Purpose We sought to describe leisure-time, aerobic, and muscle strengthening physical activity (PA) patterns in U.S. Asian Indians, in comparison to other races/ethnicities. Design, Setting, and Sample We utilized the 2011–2018 National Health Interview Surveys, a set of cross-sectional, nationally representative surveys of the U.S. noninstitutionalized population. Our study population included 257 652 adults who answered PA questions. Measures PA was classified per 2008 U.S. guidelines and continuously per estimated metabolic equivalents (METs). Race was classified into White, Black, Asian Indian, Other Asian, and American Indian/Alaskan Native/Multiracial. Analysis We used survey design-adjusted, multivariable logistic regression to determine odds of sufficient and highly active physical activity levels, adjusting for predisposing, enabling, need, and health care service factors as guided by the Anderson Model. We also used linear regression to determine racial differences in average MET-minutes/week. Analysis was additionally stratified by comorbidity status. Results While Asian Indians (N = 3049) demonstrated similar odds of sufficient aerobic PA as Whites (aOR [95% CI]: .97 [.88,1.07]), Asian Indians had 22% lower odds of meeting highly active aerobic PA levels (.78 [.71,0.87]) and 18% lower odds of meeting sufficient muscle strengthening PA levels (.82 [.73,0.91]). This translated to an average 172 (95% CI: 45 300) fewer MET-minutes. Furthermore, this decrease in MET-minutes/week was especially apparent in those without hypertension (β[95% CI]: −164 [-314,-15]) without diabetes (−185 [-319,-52]), and low/normal BMI (−422 [-623,-222]). Conclusion Asian Indians, especially those without comorbidities, are less likely to engage in high-intensity physical activity than Whites.

Introduction: Both blood pressure and heart rate (HR) are important factors that constitute hemodynamic status. Hypothesis: We aimed to determine whether HR was independently associated with all-cause mortality and whether HR modified the association between systolic blood pressure (SBP) and all-cause mortality. Methods: We included adults aged ≥20 years from the 1999-2018 National Health and Nutrition Examination Surveys without cardiovascular disease, chronic kidney disease, chronic obstructive pulmonary disease, cancer, asthma, or beta blocker use. Resting HR was categorized into 10 beats-per-min increments, and SBP in 10-20 mmHg increments as shown in Table 1. Our primary outcome was all-cause mortality, determined using linkage to the National Death Index through 2019. We used multivariable Cox regression, stratified by HTN status and adjusted for the survey design. Results: Among 27,369 participants, 5984 (22%) had diagnosed HTN. A HR ≥80 was associated with at least a 30% increase in mortality risk, regardless of HTN status (Table 1). Among normotensive participants, a HR ≥80 was associated with higher mortality risk compared to HR <80 at all SBPs except for SBP ≥180 (Table 1). While there was significant interaction between continuous HR and SBP on all-cause mortality (p=0.02), there was no evidence of significant effect modification within individual SBP categories. Conclusions: A HR ≥80 was independently associated with increased all-cause mortality risk, regardless of HTN diagnosis. HR may be a surrogate for cardiorespiratory fitness. Further studies understanding the joint associations between SBP and HR are needed in both normotensive and hypertensive individuals.

Background: Low total bilirubin (TBili) is associated with increased cardiovascular risk, in part mediated by adipose tissue-related hormones. determined whether excess adiposity (measured by BMI) is associated with low TBili levels. Methods: Our study population consisted of 14,129 (6,902 male and 7,227 non-pregnant female) adults aged ≥20 years from the 1999-2018 National Health and Nutrition Examination Surveys. Participants with elevated liver enzymes (AST>80 or ALT >112 IU/L; AST/ALT >5), excessive alcohol consumption (>20 drinks/week for males; >10 for females), iron overload (transferrin >50%), anemia (hemoglobin<12 g/dl if female; <13 g/dl if male), elevated TBili (≥1.2 mg/dl), low albumin (<3.5 g/dl), or positive hepatitis B/C serology were excluded. We categorized measured BMI into 7 categories (<18.5, 18.5-22.9, 23.0-24.9, 25.0-27.4, 27.5-29.9, 30-34.9, ≥35). Low TBili, our primary outcome, was defined as <0.4 mg/dl for both males and females. We used sex-stratified multivariable logistic regression, sequentially adjusting for demographics, cardiometabolic factors, and liver function. Results: Among 14,129 adults (mean age [SD] of 47 [15] years, 51% female, 69% White), nearly 32% had BMI ≥30. Both males and females with BMI ≥30 had >50% odds of low TBili compared to a BMI of 23-24.9, even after adjustment for covariates (Table). There was no significant association between overweight range BMIs and low TBili. Adjustment for serum albumin most significantly attenuated the associations between obese-range BMIs and low TBili, especially in males. Further classifying each BMI category into high and normal waist circumference (WC;<88cm for female, <102cm for male) groups revealed that high WC individuals, even with BMI of 23-24.9, had increased odds of low TBili (OR [95% CI]: 2.35 [1.40, 3.94]). Conclusions: Obese BMI is associated with higher likelihood of low TBili. Longitudinal studies are needed to determine directionality of association and risk of downstream cardiovascular disease.

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