Hypertension is the most common, costly, and preventable cardiovascular disease risk factor. Numerous professional organizations and committees recommend exercise as initial lifestyle therapy to prevent, treat, and control hypertension. Yet, these recommendations differ in the components of the Frequency, Intensity, Time, and Type (FITT) principle of exercise prescription (Ex R_x); the evidence upon which they are based is only of fair methodological quality; and the individual studies upon which they are based generally do not include people with hypertension, which are some of the limitations in this literature. The purposes of this review are to (1) overview the professional exercise recommendations for hypertension in terms of the FITT principle of Ex R_x; (2) discuss new and emerging research related to Ex R_x for hypertension; and (3) present an updated FITT Ex R_x for adults with hypertension that integrates the existing recommendations with this new and emerging research.

Adverse alterations in the skeletal muscle response to exercise have been noted among adults with hypertension. The influence of resting blood pressure (BP) on muscle strength is unknown. We hypothesized that adults with high BP would exhibit lower muscular strength than adults with normal BP. An isokinetic dynamometer tested 21 measures of isometric and isokinetic muscle strength. BP was measured by auscultation. Patients were categorized into having normal (<120 and 0.05). Contrary to our hypothesis, adults with high BP displayed greater muscle strength than adults with normal BP. Reasons for our findings are unclear, but may be because of shifts in muscle fiber type from type I to type IIb/x and oxidative to glycolytic metabolism; alterations may result in a more strength-adapted phenotype among adults with high BP such as we observed.

The overall pattern of a diet (diet quality) is recognized as more important to health and chronic disease risk than single foods or food groups. Indexes of diet quality can be derived theoretically from evidence-based recommendations, empirically from existing datasets, or a combination of the two. We used these methods to derive diet quality indexes (DQI), generated from a novel dietary assessment, and to evaluate relationships with cardiometabolic risk factors in young adults with (n = 106) or without (n = 106) diagnosed depression (62% female, mean age = 21). Participants completed a liking survey (proxy for usual dietary consumption). Principle component analysis of plasma (insulin, glucose, lipids) and adiposity (BMI, Waist-to-Hip ratio) measures formed a continuous cardiometabolic risk factor score (CRFS). DQIs were created: theoretically (food/beverages grouped, weighted conceptually), empirically (grouping by factor analysis, weights empirically-derived by ridge regression analysis of CRFS), and hybrid (food/beverages conceptually-grouped, weights empirically-derived). The out-of-sample CRFS predictability for the DQI was assessed by two-fold and five-fold cross validations. While moderate consistencies between theoretically- and empirically-generated weights existed, the hybrid outperformed theoretical and empirical DQIs in cross validations (five-fold showed DQI explained 2.6% theoretical, 2.7% empirical, and 6.5% hybrid of CRFS variance). These pilot data support a liking survey that can generate reliable/valid DQIs that are significantly associated with cardiometabolic risk factors, especially theoretically- plus empirically-derived DQI.

Genome-wide association studies have identified single nucleotide polymorphisms (SNPs) associated with waist circumference (WC) and waist-to-hip ratio (WHR) adjusted for BMI (WCadjBMI and WHRadjBMI), but it remains unclear whether these SNPs relate to change in WCadjBMI or WHRadjBMI with lifestyle intervention for weight loss. We hypothesized that polygenic scores (PS) comprised of 59 SNPs previously associated with central adiposity would predict less of a reduction in WCadjBMI or WHRadjBMI at 8–10 weeks in two lifestyle intervention trials, NUGENOB and DiOGenes, and at 1 year in five lifestyle intervention trials, Look AHEAD, Diabetes Prevention Program, Diabetes Prevention Study, DIETFITS, and PREDIMED-Plus. One-SD higher PS related to a smaller 1-year change in WCadjBMI in the lifestyle intervention arms at year 1 and thus predicted poorer response (β = 0.007; SE = 0.003; P = 0.03) among White participants overall and in White men (β = 0.01; SE = 0.004; P = 0.01). At average weight loss, this amounted to 0.20–0.28 cm per SD. No significant findings emerged in White women or African American men for the 8–10-week outcomes or for WHRadjBMI. Findings were heterogeneous in African American women. These results indicate that polygenic risk estimated from these 59 SNPs relates to change in WCadjBMI with lifestyle intervention, but the effects are small and not of sufficient magnitude to be clinically significant.