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Cardiovascular disease (CVD) risk factors cluster in an individual. Exercise is universally recommended to prevent and treat CVD. Yet, clinicians lack guidance on how to design an exercise prescription (ExRx) for patients with multiple CVD risk factors. To address this unmet need, we developed a novel clinical decision support system to prescribe exercise (prioritize personalize prescribe exercise [P3-EX]) for patients with multiple CVD risk factors founded upon the evidenced-based recommendations of the American College of Sports Medicine (ACSM) and American Heart Association. To develop P3-EX, we integrated (1) the ACSM exercise preparticipation health screening recommendations; (2) an adapted American Heart Association Life’s Simple 7 cardiovascular health scoring system; (3) adapted ACSM strategies for designing an ExRx for people with multiple CVD risk factors; and (4) the ACSM frequency, intensity, time, and time principle of ExRx. We have tested the clinical utility of P3-EX within a university-based online graduate program in ExRx among students that includes physicians, physical therapists, registered dietitians, exercise physiologists, kinesiologists, fitness industry professionals, and kinesiology educators in higher education. The support system P3-EX has proven to be an easy-to-use, guided, and time-efficient evidence-based approach to ExRx for patients with multiple CVD risk factors that has applicability to other chronic diseases and health conditions. Further evaluation is needed to better establish its feasibility, acceptability, and clinical utility as an ExRx tool.

Context:Compression socks have become increasingly popular with athletes due to perceived enhancement of exercise performance and recovery. However, research examining the efficacy of compression socks to reduce exercise-associated muscle damage has been equivocal, with few direct measurements of markers of muscle damage.Objective:To examine the influence of compression socks worn during a marathon on creatine kinase (CK) levels.Design:A randomized controlled trial.Setting:2013 Hartford Marathon, Hartford, CT.Participants:Adults (n = 20) randomized to control (CONTROL; n = 10) or compression sock (SOCK; n = 10) groups.Main Outcome Measures:Blood samples were collected 24 hours before, immediately after, and 24 hours following the marathon for the analysis of CK, a marker of muscle damage.Results:Baseline CK levels did not differ between CONTROL (89.3 [41.2] U/L) and SOCK (100.0 [56.2] U/L) (P = .63). Immediately following the marathon (≤1 h), CK increased 273% from baseline (P P = .60 for time × group). The day following the marathon (≤24 h), CK further increased 1094% from baseline (P P = .53 for time × group). These similar trends persisted despite controlling for potential covariates such as age, body mass index, and race finishing time (Ps > .29).Conclusions:Compression socks worn during a marathon do not appear to mitigate objectively measured markers of muscle damage immediately following and 24 hours after a marathon.

A single exercise session evokes immediate blood pressure (BP) reductions that persist for at least 24 h, termed postexercise hypotension (PEH). Self-monitoring of PEH may foster positive outcome expectations of exercise, and thus, enhance exercise adherence among adults with hypertension.To compare the efficacy of self-monitoring of exercise (EXERCISE) versus exercise and PEH (EXERCISE + PEH) to improve exercise adherence and BP control among adults with hypertension.Adults with high BP were randomized to EXERCISE (n = 12) or EXERCISE + PEH (n = 12). Participants underwent supervised, moderate intensity aerobic exercise training for 40-50 min/session, 3 days/week for 12 weeks and encouraged to exercise unsupervised at home at least 30 min/day, 1-2 days/week. EXERCISE + PEH also self-monitored BP before and after exercise. Adherence was calculated as [(no. of exercise sessions performed/no. of possible exercise sessions) × 100%]. BP was measured pre and posttraining.Healthy, middle-aged (52.3 ± 10.8 years) men (n = 11) and women (n = 13) with hypertension (136.2 ± 10.7/85.2 ± 8.9 mmHg) completed exercise training with 87.9 ± 12.1% adherence. EXERCISE + PEH demonstrated greater adherence to supervised training (94.3 ± 6.6%) than EXERCISE (81.6 ± 13.2%; P = 0.007). EXERCISE + PEH performed 32.6 ± 22.5 min/week more unsupervised home exercise than EXERCISE (P = 0.004), resulting in greater exercise adherence (107.3 ± 18.7%) than EXERCISE (82.7 ± 12.2%; P = 0.002). Post versus pretraining BP was reduced -7.4 ± 11.3/-4.9 ± 9.9 mmHg (P 0.025) with no statistical difference between EXERCISE (-5.2 ± 13.3/-3.6 ± 6.1 mmHg) and EXERCISE + PEH (-9.9 ± 11.3/-6.1 ± 6.9 mmHg; P 0.344).The current study is the first to demonstrate that PEH self-monitoring is an efficacious tool to improve exercise adherence among a small sample of adults with hypertension. Future research among a larger, more diverse sample is needed to confirm these novel findings and determine whether EXERCISE + PEH translates to better BP control relative to EXERCISE self-monitoring alone.

Venous thromboembolic (VTE) events such as deep vein thrombosis (DVT) and pulmonary embolism (PE) have been reported in otherwise low-risk healthy athletes following acute bouts of aerobic exercise.To review case reports and assess the commonalities of athletic individuals with VTE, as well as return-to-play (RTP) recommendations.We reviewed 47 reports (20 DVTs, 15 PEs, and 12 DVTs/PEs, 19 women) of trained individuals who were diagnosed with DVT and/or PE following aerobic exercise. We assessed frequency of VTE risk factors, presenting symptoms, and RTP recommendations.The age of women (24.6 ± 7.0 years) was lower (P .01) than of men (40.6 ± 13.6 years). Of the 19 women, 14 (73.7%) used oral contraceptives. Thirteen cases (27.7%) reported a recent period of prolonged inactivity (1 hour), and another 12 cases were found to have an antithrombin disorder following testing after diagnosis. The most frequently reported symptoms were muscle pain in 26 of 32 (81.3%) DVT or DVT/PE cases, and dyspnea in 21 of 27 (77.8%) PE or DVT/PE cases. Despite these common symptoms, the estimated time from first report of symptoms to confirmed diagnosis was 56.3 ± 118.7 days and 25 cases (53.2%) were initially misdiagnosed. Twenty-three cases (48.9%) did not report RTP recommendations, and those which did varied widely.Thirty-two cases (~70%) had at least one of three major risk factors, suggesting that many cases of VTE in athletes may be preventable with better education and awareness. The wide variety of RTP recommendations highlights the need for standardized guidelines in this population.

Obesity affects approximately one-third of American adults. Recent evidence suggests that weight bias may be pervasive among both exercise and nutrition professionals working with adults who have obesity. However, the published literature on this topic is limited. This review aimed to (i) systematically review existing literature examining weight bias among exercise and nutrition professionals; (ii) discuss the implications of this evidence for exercise and nutrition professionals and their clients; (iii) address gaps and limitations of this literature; and (iv) identify future research directions. Of the 31 studies that met the criteria for this review, 20 examined weight bias among exercise professionals, of which 17 (85%) found evidence of weight bias among professionals practicing physical therapy (n = 4), physical education (n = 8) and personal/group fitness training (n = 5). Of 11 studies examining weight bias among nutrition professionals, eight (73%) found evidence of weight bias. These findings demonstrate fairly consistent evidence of weight bias among exercise and nutrition professionals. However, the majority of studies were cross-sectional (90%). Given that weight bias may compromise quality of care and potentially reinforce weight gain and associated negative health consequences in patients with obesity, it is imperative for future work to examine the causes and consequences of weight bias within exercise and nutrition professions using more rigorous study designs.

Serum creatine kinase (CK) levels are higher after eccentric, muscle-damaging exercise in statin-treated patients. This could contribute to the increased statin-associated muscle symptoms reported in physically active individuals.We tested the hypothesis in this pilot study that creatine (Cr) monohydrate supplementation would reduce the CK response to eccentric exercise in patients using statins to determine if Cr supplementation could be a strategy to mitigate statin-associated muscle symptoms in physically active individuals.Healthy, nonsmoking men (n = 5) and women (n = 14) were randomized to Cr monohydrate = atorvastatin 80 mg + 10 g Cr monohydrate (n = 10, age = 60 ± 7 years) or to placebo (PL) = atorvastatin 80 mg + PL (n = 9, age = 52 ± 6 years). After 4 weeks of treatment, subjects performed 45 minutes of eccentric exercise (downhill walking at a -15% grade). Serum CK levels, muscle soreness (visual analog scale after two squats), and muscle pain severity and interference (using the brief pain inventory) were measured before and after 4 weeks of treatment, and then for 4 consecutive days after downhill walking. Vitamin D, or serum 25(OH)D, was also measured at baseline.The PL group was younger (P = .01) but not otherwise different in blood lipids, vitamin D, CK, muscle visual analog scale, and pain scores before (all P .21) or after (all P .12) treatment. CK increased in all subjects after downhill walking (P .01), but neither the relative peak change (expressed as group mean difference with 95% confidence intervals: 43.52% [-196.41, 283.45]) nor the absolute peak change (67.38 U/L [-121.55, 256.31]) relative to baseline was different between groups (P = .46 and .71, respectively). A similar lack of treatment effect was observed for muscle soreness (11.03 mm [-9.49, 31.55]), pain severity (0.77 pts [-0.95, 2.50]), and pain interference (1.02 pts [-1.25, 3.29]) with P-values for group comparisons = 0.27, 0.36, and 0.35, respectively. However, subjects with "insufficient" Vitamin D 30 ng/mL (n = 10) had an ∼2-fold greater CK increase with eccentric exercise (nominal P-value = .04) than subjects with higher vitamin D levels.Cr monohydrate did not reduce CK increases after exercise in statin-treated subjects. We did observe that low vitamin D levels are associated with a greater CK response to eccentric exercise in statin-treated subjects.

Functional magnetic resonance imaging (fMRI) has not been used to assess the effects of statins on the brain. We assessed the effect of statins on cognition using standard neuropsychological assessments and brain neural activation with fMRI on two tasks.Healthy statin-naïve men and women (48±15 years) were randomized to 80 mg/day atorvastatin (n=66; 27 men) or placebo (n=84; 48 men) for 6 months. Participants completed cognitive testing while on study drug and 2 months after treatment cessation using alternative test and task versions.There were few changes in standard neuropsychological tests with drug treatment (all P.56). Total and delayed recall from the Hopkins Verbal Learning Test-Revised increased in both groups (P.05). The Stroop Color-Word score increased (P.01) and the 18-Point Clock Test decreased in the placebo group (P=.02) after drug cessation. There were, however, small but significant group-time interactions for each fMRI task: participants on placebo had greater activation in the right putamen/dorsal striatum during the maintenance phase of the Sternberg task while on placebo but the effect was reversed after drug washout (P.001). Participants on atorvastatin had greater activation in the bilateral precuneus during the encoding phase of the Figural Memory task while on-drug but the effect was reversed after drug washout (P.001).Six months of high dose atorvastatin therapy is not associated with measurable changes in neuropsychological test scores, but did evoke transient differences in brain activation patterns. Larger, longer-term clinical trials are necessary to confirm these findings and evaluate their clinical implications.

Considerable variability exists in the cardiometabolic disease biomarker response to exercise. We propose that a major contributor to this heterogeneity is underpowered studies due to small sample sizes. To test our hypothesis, we conducted a systematic review to identify meta-analyses/reviews of randomized controlled trials (RCT) and RCT that examined the cardiometabolic disease biomarker response to aerobic and resistance exercise.

Aerobic exercise reduces blood pressure (BP) on average 5-7 mmHg among those with hypertension; limited evidence suggests similar or even greater BP benefits may result from isometric handgrip (IHG) resistance exercise.We conducted a randomized controlled trial investigating the antihypertensive effects of an acute bout of aerobic compared with IHG exercise in the same individuals. Middle-aged adults (n = 27) with prehypertension and obesity randomly completed three experiments: aerobic (60% peak oxygen uptake, 30 min); IHG (30% maximum voluntary contraction, 4 × 2 min bilateral); and nonexercise control. Study participants were assessed for carotid-femoral pulse wave velocity pre and post exercise, and left the laboratory wearing an ambulatory BP monitor.SBP and DBP were lower after aerobic versus IHG (4.8 ± 1.8/3.1 ± 1.3 mmHg, P = 0.01/0.04) and control (5.6 ± 1.8/3.6 ± 1.3 mmHg, P = 0.02/0.04) over the awake hours, with no difference between IHG versus control (P = 0.80/0.83). Pulse wave velocity changes following acute exercise did not differ by modality (aerobic increased 0.01 ± 0.21 ms, IHG decreased 0.06 ± 0.15 ms, control increased 0.25 ± 0.17 ms, P 0.05). A subset of participants then completed either 8 weeks of aerobic or IHG training. Awake SBP was lower after versus before aerobic training (7.6 ± 3.1 mmHg, P = 0.02), whereas sleep DBP was higher after IHG training (7.7 ± 2.3 mmHg, P = 0.02).Our findings did not support IHG as antihypertensive therapy but that aerobic exercise should continue to be recommended as the primary exercise modality for its immediate and sustained BP benefits.

BackgroundThere is a high prevalence of cardiovascular disease across diverse groups in the U.S. population, and increasing research has identified stigma as a potential barrier to cardiovascular disease prevention and treatment. This systematic review examines evidence linking discrimination and cardiovascular health among socially stigmatized groups.Study designSix databases were systematically reviewed from inception through February 2018 for studies with adult subjects, focusing on cardiovascular health indicators among social groups stigmatized because of their gender, race/ethnicity, age, body weight/obesity, or sexual orientation. The Newcastle-Ottawa Scale was used to evaluate the methodological quality and risk of bias for nonrandomized studies, and the Cochrane Collaboration 7-item domain for randomized controlled and experimental trials.ResultsThe search identified 84 eligible studies published between 1984 and 2017. Studies retrieved were categorized according to demonstrated links between stigma and cardiovascular disease risk factors including blood pressure (n = 45), heart rate variability (n = 6), blood/saliva cardiovascular biomarkers (n = 18), as well as other indicators of cardiovascular health (n = 15). Based on the findings from included studies, 86% concluded that there was a significant relationship among stigma or discrimination and cardiovascular health indicators among socially stigmatized groups. However, there were varying degrees of evidence supporting these relationships, depending on the type of discrimination and cardiovascular health indicator. The current evidence implies an association between perceived discrimination and cardiovascular health. However, a majority of these studies are cross-sectional (73%) and focus on racial discrimination (79%), while using a wide variety of measurements to assess social discrimination and cardiovascular health.ConclusionsFuture research should include longitudinal and randomized controlled trial designs, with larger and more diverse samples of individuals with stigmatized identities, using consistent measurement approaches to assess social discrimination and its relationship with cardiovascular health.

Objectives To examine the effects of exercise training on cognitive function in individuals at risk of or diagnosed with Alzheimer's disease (AD). Design Meta‐analysis. Setting PubMed, Scopus, ClinicalTrials.gov, and ProQuest were searched from inception until August 1, 2017. Participants Nineteen studies with 23 interventions including 1,145 subjects with a mean age of 77.0 ± 7.5 were included. Most subjects were at risk of AD because they had mild cognitive impairment (64%) or a parent diagnosed with AD (1%), and 35% presented with AD. Intervention Controlled studies that included an exercise‐only intervention and a nondiet, nonexercise control group and reported pre‐ and post‐intervention cognitive function measurements. Measurements Cognitive function before and after the intervention and features of the exercise intervention. Results Exercise interventions were performed 3.4 ± 1.4 days per week at moderate intensity (3.7 ± 0.6 metabolic equivalents) for 45.2 ± 17.0 minutes per session for 18.6 ± 10.0 weeks and consisted primarily of aerobic exercise (65%). Overall, there was a modest favorable effect of exercise on cognitive function (d+ = 0.47, 95% confidence interval (CI) = 0.26–0.68). Within‐group analyses revealed that exercise improved cognitive function (d+w = 0.20, 95% CI = 0.11–0.28), whereas cognitive function declined in the control group (d+w = −0.18, 95% CI = −0.36 to 0.00). Aerobic exercise had a moderate favorable effect on cognitive function (d+w = 0.65, 95% CI = 0.35–0.95), but other exercise types did not (d+w = 0.19, 95% CI = −0.06–0.43). Conclusion Our findings suggest that exercise training may delay the decline in cognitive function that occurs in individuals who are at risk of or have AD, with aerobic exercise possibly having the most favorable effect. Additional randomized controlled clinical trials that include objective measurements of cognitive function are needed to confirm our findings.

Recent data suggest that rapid infusion of intravenous (IV) cold saline for Targeted Temperature Management (TTM) after cardiac arrest is associated with higher rates of rearrest, pulmonary edema, and hypoxia, with no difference in neurologic outcomes or survival when administered by Emergency Medical Services. We sought to determine the effects of IV cold saline administration in the hospital setting in postcardiac arrest patients to achieve TTM and its effect on clinical parameters and neurologic outcomes.A cohort of 132 patients who completed TTM after cardiac arrest in a single institution was retrospectively studied. Patients who did not receive cold saline were matched by age, gender, Glasgow coma scale, downtime, and presenting rhythm to patients who received cold saline. Demographics, cardiac rearrest, diuretic use, time to target temperature, and Cerebral Performance Category (CPC) scores were recorded among other variables. Patients who received cold saline achieved target temperature sooner (280 vs. 345 minutes, p = 0.05), had lower lactate levels on day 1 (4.2 ± 3.5 mM vs. 6.0 ± 4.9 mM, p = 0.019) and day 2 (1.3 ± 2.2 mM vs. 2.2 ± 3.2 mM, p = 0.046), increased incidence of pulmonary edema (51.5% vs. 31.8%, p = 0.006), and increased diuretic utilization (63.6% vs. 42.4%, p = 0.014). There was no significant difference in cardiac rearrest, arterial oxygenation, and CPC scores (ps 0.05).Infusion of IV cold saline is associated with shorter time to target temperature, increased incidence of pulmonary edema, and diuretic use, with no difference in cardiac rearrest, survival, and neurologic outcomes.

OBJECTIVE To investigate the effect of oral contraceptive (OC) use and compression socks on hemostatic activation in women flying cross-country to and from a marathon. DESIGN Prospective study. SETTING 2015 Boston Marathon. PARTICIPANTS Women were divided into non-OC using (CONTROL; n = 12), OC-using (OC; n = 15), and OC-using plus compression sock (OC + SOCK; n = 14) groups. INTERVENTION Women in OC + SOCK wore compression socks during flights to and from the marathon. MAIN OUTCOME MEASURES Venous blood samples were collected within 24 hours of arriving in Boston (EXPO), immediately after the marathon (RUN), and within 24 hours after a return flight home (Post-Flight) for analysis of thrombin-antithrombin complex (TAT), d-dimer, and tissue plasminogen activator (t-PA). RESULTS TAT did not increase with exercise (P = 0.48) and was not affected by group (P = 0.08) or the interaction between these 2 factors (P = 0.80). Group, time, and their interaction were significant for d-dimer (all P < 0.05) such that d-dimer increased with acute exercise to a greater extent (Δ d-dimer from expo to postrace = 909.5 ± 1021.9 ng/mL) in the OC + SOCK group relative to OC (Δ d-dimer = 240.0 ± 178.5 ng/mL; P = 0.02) and CONTROL (Δ d-dimer = 230.3 ± 120.3 ng/mL; P = 0.02). There was a significant effect of time, group, and the interaction on t-PA (all P < 0.01) such that t-PA increased with acute exercise to a greater extent (Δ t-PA from expo to postrace = 19.6 ± 10.0 ng/mL) in the CONTROL group relative to OC (Δ t-PA = 4.0 ± 1.8 ng/mL; P < 0.01) and OC + SOCK (Δ t-PA = 3.3 ± 1.2 ng/mL; P < 0.01). CONCLUSIONS Female runners using OCs did not exhibit disproportionately increased coagulation. The use of compression socks in women on OCs, surprisingly, resulted in a greater increase in d-dimer after exercise.

The mechanisms underlying statin-associated muscle symptoms (SAMS) are not understood. Mitochondrial dysfunction and atrogin-1 activation are among the leading possible explanations for SAMS. Interestingly, metformin can enhance mitochondrial function and may affect atrogin-1 expression. Therefore, we sought to perform a systematic search of the literature to explore the relationship among statins, metformin, and SAMS.

FURIN is a proprotein convertase subtilisin/kexin enzyme important in pro‐renin receptor processing, and FURIN (furin, paired basic amino acid cleaving enzyme) variants are involved in multiple aspects of blood pressure (BP) regulation. Therefore, we examined associations among FURIN variants and the immediate blood pressure (BP) response to bouts of aerobic exercise, termed postexercise hypotension (PEH). Obese (30.9 ± 3.6 kg m−2) Black‐ (n = 14) and White‐ (n = 9) adults 42.0 ± 9.8 year with hypertension (139.8 ± 10.4/84.6 ± 6.2 mmHg) performed three random experiments: bouts of vigorous (VIGOROUS) and moderate (MODERATE) intensity cycling and control. Subjects were then attached to an ambulatory BP monitor for 19 h. We performed deep‐targeted exon sequencing with the Illumina TruSeq Custom Amplicon kit. FURIN genotypes were coded as the number of minor alleles (#MA) and selected for additional statistical analysis based upon Bonferonni or Benjamini–Yekutieli multiple testing corrected P‐values under time‐adjusted linear models for 19 hourly BP measurements. After VIGOROUS over 19 h, as FURIN #MA increased in rs12917264 (P = 2.4E‐04) and rs75493298 (P = 6.4E‐04), systolic BP (SBP) decreased 30.4–33.7 mmHg; and in rs12917264 (P = 1.6E‐03) and rs75493298 (P = 9.7E‐05), diastolic BP (DBP) decreased 17.6–20.3 mmHg among Blacks only. In addition, after MODERATE over 19 h in FURIN rs74037507 (P = 8.0E‐04), as #MA increased, SBP increased 20.8 mmHg among Blacks only. Whereas, after MODERATE over the awake hours in FURIN rs1573644 (P = 6.2E‐04), as #MA increased, DBP decreased 12.5 mmHg among Whites only. FURIN appears to exhibit intensity and race‐dependent associations with PEH that merit further exploration among a larger, ethnically diverse sample of adults with hypertension.

This review examined studies published within the last 16 months that investigated the relationship between statins and physical activity.These recent studies suggest that statins do not adversely affect cardiorespiratory fitness, muscle strength, athletic performance, or physical activity adherence. One recent study comparing patients with statin-associated myalgia and nonstatin-using controls did report that statins are associated with a slowing of time to peak power output, increased abdominal adiposity, and insulin resistance. Statin users also had different muscle gene expression than controls, but conclusions are limited by the design of that study.Previous reports suggest that statin-associated muscle symptoms such as myalgia, cramps, and weakness occur more frequently in physically active individuals, but the recent studies we reviewed do not provide additional support for this possibility. Well-designed clinical trials are needed to determine whether different statins or statin doses evoke statin-associated muscle symptoms or muscle damage that may reduce cardiorespiratory fitness and adherence to physical activity.

Hydroxy-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors or statins are well tolerated, but associated with various statin-associated symptoms (SAS), including statin-associated muscle symptoms (SAMS), diabetes mellitus (DM), and central nervous system complaints. These are "statin-associated symptoms" because they are rare in clinical trials, making their causative relationship to statins unclear. SAS are, nevertheless, important because they prompt dose reduction or discontinuation of these life-saving mediations. SAMS is the most frequent SAS, and mild myalgia may affect 5% to 10% of statin users. Clinically important muscle symptoms, including rhabdomyolysis and statin-induced necrotizing autoimmune myopathy (SINAM), are rare. Antibodies against HMG-CoA reductase apparently provoke SINAM. Good evidence links statins to DM, but evidence linking statins to other SAS is largely anecdotal. Management of SAS requires making the possible diagnosis, altering or discontinuing the statin treatment, and using alternative lipid-lowering therapy.

In previous studies, we found an endothelial nitric oxide synthase gene ( NOS3 ) variant rs2070744 associated with the ambulatory blood pressure (BP) response following bouts of moderate and vigorous intensity acute exercise, termed post‐exercise hypotension (PEH). In a validation cohort, we sequenced NOS3 exons for associations with PEH. Obese (30.9 ± 3.6 kg . m −2 ) African American ( n = 14) [AF] and Caucasian ( n = 9) adults 42.0 ± 9.8 years with hypertension (139.8 ± 10.4/84.6 ± 6.2 mmHg) performed three random experiments: bouts of vigorous and moderate intensity cycling and control. Subjects were attached to an ambulatory BP monitor for 19 h. We performed deep‐targeted exon sequencing with the Illumina TruSeq Custom Amplicon kit. Variant genotypes were coded as number of minor alleles (#MA) and selected for additional statistical analysis based upon Bonferonni or Benjamini–Yekutieli multiple testing‐corrected P ‐values under time‐adjusted linear models for 19 hourly BP measurements for each subject. After vigorous intensity over 19 h, among NOS3 variants passing multiple testing thresholds, as the #MA increased in rs891512 ( P = 6.4E‐04), rs867225 ( P = 6.5E‐04), rs743507 ( P = 2.6E‐06), and rs41483644 ( P = 2.4E‐04), systolic (SBP) decreased from 17.5 to 33.7 mmHg; and in rs891512 ( P = 9.7E‐05), rs867225 ( P = 2.6E‐05), rs41483644 ( P = 1.6E‐03), rs3730009 ( P = 2.6E‐04), and rs77325852 ( P = 5.6E‐04), diastolic BP decreased from 11.1 mmHg to 20.3 mmHg among AF only. In contrast, after moderate intensity over 19 h in NOS3 rs3918164, as the #MA increased, SBP increased by 16.6 mmHg ( P = 2.4E‐04) among AF only. NOS3 variants exhibited associations with PEH after vigorous, but not moderate intensity exercise among AF only. NOS3 should be studied further for its effects on PEH in a large, ethnically diverse sample of adults with hypertension to confirm our findings.

We found variants from the Angiotensinogen‐Converting Enzyme ( ACE ), Angiotensin Type 1 Receptor ( AGTR1 ), Aldosterone Synthase ( CYP11B2 ), and Adducin ( ADD1 ) genes exhibited intensity‐dependent associations with the ambulatory blood pressure (BP) response following acute exercise, or postexercise hypotension (PEH). In a validation cohort, we sequenced exons from these genes for their associations with PEH. Obese (30.9 ± 3.6 kg m −2 ) adults ( n = 23; 61% African Americans [AF], 39% Caucasian) 42.0 ± 9.8 years with hypertension (139.8 ± 10.4/84.6 ± 6.2 mmHg) completed three random experiments: bouts of vigorous and moderate intensity cycling and control. Subjects wore an ambulatory BP monitor for 19 h. We performed deep‐targeted exon sequencing using the Illumina TruSeq Custom Amplicon kit. Variant genotypes were coded as number of minor alleles (#MA) and selected for further statistical analysis based upon Bonferonni or Benjamini–Yekutieli multiple testing corrected p‐values under time adjusted linear models for 19 hourly BP measurements per subject. After vigorous intensity over 19 h among ACE , AGTR1 , CYP11B2 , and ADD1 variants passing multiple testing thresholds, as the #MA increased, systolic (SBP) and/or diastolic BP decreased 12 mmHg ( P = 4.5E‐05) to 30 mmHg ( P = 6.4E‐04) among AF only. In contrast, after moderate intensity over 19 h among ACE and CYP11B2 variants passing multiple testing thresholds, as the #MA increased, SBP increased 21 mmHg ( P = 8.0E‐04) to 22 mmHg ( P = 8.2E‐04) among AF only. In this replication study, ACE , AGTR1 , CYP11B2 , and ADD1 variants exhibited associations with PEH after vigorous, but not moderate intensity exercise among AF only. Renal variants should be explored further with a multi‐level “omics” approach for associations with PEH among a large, ethnically diverse sample of adults with hypertension.

Exercise prescription is quantified based on frequency, intensity, time, type, volume, and progression, but differing injury rates associated with various modalities and types of exercise are often not accounted for. We propose an effectiveness ratio, a quantification of benefits associated with exercise relative to the injury risk associated with training.

Older adults represent the fastest-growing age demographic of the population. Physiological changes associated with primary aging and concurrent chronic disease adversely impact functional capacity, health outcomes, and quality of life. For these reasons, there is a national emphasis for healthcare providers to improve the health, function, and quality of life of older adults to preserve independent living and psychological well-being. The benefits of regular physical activity or exercise with regard to aging and disease are indisputable, yet many clinicians do not prescribe exercise to older adults. This reluctance may be attributable to a lack of knowledge regarding appropriate exercise prescription for older adults in light of the potential risks and benefits of various doses and types of exercise. In addition, clinicians and patients may have concerns about potential health considerations relevant to older adults such as comprehensive pre-exercise screening and exercise-drug interactions. In light of this, the following review presents (1) guidelines for exercise prescription in older adults and modification of these guidelines for patients with the most common age-associated comorbidities; (2) recommendations for pre-exercise screening prior to initiating an exercise program in older adults; (3) considerations for older adults on one or more medications; and (4) common barriers to adopting and maintaining exercise in an older population. Our goal is to provide a framework that clinicians can follow when prescribing exercise in older adults while considering the unique characteristics and concerns present in this population.