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Do exercise-associated genes explain phenotypic variance in the three components of fitness? a systematic review & meta-analysis.

ABSTRACT: The aim of this systematic review and meta-analysis was to identify a list of common, candidate genes associated with the three components of fitness, specifically cardiovascular fitness, muscular strength, and anaerobic power, and how these genes are associated with exercise response phenotype variability, in previously untrained participants. A total of 3,969 potentially relevant papers were identified and processed for inclusion. After eligibility and study selection assessment, 24 studies were selected for meta-analysis, comprising a total of 3,012 participants (male n = 1,512; females n = 1,239; not stated n = 261; age 28 ± 9 years). Meta-Essentials spreadsheet 1.4 (Microsoft Excel) was used in creating the forest plots and meta-analysis. IBM SPSS statistics V24 was implemented for the statistical analyses and the alpha was set at p ≤ 0.05. 13 candidate genes and their associated alleles were identified, which were associated with the phenotypes of interest. Analysis of training group data showed significant differential phenotypic responses. Subgroup analysis showed; 44%, 72% and 10% of the response variance in aerobic, strength and power phenotypes, respectively, were explained by genetic influences. This analysis established that genetic variability explained a significant proportion of the adaptation differences across the three components of fitness in the participants post-training. The results also showed the importance of analysing and reporting specific gene alleles. Information obtained from these findings has the potential to inform and influence future exercise-related genes and training studies.

SUBMITTER: Chung HC

PROVIDER: S-EPMC8516263 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundDiurnal variation in blood pressure (BP) is regulated, in part, by an endogenous circadian clock; however, few human studies have identified associations between clock genes and BP. Accounting for environmental temperature may be necessary to correct for seasonal bias.MethodsWe examined whether environmental temperature on the day of participants' assessment was associated with BP, using adjusted linear regression models in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) (n = 819) and the Boston Puerto Rican Health Study (BPRHS) (n = 1,248) cohorts. We estimated phenotypic variance in BP by 18 clock genes and examined individual single-nucleotide polymorphism (SNP) associations with BP using an additive genetic model, with further consideration of environmental temperature.ResultsIn GOLDN, each additional 1 °C increase in environmental temperature was associated with 0.18 mm Hg lower systolic BP [SBP; β ± SE = -0.18 ± 0.05 mm Hg; P = 0.0001] and 0.10mm Hg lower diastolic BP [DBP; -0.10 ± 0.03 mm Hg; P = 0.001]. Similar results were seen in the BPRHS for SBP only. Clock genes explained a statistically significant proportion of the variance in SBP [V G/V P ± SE = 0.071 ± 0.03; P = 0.001] in GOLDN, but not in the BPRHS, and we did not observe associations between individual SNPs and BP. Environmental temperature did not influence the identified genetic associations.ConclusionsWe identified clock genes that explained a statistically significant proportion of the phenotypic variance in SBP, supporting the importance of the circadian pathway underlying cardiac physiology. Although temperature was associated with BP, it did not affect results with genetic markers in either study. Therefore, it does not appear that temperature measures are necessary for interpreting associations between clock genes and BP.Clinical trial registrationTrials related to this study were registered at clinicaltrials.gov as NCT00083369 (Genetic and Environmental Determinants of Triglycerides) and NCT01231958 (Boston Puerto Rican Health Study).

Project description:Background: Sarcopenia is a muscle disease in loss of muscle strength, mass, and function associated with aging. Although protective effects of exercise on muscle mass and function are generally recognized, research findings in sarcopenic adults are inconsistent. It is necessary to conduct a systematic review to determine the effects of exercise on muscle strength, body composition, and physical performance in older adults with sarcopenia, and to examine the potential moderators including sociodemographic characteristics and exercise-related factors. Methods: Six electronical academic databases (Medline, Embase, CINAHL, Scopus, Cochrane Library, and SPORTDiscus) were used to retrieve the eligible studies from inception to May 2020. Two reviewers independently selected and extracted the data from each included study, and effect sizes were calculated by employing random-effect models with 95% confidential interval (CI). The Physiotherapy Evidence Database (PEDro) scale was used to assess study quality. Results: Seventeen studies (985 participants with sarcopenia, aged 67.6-86 years) were included in this review study. The meta-analytic results showed significant improvements in muscle strength [grip strength, SMD = 0.30, 95% CI (0.15, 0.45), I 2 = 6%, p < 0.01; knee extension, SMD = 0.32, 95% CI (0.15, 0.50), I 2 = 0%, p < 0.01; and chair and stand, SMD = 0.56, 95% CI (0.30, 0.81), I 2 = 36%, p < 0.01], in physical performance [timed up and go, SMD = 0.74, 95% CI (0.48, 1.00), I 2 = 0%, p < 0.01; and gait speed, SMD = 0.59, 95% CI (0.35, 0.82), I 2 = 62%, p < 0.01], and in body composition [skeletal muscle mass index, SMD = 0.37, 95% CI (0.15, 0.58), I 2 = 16%, p < 0.01; and appendicular skeletal muscle, SMD = 0.31, 95% CI (0.13, 0.49), I 2 = 20%, p < 0.01]. However, there were no significant differences in other body composition (SMD = 0.20-0.36). Additionally, meta-regression revealed that the higher percent of female participants was significantly associated with improved gait speed (β = 0.0096, p = 0.03) and decreased skeletal muscle mass index (β = -0.0092, p = 0.01). Conclusions: The current meta-analysis suggests that exercise is a beneficial therapy, which has protective effects for older adults with sarcopenia. Some beneficial effects may be moderated by gender and exercise intensity.

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Do exercise-associated genes explain phenotypic variance in the three components of fitness? a systematic review & meta-analysis.

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