Dataset Information

Aerobic Training Protects Cardiac Function During Advancing Age: A Meta-Analysis of Four Decades of Controlled Studies.

ABSTRACT:

Background

In contrast to younger athletes, there is comparatively less literature examining cardiac structure and function in older athletes. However, a progressive accumulation of studies during the past four decades offers a body of literature worthy of systematic scrutiny.

Objectives

We conducted a systematic review, meta-analysis and meta-regression of controlled echocardiography studies comparing left ventricular (LV) structure and function in aerobically trained older athletes (> 45 years) with age-matched untrained controls, in addition to investigating the influence of chronological age.

Methods

Electronic databases were searched from inception to January 2018 before conducting a random-effects meta-analysis to calculate pooled differences in means, effect size and 95% confidence intervals (CIs). Study heterogeneity was reported using Cochran's Q and I² statistic.

Results

Overall, 32 studies (644 athletes; 582 controls) were included. Athletes had greater LV end-diastolic diameter (3.65 mm, 95% CI 2.66-4.64), interventricular septal thickness (1.23 mm, 95% CI 0.85-1.60), posterior wall thickness (1.20 mm, 95% CI 0.83-1.56), LV mass (72 g, 95% CI 46-98), LV mass index (28.17 g·m², 95% CI 19.84-36.49) and stroke volume (13.59 mL, 95% CI 7.20-19.98) (all p < 0.01). Athletes had superior global diastolic function [ratio of early (E) to late (A) mitral inflow velocity (E/A) 0.18, 95% CI 0.13-0.24, p < 0.01; ratio of early (e') to late (a') diastolic annular tissue velocity (e'/a') 0.23, 95% CI 0.06-0.40, p = 0.01], lower A (-8.20 cm·s^-1, 95% CI -11.90 to -4.51, p < 0.01) and a' (-0.72 cm·s^-1, 95% CI -1.31 to -0.12, p = 0.02), and more rapid e' (0.96 cm·s^-1, 95% CI 0.05-1.86, p = 0.04). Meta-regression for chronological age identified that athlete-control differences, in the main, are maintained during advancing age.

Conclusions

Athletic older men have larger cardiac dimensions and enjoy more favourable cardiac function than healthy, non-athletic counterparts. Notably, the athlete groups maintain these effects during chronological ageing.

SUBMITTER: Beaumont AJ

PROVIDER: S-EPMC6513799 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature

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Publications

Aerobic Training Protects Cardiac Function During Advancing Age: A Meta-Analysis of Four Decades of Controlled Studies.

Beaumont Alexander J AJ Grace Fergal M FM Richards Joanna C JC Campbell Amy K AK Sculthorpe Nicholas F NF

Sports medicine (Auckland, N.Z.) 20190201 2

<h4>Background</h4>In contrast to younger athletes, there is comparatively less literature examining cardiac structure and function in older athletes. However, a progressive accumulation of studies during the past four decades offers a body of literature worthy of systematic scrutiny.<h4>Objectives</h4>We conducted a systematic review, meta-analysis and meta-regression of controlled echocardiography studies comparing left ventricular (LV) structure and function in aerobically trained older athle ...[more]

PMID: 30374946

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Project description:ObjectiveCardiac function declines with age, impairing exercise tolerance and negatively impacting healthy aging. However, mechanisms driving age-related declines in cardiac function are not fully understood.MethodsWe examined mechanisms underlying age-related cardiac dysfunction using 3- and 24-month-old wild-type mice fed ad libitum or 24-month-old wild-type mice subjected to 70% calorie restriction (CR) starting at 2-month-old. In addition, cardiac aging phenotypes and mitochondrial biogenesis were also analyzed in 25-month-old cardiac-specific Hint1 knockout mice, 24-month-old CAG-Caren Tg mice, and 24-month-old wild-type mice injected with AAV6-Caren.ResultsWe observed inactivation of mitochondrial biogenesis in hearts of aged mice. We also showed that activity of the BAF chromatin remodeling complex is repressed by HINT1, whose expression in heart increases with age, leading to decreased transcription of Tfam, which promotes mitochondrial biogenesis. Interestingly, CR not only suppressed age-related declines in cardiac function and mitochondrial biogenesis but blocked concomitant increases in cardiac HINT1 protein levels and maintained Tfam transcription. Furthermore, expression of the lncRNA Caren, which inhibits Hint1 mRNA translation, decreased with age in heart, and CR suppressed this effect. Finally, decreased HINT1 expression due to Caren overexpression antagonized age-related declines in mitochondrial biogenesis, ameliorating age-related cardiac dysfunction, exercise intolerance, and exercise-induced cardiac damage and subsequent death of mice.ConclusionOur findings suggest that mitochondrial biogenesis in cardiomyocytes decreases with age and could underlie cardiac dysfunction, and that the Caren-HINT1-mitochondrial biogenesis axis may constitute a mechanism linking CR to resistance to cardiac aging. We also show that ameliorating declines in mitochondrial biogenesis in cardiomyocytes could counteract age-related declines in cardiac function, and that this strategy may improve exercise tolerance and extend so-called "healthy life span".

Project description:Aerobic exercise confers sustainable protection against cardiac hypertrophy and heart failure (HF). Nitric oxide synthase (NOS) and nitric oxide (NO) are known to play an important role in exercise-mediated cardioprotection, but the mechanism of NOS/NO stimulation during exercise remains unclear. The aim of this study is to determine the role of β3-adrenergic receptors (β3-ARs), NOS activation, and NO metabolites (nitrite and nitrosothiols) in the sustained cardioprotective effects of aerobic exercise. An HF model was constructed by transverse aortic constriction (TAC). Animals were treated with either moderate aerobic exercise by swimming for 9 weeks and/or the β3-AR-specific inhibitor SR59230A at 0.1 mg/kg/hour one day after TAC operation. Myocardial fibrosis, myocyte size, plasma catecholamine (CA) level, cardiac function and geometry were assessed using Masson's trichrome staining, FITC-labeled wheat germ agglutinin staining, enzyme-linked immuno sorbent assay (ELISA) and echocardiography, respectively. Western blot analysis was performed to elucidate the expression of target proteins. The concentration of myocardial NO production was evaluated using the nitrate reductase method. Myocardial oxidative stress was assessed by detecting the concentration of myocardial super oxidative dismutase (SOD), malonyldialdehyde (MDA), and reactive oxygen species (ROS). Aerobic exercise training improved dilated left ventricular function and partially attenuated the degree of cardiac hypertrophy and fibrosis in TAC mice. Moreover, the increased expression of β3-AR, activation of neuronal NOS (nNOS), and production of NO were detected after aerobic exercise training in TAC mice. However, selective inhibition of β3-AR by SR59230A abolished the upregulation and activation of nNOS induced NO production. Furthermore, aerobic exercise training decreased the myocardial ROS and MDA contents and increased myocardial levels of SOD; both effects were partially attenuated by SR59230A. Our study suggested that aerobic exercise training could improve cardiac systolic function and alleviate LV chamber dilation, cardiac fibrosis and hypertrophy in HF mice. The mechanism responsible for the protective effects of aerobic exercise is associated with the activation of the β3-AR-nNOS-NO pathway.

Dataset Information

Aerobic Training Protects Cardiac Function During Advancing Age: A Meta-Analysis of Four Decades of Controlled Studies.

Background

Objectives

Methods

Results

Conclusions

Publications

Aerobic Training Protects Cardiac Function During Advancing Age: A Meta-Analysis of Four Decades of Controlled Studies.

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