Filtering by
Methods: Participants were recruited from the parent REasons for Geographic and Racial Differences in Stroke (REGARDS) Study. ActicalTM accelerometers provided estimates of PA variables, including moderate-to-vigorous PA (MVPA), high light PA (HLPA), low light PA (LLPA) and sedentary time, for 4-7 consecutive days. Prevalence and incidence of cognitive impairment were defined by the Six-Item Screener. Letter fluency, animal fluency, word list learning and Montreal Cognitive Assessment (orientation and recall) were conducted to assess executive function and memory.
Results: Of the 7,339 participants who provided accelerometer wear data > 4 days (70.1 ± 8.6 yr, 54.2% women, 31.7% African American), 320 participants exhibited impaired cognition. In cross-sectional analysis, participants in the highest MVPA% quartile had 39% lower odds of cognitive impairment than those in the lowest quartile (OR: 0.61, 95% C.I.: 0.39-0.95) after full adjustment. Further analysis shows most quartiles of MVPA% and HLPA% were significantly associated with executive function and memory (P<0.01). During 2.7 ± 0.5 years of follow-up, 3,385 participants were included in the longitudinal analysis, with 157 incident cases of cognitive impairment. After adjustments, participants in the highest MVPA% quartile had 51% lower hazards of cognitive impairment (HR: 0.49, 95% C.I.: 0.28-0.86). Additionally, MVPA% was inversely associated with change in memory z-scores (P<0.01), while the highest quartile of HLPA% was inversely associated with change in executive function and memory z-scores (P<0.01).
Conclusion: Higher levels of objectively measured MVPA% were independently associated with lower prevalence and incidence of cognitive impairment, and better memory and executive function in older adults. Higher levels of HLPA% were also independently associated with better memory and executive function. The amount of MVPA associated with lower risk of cognitive impairment (259 min/week) is >70% higher than the minimal amount of MVPA recommended by PA guidelines.
Vegetarian diets are typically more sustainable than omnivorous ones due to using less environmental resources in the production of food. An important consideration with plant protein and vegetarian diets, however, is whether this would affect athletic performance. To examine this, 70 male and female endurance athletes were compared for maximal oxygen uptake (VO2 max), peak torque when doing leg extensions, and body composition. Vegetarians had higher VO2 max, but peak torque was not significantly different by diet. Omnivores had higher total body mass, lean body mass, and there was a trend for peak torque to be higher.
To investigate whether plant-protein can comparably support development of lean body mass and strength development in conjunction with strength training, 61 healthy young males and females began a 12-week training and protein supplementation study. While previous training studies have shown no differences for lean body mass or strength development when consuming either soy (plant) or whey (animal) protein supplements in very large amounts (>48 grams), when consuming around 15-20 grams, whey has contributed to greater lean body mass accrual, although strength increases remain similar. The present study matched supplements by leucine content instead of by total protein amount since leucine has been shown to be a key stimulator of muscle protein synthesis and is more concentrated in animal protein. There were no significant differences between the whey or soy group for lean body mass or strength development, as assessed using isokinetic dynamometry doing leg extensions and flexions.
Background: Healthy individuals on the lower end of the insulin sensitivity spectrum also have a reduced gene expression response to exercise for specific genes. The goal of this study was to determine the relationship between insulin sensitivity and exercise-induced gene expression in an unbiased, global manner.
Methods and Findings: Euglycemic clamps were used to measure insulin sensitivity and muscle biopsies were done at rest and 30 minutes after a single acute exercise bout in 14 healthy participants. Changes in mRNA expression were assessed using microarrays, and miRNA analysis was performed in a subset of 6 of the participants using sequencing techniques. Following exercise, 215 mRNAs were changed at the probe level (Bonferroni-corrected P<0.00000115). Pathway and Gene Ontology analysis showed enrichment in MAP kinase signaling, transcriptional regulation and DNA binding. Changes in several transcription factor mRNAs were correlated with insulin sensitivity, including MYC, r=0.71; SNF1LK, r=0.69; and ATF3, r= 0.61 (5 corrected for false discovery rate). Enrichment in the 5’-UTRs of exercise-responsive genes suggested regulation by common transcription factors, especially EGR1. miRNA species of interest that changed after exercise included miR-378, which is located in an intron of the PPARGC1B gene.
Conclusions: These results indicate that transcription factor gene expression responses to exercise depend highly on insulin sensitivity in healthy people. The overall pattern suggests a coordinated cycle by which exercise and insulin sensitivity regulate gene expression in muscle.
Although insulin resistance in skeletal muscle is well-characterized, the role of circulating whole blood in the metabolic syndrome phenotype is not well understood. We set out to test the hypothesis that genes involved in inflammation, insulin signaling and mitochondrial function would be altered in expression in the whole blood of individuals with metabolic syndrome. We further wanted to examine whether similar relationships that we have found previously in skeletal muscle exist in peripheral whole blood cells. All subjects (n=184) were Latino descent from the Arizona Insulin Resistance registry. Subjects were classified based on the metabolic syndrome phenotype according to the National Cholesterol Education Program’s Adult Treatment Panel III. Of the 184 Latino subjects in the study, 74 were classified with the metabolic syndrome and 110 were without. Whole blood gene expression profiling was performed using the Agilent 4x44K Whole Human Genome Microarray. Whole blood microarray analysis identified 1,432 probes that were altered in expression ≥1.2 fold and P<0.05 after Benjamini-Hochberg in the metabolic syndrome subjects. KEGG pathway analysis revealed significant enrichment for pathways including ribosome, oxidative phosphorylation and MAPK signaling (all Benjamini-Hochberg P<0.05). Whole blood mRNA expression changes observed in the microarray data were confirmed by quantitative RT-PCR. Transcription factor binding motif enrichment analysis revealed E2F1, ELK1, NF-kappaB, STAT1 and STAT3 significantly enriched after Bonferroni correction (all P<0.05). The results of the present study demonstrate that whole blood is a useful tissue for studying the metabolic syndrome and its underlying insulin resistance although the relationship between blood and skeletal muscle differs.
Background: Although the effect of the fat mass and obesity-associated (FTO) gene on adiposity is well established, there is a lack of evidence whether physical activity (PA) modifies the effect of FTO variants on obesity in Latino populations. Therefore, the purpose of this study was to examine PA influences and interactive effects between FTO variants and PA on measures of adiposity in Latinos.
Results: After controlling for age and sex, participants who did not engage in regular PA exhibited higher BMI, fat mass, HC, and WC with statistical significance (P < 0.001). Although significant associations between the three FTO genotypes and adiposity measures were found, none of the FTO genotype by PA interaction assessments revealed nominally significant associations. However, several of such interactive influences exhibited considerable trend towards association.
Conclusions: These data suggest that adiposity measures are associated with PA and FTO variants in Latinos, but the impact of their interactive influences on these obesity measures appear to be minimal. Future studies with large sample sizes may help to determine whether individuals with specific FTO variants exhibit differential responses to PA interventions.
Background: Obesity is a metabolic disease caused by environmental and genetic factors. However, the epigenetic mechanisms of obesity are incompletely understood. The aim of our study was to investigate the role of skeletal muscle DNA methylation in combination with transcriptomic changes in obesity.
Results: Muscle biopsies were obtained basally from lean (n = 12; BMI = 23.4 ± 0.7 kg/m[superscript 2]) and obese (n = 10; BMI = 32.9 ± 0.7 kg/m[superscript 2]) participants in combination with euglycemic-hyperinsulinemic clamps to assess insulin sensitivity. We performed reduced representation bisulfite sequencing (RRBS) next-generation methylation and microarray analyses on DNA and RNA isolated from vastus lateralis muscle biopsies. There were 13,130 differentially methylated cytosines (DMC; uncorrected P < 0.05) that were altered in the promoter and untranslated (5' and 3'UTR) regions in the obese versus lean analysis. Microarray analysis revealed 99 probes that were significantly (corrected P < 0.05) altered. Of these, 12 genes (encompassing 22 methylation sites) demonstrated a negative relationship between gene expression and DNA methylation. Specifically, sorbin and SH3 domain containing 3 (SORBS3) which codes for the adapter protein vinexin was significantly decreased in gene expression (fold change −1.9) and had nine DMCs that were significantly increased in methylation in obesity (methylation differences ranged from 5.0 to 24.4 %). Moreover, differentially methylated region (DMR) analysis identified a region in the 5'UTR (Chr.8:22,423,530–22,423,569) of SORBS3 that was increased in methylation by 11.2 % in the obese group. The negative relationship observed between DNA methylation and gene expression for SORBS3 was validated by a site-specific sequencing approach, pyrosequencing, and qRT-PCR. Additionally, we performed transcription factor binding analysis and identified a number of transcription factors whose binding to the differentially methylated sites or region may contribute to obesity.
Conclusions: These results demonstrate that obesity alters the epigenome through DNA methylation and highlights novel transcriptomic changes in SORBS3 in skeletal muscle.