of reproductive success are suggestive of effects of mutation number per se on embryo viability. Overall, our results highlight the potential for early life mortality to remove deleterious mutations, and the need to account for this mortality when investigating the evolutionary dynamics of mutation load.

Project description:While high-load resistance training increases muscle hypertrophy, the intramuscular protein responses to this form of training remains largely unknown. In the current study, recreationally resistance-trained college-aged males (N = 15; mean ± SD: 23 ± 3 years old, 6 ± 5 years training) performed full-body, low-volume, high-load [68-90% of one repetition maximum (1RM)] resistance training over 10 weeks. Back squat strength testing, body composition testing, and a vastus lateralis biopsy were performed before (PRE) and 72 h after the 10-week training program (POST). Fiber type-specific cross-sectional area (fCSA), myofibrillar protein concentrations, sarcoplasmic protein concentrations, myosin heavy chain and actin protein abundances, and muscle tissue percent fluid were analyzed. The abundances of individual sarcoplasmic proteins in 10 of the 15 participants were also assessed using proteomics. Significant increases (p < 0.05) in type II fCSA and back squat strength occurred with training, although whole-body fat-free mass paradoxically decreased (p = 0.026). No changes in sarcoplasmic protein concentrations or muscle tissue percent fluid were observed. Myosin heavy chain protein abundance trended downward (-2.9 ± 5.8%, p = 0.069) and actin protein abundance decreased (-3.2 ± 5.3%, p = 0.034) with training. Proteomics indicated only 13 sarcoplasmic proteins were altered with training (12 up-regulated, 1 down-regulated, p < 0.05). Bioinformatics indicated no signaling pathways were affected, and proteins involved with metabolism (e.g., ATP-PCr, glycolysis, TCA cycle, or beta-oxidation) were not affected. These data comprehensively describe intramuscular protein adaptations that occur following 10 weeks of high-load resistance training. Although previous data from our laboratory suggests high-volume resistance training enhances the ATP-PCr and glycolytic pathways, we observed different changes in metabolism-related proteins in the current study with high-load training.

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Genome-wide DNA methylation and mRNA responses to a bout of higher versus lower load resistance training in previously trained men

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