EXERCISE & CARDIOVASCULAR DISEASE

1. EXERCISE & CARDIOVASCULAR DISEASE

2. CHOLESTEROL • Cholesterol is an important part of a healthy body • It is used for producing cell membranes, some hormones, and vitamin D.

3. CHOLESTEROL • You get cholesterol in two ways. • Your body makes some of it, and the rest comes from cholesterol in animal products that you eat, such as meats, poultry, fish, eggs, butter, cheese and whole milk. • Food from plants — like fruits, vegetables and cereals — doesn't have cholesterol. • Some foods that don't contain animal products may contain trans-fats, which cause your body to make more cholesterol. • Foods with saturated fats also cause the body to make more cholesterol.

4. CHOLESTEROL • Cholesterol and other fats can't dissolve in the blood. They have to be transported to and from the cells by special carriers called lipoproteins. • There are two kinds that you need to know about. Low-density lipoprotein, or LDL, is known as the "bad" cholesterol. • Too much LDL cholesterol can clog your arteries, increasing your risk of heart attack and stroke. • High-density lipoprotein, or HDL, is known as the "good" cholesterol. Your body makes HDL cholesterol for your protection. It carries cholesterol away from your arteries. • Studies suggest that high levels of HDL cholesterol reduce your risk of heart attack.

9. How is cholesterol involved with atherosclerosis? • Injury – HTN, inflammation, infection, trauma, toxic materials, etc. • Fatty streak – monocytes form foam cells which become fatty streaks and plaques • Migration and aggregation – macrophages secret growth factors for smooth muscle cells, produce reactive oxygen materials which cause LDL to accumulate • Lipid accumulation • Maturation of the lesion

14. CHOLESTEROL MISCONCEPTIONS • Using margarine instead of butter will help lower my cholesterol. • Thin people don’t have to worry about high cholesterol. • Since the nutrition label on my favorite food says there’s no cholesterol, I can be sure that it’s a “heart-healthy” choice. • I recently read that eggs aren’t so bad for your cholesterol after all, so I guess I can go back to having my two eggs for breakfast every morning.

15. Physical activity and cardiovascular disease: evidence for a dose response KOHL, HAROLD W. III. Medicine and Science in Sports and Exercise: Volume 33(6) Supplement June 2001 pp S472-S483

16. CARDIOVASCULAR DISEASE • The major observational studies relating the risk of CVD incidence and mortality to physical activity indicate that the relation is likely causal, and the majority provide convincing evidence for a dose-response relation. • A limitation of these studies, however, is that CVD is a large collection of diseases and disorders, many which may not be related to the atherosclerotic process or other biologic mechanisms that may be affected by physical activity

17. CORONARY HEART DISEASE • 31 publications relating dose of physical activity to risk of CHD have been published since 1958 • Twenty of the reviewed studies were judged to provide support for a dose-response relation between physical activity and CHD • Three studies provided mixed support for such a relation depending on the indices of physical activity used or cohort characteristics (data stratification) presented. • Eight studies did not support the conclusion of a dose-response relation between physical activity and CHD • Physical activity is inversely related to risk of CHD, and the bulk of the observational studies suggest this inverse relation to be a dose response.

18. STROKE • Fifteen major studies (16 separate publications) that provide evidence toward evaluation of a physical activity dose-stroke response are available for review. • Six of the studies were judged to provide evidence of a dose-response relation • Eight studies provided no support for a dose-response relation • Two provided mixed support (varying results in separate subanalyses) Strikingly, several studies reported prominent U-shaped distributions of the relation between physical activity and risk of stroke • The importance of this observation lies in the fact that the pathophysiology of the two types of stroke is very different, and it is possible that physical activity may be differentially related to one type (occlusive) and not the other.

19. SUMMARY • Physical activity is causally and inversely related to the risk of death due to CHD. • A variety of mechanisms are available. • Physical activity is known to indirectly do so and to positively be associated with blood pressure, clotting factors, glucose tolerance, and smoking habits all factors that have been associated with increased risk of stroke.

20. SUMMARY • Given the probability of common pathophysiologic mechanisms in CHD and ischemic stroke, namely atherosclerosis, it follows that physical inactivity would also adversely affect the risk of stroke. • Although attractive as a hypothesis, the currently available data are equivocal concerning the role that physical activity may play in the risk of stroke. • Existing studies do not show the consistencies noted in the association that are seen for CVD and CHD and do not support the conclusion of a dose-response relation.

21. Response of blood lipids to exercise training alone or combined with dietary intervention Medicine and Science in Sports and Exercise: Volume 33(6) Supplement June 2001 pp S502-S515 LEON, ARTHUR S.; SANCHEZ, OTTO A.

22. The National Cholesterol Education Program (NCEP) • Total cholesterol (TC) level of ≥ 6.2 mmol·L- 1 (>240 mg·dL- 1) • LDL-C level of ≥ 4.1 mmol·L- 1 (>160 mg·dL- 1) • TC levels of 5.2 mmol·L- 1 to 4.0 mmol·L-1 (200-239 mg·dL- 1) • LDL-C levels of ≥ 34 mmol·L- 1 (130 mg·dL- 1) as borderline high. • In the presence of CVD or two or more other risk factors, borderline levels of TC and LDL-C are considered elevated. • HDL-C levels ≤ 0.9 mmol·L- 1 (≤35 mg·dL- 1) classified as low • HDL-C levels ≥ 1.6 mmol·L-1 (≥60 mg·dL) as a negative risk factor or a protective factor against CHD

23. PHYSICAL ACTIVITY • A consensus exists that physical inactivity and reduced cardiorespiratory endurance contribute to risk of CHD • A consensus already exists that at least 12 wk of endurance exercise is required to have a training effect on blood lipids • Particularly an increase in HDL-C and a reduction in TG levels

24. EXERCISE TRAINING • 51 studies uncovered in this literature search, of which 28 were randomized RCT. • Exercise training was performed at a moderate to hard intensity, three to five times per week for 30 min or more per session. • The duration of exercise training ranged from 12 wk to 2 yr. • Training generally resulted in significant improvements in VO2max ranging from <3% to over 50%, with the mean increase across studies of 15.7%.

25. EXERCISE TRAINING • The most commonly observed lipid change was a significant (P < 0.05) increase in HDL-C in 24 of the 51 studies (47%). • The exercise-induced change in HDL-C ranged from a decrease of 5.8% to an increase of about 25%, with a mean increase of 4.6% across these studies (P < 0.05) • It has been well documented by feeding experiments that a reduced saturated fat intake in addition to reducing targeted LDL-C also is likely to reduce HDL-C • It appears from this review that aerobic exercise training negates or attenuates this dietary-induced reduction in HDL-C, particularly if there is an associated substantial weight loss, i.e., ≥ 4 kg.

26. EXERCISE TRAINING • Exercise training in the absence of simultaneous dietary interventions resulted in mean reductions in TG, LDL-C, and TC of about 3.7% (P < 0.05), 5.0% (P < 0.05), and 1.0% (P = NS), respectively, across studies. • This review confirms the observations of previous reviewers of a marked inconsistency in blood lipid changes with endurance exercise training with an increase in HDL-C noted in only about half of the reported studies.

27. SUMMARY • Although there is a great deal of inconsistency in the response of blood lipids to endurance exercise training in both RCT and non-RCT, the bulk of the evidence supports this hypothesis. • It is estimated that for every 0.026 mmol·L-1 (1 mg·dL-1) increase in HDL-C, the risk for a CHD event is reduced by 2% in men and at least 3% in women. • The data reviewed here suggest that sex is not a predictor of responsiveness of HDL-C to training, with adult men and women appearing to respond similarly.

28. SUMMARY • Age also does not appear to be a predictor of lipid responsiveness to exercise training, with elderly men and women as likely, or perhaps even more likely, than younger individuals to increase HDL-C with training. • On the basis of this review, baseline lipid levels appear to strongly influence the lipid response to training. • A low pre-training HDL-C was shown to be a moderately strong predictor of a positive HDL-C response to training.

29. SUMMARY • There currently are insufficient data from available training studies to conclusively establish a dose-response relationship between intensity and volume of exercise and lipid responses, suggested by observational studies.

30. AHA Scientific Statement Exercise and Physical Activity in the Prevention and Treatment of Atherosclerotic Cardiovascular Disease Circulation. 2003;107:3109

31. EXERCISE AND CAD • Epidemiological studies, combined with studies providing biological plausibility, provide conclusive evidence that physical activity reduces the incidence of CAD. • Physical activity both prevents and helps treat many established atherosclerotic risk factors, including elevated blood pressure, insulin resistance and glucose intolerance, elevated triglyceride concentrations, low high-density lipoprotein cholesterol (HDL-C) concentrations, and obesity. • Exercise in combination with weight reduction can decrease low-density lipoprotein cholesterol (LDL-C) concentrations and limit the reduction in HDL-C that often occurs with a reduction in dietary saturated fat.

32. EXERCISE AND CAD • Cardiac mortality was reduced 31% (P<0.05) and 26% (P<0.05) for the exercise-only and comprehensive programs, respectively. • Neither the exercise-only program nor the comprehensive intervention significantly reduced the rate of nonfatal myocardial infarction. • Rates of sudden cardiac death were not reduced, although only 4 exercise-only and 14 comprehensive rehabilitation trials analyzed this outcome. • Only 5 exercise-only trials and 10 comprehensive trials examined the rate of coronary artery bypass grafting.

33. EXERCISE AND CAD • Exercise-based cardiac rehabilitation reduces cardiac mortality (27%) but does not reduce the risk of recurrent myocardial infarction. • Exercise is useful for patients with angina • Exercise may improve electrical stability and coronary vasomotor responses.

34. EXERCISE AND CAD • The most common risk of physical activity is musculoskeletal injury • Increase risk due to obesity, volume of exercise, and vigorous exercise • Vigorous exercise (> 60%) increases the risk of sudden cardiac death and MI • The incidence of sudden death is not well defined • Approximately 5-10% of MI are associated with vigorous exercise

35. SUMMARY 1. Physical activity and exercise training have important roles in: A. Preventing atherosclerotic CAD; B. Managing selected CAD risk factors, including elevated triglyceride levels, low HDL-C, hypertension, glucose intolerance, hypertension, obesity, and possibly cigarette use; C. Treating patients with CAD, HF, and claudication.

36. SUMMARY 2. Healthcare professionals should: A. Engage in an active lifestyle; B. Encourage schools to teach skills required for physically active lifestyles and communities to develop programs and facilities conducive to physical activity; C. Be educated about exercise as a therapeutic modality and the importance of lifelong physical activity in their patients; D. Routinely prescribe exercise and increased physical activity to their patients in accordance with recommendations provided by the CDC/ACSM7 and the AHA; E. Perform exercise testing before vigorous exercise in selected patients with cardiovascular disease and other patients with symptoms or those at high risk.

37. SUMMARY 3. Additional research should: A. Address behavioral strategies to increase and maintain physical activity over the lifespan; B. Increase the scientific rationale supporting the importance of physical activity by examining the amount of exercise required to alter CAD risk, the effect of exercise on morbidity and mortality, and its cost-effectiveness.