Deep Dive: VO2max ab 45 gezielt steigern

<h4>Introduction</h4>As wearable technology becomes increasingly popular and sophisticated, independent validation is needed to determine its accuracy and potential applications. Therefore, the purpose of this study was to evaluate the accuracy (validity) of VO2max estimates and blood oxygen saturation measured via pulse oximetry using the Garmin fēnix 6 with a general population participant pool.<h4>Methods</h4>We recruited apparently healthy individuals (both active and sedentary) for VO2max (n = 19) and pulse oximetry testing (n = 22). VO2max was assessed through a graded exercise test and an outdoor run, comparing results from the Garmin fēnix 6 to a criterion measurement obtained from a metabolic system. Pulse oximetry involved comparing fēnix 6 readings under normoxic and hypoxic conditions against a medical-grade pulse oximeter. Data analysis included descriptive statistics, error analysis, correlation analysis, equivalence testing, and bias assessment, with the validation criteria set at a concordance correlation coefficient (CCC) > 0.7 and a mean absolute percentage error (MAPE) < 10%.<h4>Results</h4>The Garmin fēnix 6 provided accurate VO2max estimates, closely aligning with the 15 s and 30 s averaged laboratory data (MAPE for 30 s avg = 7.05%; Lin's concordance correlation coefficient for 30 s avg = 0.73). However, it failed to accurately measure blood oxygen saturation (BOS) under any condition or combined analysis (MAPE for combined conditions BOS = 4.29%; Lin's

Cardiorespiratory fitness (CRF) has a strong genetic component and low CRF is a major risk factor for cardiovascular morbidity and mortality. The purpose of this study was to develop and validate a polygenic score (PGS) for CRF (CRF_PGS) and assess its associations with cardiovascular disease (CVD) and all-cause mortality. We hypothesized that the CRF_PGS would demonstrate similar cardioprotective benefits as the CRF phenotype. Effect estimates from a genome-wide association study on directly measured CRF in the Trøndelag Health Study (HUNT; n = 4525) were used in a Bayesian regression framework to develop multiple PGSs in an independent cohort from the UK Biobank (n = 65,165). The top performing score was applied in the HUNT target cohort, excluding the discovery sample (n = 82,109). The PGS-CRF association varied considerably as a function of model fit and phenotypic accuracy. There was a difference of 1.55 [95% confidence interval: 1.26, 1.84]  mL·kg^-1·min^-1 between the bottom and top decile of the CRF_PGS. Moreover, a high CRF_PGS demonstrated cardioprotective effects, with reduced risk for CVD, myocardial infarction, hypertension, and all-cause mortality. Additionally, in women, we observed that the CRF_PGS predisposed to lower risk of heart failure and hypertrophic cardiomyopathy. We developed the first PGS for CRF using gold standard phenotypes and multiple independent cohorts. Genetic susceptibili

<h4>Background</h4>Cardiorespiratory fitness (CRF) has been linked to lower risk of individual chronic diseases, but little is known about the CRF in relation to multimorbidity.<h4>Objectives</h4>The authors investigated the association between CRF and multimorbidity risk and explored differences in the trajectories of chronic disease accumulation at varying levels of CRF.<h4>Methods</h4>The study included 38,348 adults from the UK Biobank (mean age 55.21 ± 8.15 years; 51.95% female) who were followed for up to 15 years to detect the incidence of 59 common chronic diseases. CRF was estimated using a 6-minute submaximal exercise test and tertiled as low, moderate, and high (after standardization by age and sex). Multimorbidity was defined as the presence of 2 or more chronic diseases. Data were analyzed using Cox regression, Laplace regression, and linear mixed-effects models.<h4>Results</h4>During the follow-up (median [IQR]: 11.57 [7.39-11.76] years), 15,368 (40.08%) participants developed multimorbidity. The risk of multimorbidity was 21% lower in participants with high compared to low CRF (HR: 0.79 [95% CI: 0.76-0.83]). The median time to multimorbidity onset was 1.27 (95% CI: 1.01-1.54) years later for those with high compared to low CRF. Moreover, participants with high CRF experienced a significantly slower annual rate of chronic disease accumulation (β = -0.043 [-0.050 to -0.036]).<h4>Conclusions</h4>High CRF is associated with lower multimorbidity risk, delayed onset

<b>Background:</b> Cardiorespiratory fitness plays a crucial role in cardiovascular health; however, its effects on adverse cardiovascular outcomes across different diseases remain poorly defined. Specifically, the differential impact of cardiorespiratory fitness on patients with and without atrial fibrillation (AF) is yet to be fully understood. This study aimed to explore the relationships between resting heart rate (RHR), maximal heart rate (HRmax), and maximal oxygen uptake (VO₂max) in relation to adverse cardiovascular outcomes, providing valuable insights to inform exercise prescriptions and cardiac rehabilitation practices. <b>Methods:</b> Participants were classified into two groups: those with AF diagnosed prior to baseline (AF group) and those without AF at baseline (non-AF group). In the AF group, outcomes included heart failure (HF), stroke, and all-cause mortality; in the non-AF group, incident AF, stroke, HF, and mortality were assessed. Associations between cardiorespiratory indices-RHR, HRmax, and VO₂max-and adverse cardiovascular events were evaluated using Cox proportional hazards models. Dose-response relationships were examined via restricted cubic spline (RCS) models with three knots. <b>Results:</b> In the non-AF population, higher resting heart rate was significantly associated with an increased risk of adverse cardiovascular outcomes, including heart failure (HF: HR = 1.008, 95% CI 1.001-1.014, P = 0.0182), stroke (HR = 1.010, 95% CI 1.004-1.016, P = 0

Sudden cardiac death (SCD) remains one of the most devastating manifestations of cardiovascular disease. While traditional risk stratification has focused on structural heart disease and electrophysiological markers, growing evidence suggests that modifiable lifestyle factors-particularly physical activity (PA) and cardiorespiratory fitness (CRF)-play a critical role in mitigating the risk of SCD. This narrative review synthesizes evidence on the associations between PA, CRF, and SCD risk. It explores potential biological mechanisms underlying these relationships, identifies key gaps in the literature, and discusses the clinical and public health implications. A substantial body of prospective cohort studies and meta-analyses demonstrates a strong, inverse, and dose-dependent association between both PA and CRF and the risk of SCD. Engaging in ⩾4 hours/week of moderate-to-vigorous PA or achieving CRF levels of ⩾8 to 10 METs is associated with 40% to 50% reductions in SCD risk. CRF also modifies the risk conferred by traditional cardiovascular risk factors such as hypertension, diabetes, and systemic inflammation. Proposed mechanisms include favorable modulation of cardiovascular risk profiles, improved autonomic regulation, anti-arrhythmic and anti-ischemic effects, and enhanced myocardial function. However, evidence gaps persist regarding causal inference (absence of Mendelian randomization studies), optimal PA and CRF thresholds, sex- and age-specific effects, and interacti