Roberta K. Oka

Long-term Effects of Varying Intensities and Formats of Physical Activity on Participation Rates, Fitness, and Lipoproteins in Men and Women Aged 50 to 65 Years

BACKGROUND Although exercise parameters such as intensity and format have been shown to influence exercise participation rates and physiological outcomes in the short term, few data are available evaluating their longer-term effects. The study objective was to determine the 2-year effects of differing intensities and formats of endurance exercise on exercise participation rates, fitness, and plasma HDL cholesterol levels among healthy older adults. METHODS AND RESULTS Higher-intensity, group-based exercise training; higher-intensity, home-based exercise; and lower-intensity, home-based exercise were compared in a 2-year randomized trial. Participants were 149 men and 120 postmenopausal women 50 to 65 years of age who were sedentary and free of cardiovascular disease. Recruitment was achieved through a random digit-dial community telephone survey and media promotion. All exercise occurred in community settings. For higher-intensity exercise training, three 40-minute endurance training sessions per week were prescribed at 73% to 88% of peak treadmill heart rate. For lower-intensity exercise, five 30-minute endurance training sessions per week were prescribed at 60% to 73% of peak treadmill heart rate. Treadmill exercise performance, lipoprotein levels and other heart disease risk factors, and exercise adherence were evaluated at baseline and across the 2-year period. Treadmill exercise test performance improved for all three training conditions during year 1 and was successfully maintained during year 2, particularly for subjects in the higher-intensity, home-based condition. Subjects in that condition also showed the greatest year 2 exercise adherence rates (P < .003). Although no significant increases in HDL cholesterol were observed during year 1, by the end of year 2 subjects in the two home-based training conditions showed small but significant HDL cholesterol increases over baseline (P < .01). The increases were particularly pronounced for subjects in the lower-intensity condition, whose exercise prescription required more frequent exercise sessions per week. For all exercise conditions, increases in HDL cholesterol were associated with decreases in waist-to-hip ratio in both men and women (P < .04). CONCLUSIONS While older adults can benefit from initiating a regular regimen of moderate-intensity exercise in terms of improved fitness levels and small improvements in HDL cholesterol levels, the time frame needed to achieve HDL cholesterol change (2 years) may be longer than that reported previously for younger populations. Frequency of participation may be particularly important for achieving such changes. Supervised home-based exercise regimens represent a safe, attractive alternative for achieving sustained participation.

Endothelial Dysfunction Induced by Hyperhomocyst(e)inemia Role of Asymmetric Dimethylarginine

Background—Endothelial function is impaired by hyperhomocyst(e)inemia. We have previously shown that homocyst(e)ine (Hcy) inhibits NO production by cultured endothelial cells by causing the accumulation of asymmetric dimethylarginine (ADMA). The present study was designed to determine if the same mechanism is operative in humans. Methods and Results—We studied 9 patients with documented peripheral arterial disease (6 men; 3 women; age, 64±3 years), 9 age-matched individuals at risk for atherosclerosis (older adults; 9 men; age, 65±1 years), and 5 young control subjects (younger adults; 5 men; age, 31±1 years) without evidence of or risk factors for atherosclerosis. Endothelial function was measured by flow-mediated vasodilatation of the brachial artery before and 4 hours after a methionine-loading test (100 mg/kg body weight, administered orally). In addition, blood was drawn at both time points for measurements of Hcy and ADMA concentrations. Plasma Hcy increased after the methionine-loading test in each group (all, P <0.001). Plasma ADMA levels rose in all subjects, from 0.9±0.2 to 1.6±0.2 &mgr;mol/L in younger adults, from 1.5±0.2 to 3.0±0.4 &mgr;mol/L in older adults, and from 1.8±0.1 to 3.9±0.3 &mgr;mol/L in peripheral arterial disease patients (all, P <0.001). Flow-mediated vasodilatation was reduced from 13±2% to 10±1% in younger adults, from 6±1% to 5±1% in older adults, and from 7±1% to 3±1% in peripheral arterial disease patients (all, P <0.001). Furthermore, we found positive correlations between plasma Hcy and ADMA concentrations (P =0.03, r =0.450), as well as ADMA and flow-mediated vasodilatation (P =0.002, r =0.623). Conclusions—Our results suggest that experimental hyperhomocyst(e)inemia leads to accumulation of the endogenous NO synthase inhibitor ADMA, accompanied by varying degrees of endothelial dysfunction according to the preexisting state of cardiovascular health.

Does Leptin Cause Vascular Disease

In the past two decades, there has been a 2- to 4-fold increase in childhood obesity in the United States. The current epidemic of childhood obesity in the United States can be expected to cause a surge in cardiovascular disease in this generation.1,2⇓ Already, obesity-related illnesses account for nearly 300 000 deaths and about

Psychophysiological and Cortisol Responses to Psychological Stress in Depressed and Nondepressed Older Men and Women With Elevated Cardiovascular Disease Risk

100 billion in economic costs per year in the United States. Therefore, understanding the mechanisms by which obesity accelerates vascular disease has become ever more important. See p 1919 Obesity is associated with hypercholesterolemia, which is in some cases due to elevated levels of low-density lipoprotein cholesterol. Obesity-associated dyslipidemia is often due to metabolic syndrome, which is characterized by hypertriglyceridemia, hyperinsulinemia, hypertension, and reduced high-density lipoprotein cholesterol.3 Each component of the metabolic syndrome may contribute to the increased risk of cardiovascular disease observed in obesity. In addition, plasma levels of C-reactive peptide (CRP) increase with fat mass and decline with weight loss.4 Recently, CRP has been demonstrated to directly impair endothelium-dependent vasodilation,5 and it is also known to be predictive of increased cardiovascular events in patients with other risk factors or with vascular disease.6 Obesity is also known to reduce vascular compliance.7 An increase in vascular stiffness has long-term adverse effects on the cardiovascular system by increasing impedance to blood flow and thereby increasing cardiovascular work and contributing to the development of left ventricular hypertrophy. Traditional risk …

Differences in treatment of acute myocardial infarction by sex, age, and other factors (the Stanford Five-City Project).

Objective: The objective of this study was to compare psychophysiological and cortisol reactions to psychological stress in older depressed and nondepressed patients at risk for cardiovascular disease (CVD). Methods: Forty-eight depressed participants and 20 controls with elevated cardiovascular risk factors underwent a psychological stress test during which cardiovascular variables were measured. Salivary cortisol was collected after each test segment. Traditional (e.g., lipids) and atypical (e.g., C-reactive protein) CVD risk factors were also obtained. Results: At baseline, the groups did not differ on lipid levels, flow-mediated vasodilation, body mass index, or asymmetric dimethylarginine. However, the depressed patients had significantly higher C-reactive protein levels. Contrary to our hypothesis, there were no differences in baseline cortisol levels or diurnal cortisol slopes, but depressed patients showed significantly lower cortisol levels during the stress test (p = .03) and less cortisol response to stress. Compared with nondepressed subjects, depressed subjects also showed lower levels of respiratory sinus arrhythmia (RSATF) during the stress test (p = .02). Conclusions: In this sample, older depressed subjects with elevated risk for CVD exhibited a hypocortisol response to acute stress. This impaired cortisol response might contribute to chronic inflammation (as reflected in the elevated C-reactive proteins in depressed patients) and in other ways increase CVD risk. The reduced RSATF activity may also increase CVD risk in depressed patients through impaired autonomic nervous system response to cardiophysiological demands. ACTH = adrenocorticotropic hormone; ADH = antidiuretic hormone; ADMA = asymmetric dimethylarginine; ANS = autonomic nervous system; BMI = body mass index; BP = blood pressure; BRC = baroreflex control; CAD = coronary artery disease; CBT = cognitive behavioral therapy; CHD = coronary heart disease; CO = cardiac output; CON = nondepressed control; CPM = cycles per minute; CVD = cardiovascular disease; DBP = diastolic blood pressure; DISH = Depression Interview and Structured Hamilton; ECG = electrocardiogram; FMVD = flow-mediated vasodilation; HDL = high-density lipoprotein; HPA = hypothalamic–pituitary–adrenal axis; HR = heart rate; HRSD = Hamilton Rating Scale of Depression; HRV = heart rate variability; LDL = low-density lipoprotein; MDD = major depressive disorder; MI = myocardial infarction; NO = nitric oxide; PANAS = Positive and Negative Affect Schedule; pCO2 = partial pressure of carbon dioxide; PEP = preejection period; PSS = Perceived Stress Scale; RSA = respiratory sinus arrhythmia; RSATF = transfer function respiratory sinus arrhythmia; SBP = systolic blood pressure; SVR = systemic vascular resistance; TSST = Trier Social Stress Test; VLDL = very-low-density lipoprotein.

Atherosclerotic Peripheral Vascular Disease Symposium II: Nomenclature for Vascular Diseases

This study examines the temporal trends in the use of angiography followed by revascularization procedures for acute myocardial infarction (AMI) in 2,021 hospitalized men and 995 women aged 30 to 74 years who participated in the Stanford Five-City Project during the years 1986 to 1992. Our sample included hospitalized patients who received a discharge diagnosis code of 410 through 414 and met study criteria for either a definite or possible AMI. Incident and recurrent infarctions occurring in the years 1986 through 1992 were included, but only the first event in this period for each patient. We performed stepwise multiple logistic regression analysis to determine the probability of: (1) receiving coronary angiography, (2) revascularization by either coronary bypass surgery or angioplasty among those with angiogram, and (3) thrombolytic therapy. Age, year of procedure, disease severity, and time between symptom onset and medical treatment were included as covariates. After adjustment of these factors, women were less likely than men to undergo angiography but were equally likely to undergo revascularization and thrombolysis. Hispanics and whites were equally likely to receive angiography and thrombolysis, but Hispanics were less likely than whites to undergo revascularization. Age and disease severity were inverse predictors of coronary angiography but not of revascularization. Age, severity, and delay time between onset of symptoms and medical therapy were inverse predictors of thrombolysis; delay time was significantly greater in women than in men and averaged > 6 hours in both sexes. The likelihood of receiving angiography, revascularization, and thrombolysis increased sharply over the study period.

Predictors of physical activity in patients with chronic heart failure secondary to either ischemic or idiopathic dilated cardiomyopathy

Peripheral vascular diseases are important components of cardiovascular medicine. The high prevalence of these disorders in the clinical setting mandates effective communication among healthcare providers. The public health significance of these conditions requires clear and consistent terminology for community audiences. Therefore, the goal of this writing group was to suggest definitions, usage, and nomenclature of specific terms commonly used to describe vascular diseases by cardiovascular specialists and primary care communities. The need for clarity is driven by 2 major challenges: (1) the need for use of common keywords for literature searches; and (2) the need for healthcare professionals to use common, reasoned terminology when communicating with each other and with the public. The major structural components of the vascular system are the veins, lymphatic vessels, and arteries. These serve as the basis of the nomenclature system for vascular diseases (Figure). Figure. Major classification of vascular diseases. *Includes inflammatory, artery dysplasias, congenital, traumatic, and infections. In this report, the writing group focuses only on nomenclature that applies to non–coronary artery diseases. Venous and lymphatic diseases were outside the scope of this conference. Diseases of arteries are classified further into atherosclerotic occlusive disorders, nonatherosclerotic occlusive disorders, and aneurysms. …

Isoflavones improve vascular reactivity in post-menopausal women with hypercholesterolemia.

To identify predictors of physical activity levels in patients with chronic heart failure, 43 patients, aged 33 to 91 years, who had well-compensated heart failure were asked to perform a symptom-limited exercise treadmill test and to complete activity logs for 2 consecutive days while wearing an ambulatory heart rate activity monitor. Activity logs included information on the type of activity, duration, rating of perceived exertion, symptoms experienced, and the intensity of symptoms. Subjects also completed the Duke Activity Status Index, a brief self-administered questionnaire that assesses physical functioning, and a self-efficacy for general activity questionnaire. Simultaneous multiple regression analysis was used to predict physical activity levels from a model that included: personal variables of physical fitness (peak oxygen consumption); knowledge, attitudes, and beliefs including self-efficacy for general activity, and rating of perceived exertion during daily activity; and environmental factors such as social support (marital status). The overall model explained 38% of the variance (p < 0.001). Self-efficacy (p = 0.015) was the strongest predictor of physical activity in this group. From this initial descriptive study, we conclude that self-efficacy is a better predictor of performance of physical activity than measures of physical fitness or rating of perceived exertion during activity. Additional studies are needed to examine other behavioral and physiologic mediators as well as behavioral strategies that may be used to increase participation in physical activity programs. Particularly promising are strategies to enhance self-efficacy for exercise.

Limb hemodynamics are not predictive of functional capacity in patients with PAD

This randomized clinical trial was designed to assess the effects of dietary isoflavones on vascular reactivity, lipid levels, and markers of inflammation in post-menopausal women. Epidemiological studies have revealed that populations consuming large amounts of soy protein have lower cardiovascular morbidity and mortality. The benefits of soy protein may be due to its hypolipidemic effects; its anti-oxidant properties; its high content of L-arginine; and=or or its phytoestrogen content. Two putative mediators of the effects of soy protein are the isoflavones genistein and daidzein. Forty post-menopausal, hypercholesterolemic women who did not take estrogen replacement therapy were recruited for this study of isoflavone supplementation. Baseline flow-mediated vasodilation and response to nitroglycerin were measured, along with urinary isoflavone and nitrite=nitrate levels and serum lipids. After 6 weeks of 90 mg of isoflavones daily versus placebo, women receiving isoflavones demonstrated improved responsiveness to nitroglycerin, an assessment of endothelium-independent vasodilation, with an effect size (percentage points change from baseline) of 7.2 1.9 versus 1.2 1.3; p = 0.01. There was a trend towards improvement of flow-mediated vasodilation, which is an endothelium-dependent response (effect size: 3.4 2.0% versus -0.6 1.7%; p = 0.12). Lipid levels were unchanged after isoflavone treatment. In conclusion, dietary isoflavones may have cardiovascular benefit in the form of improved vascular reactivity, but not by lowering cholesterol, for women who do not take estrogen replacement therapy.

Daily physical activity levels in congestive heart failure

To the practicing clinician, it seems obvious that limb hemodynamics would be the primary determinant of walking distance. However, other determinants, such as skeletal muscle metabolism, may play a role. Accordingly, in the current study, we examined the relationship between measures of limb hemodynamics and walking capacity in patients with peripheral arterial disease (PAD). We measured toe and ankle pressures for calculation of toe-(TBI) and ankle (ABI)-brachial indices; basal and hyperemic calf blood flow (CBF; by plethysmography); and initial (ICT) and absolute (ACT) claudication time using the Skinner-Gardner protocol. As expected, PAD patients had impaired limb hemodynamics with reduced TBI, ABI and a reduction in ABI post-exercise. However, there was no relationship between any of the hemodynamic variables (including ABI, ABI reduction post-exercise, TBI, baseline or maximal CBF) and walking distance as assessed by ICT or ACT. A subset of PAD patients with an ACT >750 s (n =16; ‘long claudicators’) were compared with a subset of PAD patients with an ACT <260 s (n = 16; ‘short claudicators’). The average ACT in the long claudicants was over fivefold greater than the short claudicators. Surprisingly, there were no differences between the two groups in any of the hemo-dynamic variables. There was also no relationship between the initial ABI, TBI, toe pressure, baseline or hyperemic CBF, and the improvement in ACT over the 3-month course of the study. This study found little relationship between hemodynamic variables and functional capacity in PAD. Accordingly, to assess the response to therapeutic interventions, exercise performance and functional status need to be directly measured, and cannot be predicted from hemodynamic measurements.