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Chronic heart failure and all cardiac diseases have now fast become the most common cause of mortality and morbidity in the western countries. This has also become the cause of decrease in the quality of life. There have been leaps in the discovery of medications and treatments of these life threatening diseases. (QoL; Hunt et al., 2001) Due to this fact, there are more and more people who are surviving and living with these diseases.
In the United States, approximately 5 million people are afflicted with HF and more than 550,000 new cases of HF are diagnosed annually; the prevalence increases significantly by the age of 55 in both men and women (Centers for Disease Control and Prevention, 2006). Although the overall death rate declined 2% from 1993 to 2003, the rate of deaths from HF increased 20.5% during the same period (Thom et al., 2006).
But these advancements have not changed the fact that the prognosis in these patients is not very good. And mortality among severe patients still remains on the higher side of the graph.
Chronic heart failure patients do not have the ability to exercise like normal people. The main complaints of the severe patients are usually fatigue, breathlessness and inability to do any kid of physical activity.
All the studies and observations that have been made recently have placed their emphasis on the reason behind the exercise intolerance to be peripheral factors. This maybe due to the fact that there is a very poor relationship between the systolic functions of the ventricles and the capacity to exercise. Usually drugs are relied upon to improve the central hemodynamic factors. But the importance given to the capacity to tolerate physical activity is usually delayed for months!
There have been many studies in the last few decades that have proved that training and exercise in normal people(people who have not had or are not at a risk of cardiac events) have an increase in the oxygen consumption during and due to exercise. This is achieved due to both peripheral and central effects and adaptations. The muscles that are being exercised receive more blood supply from the heart(an increase in heart rate) (Sullivan et al,1988)
Central adaptations to exercise and endurance training in patients with chronic heart failure have been researched and the results are all contradictory. Few researchers also suggest that if a patient has had a myocardial infarction or any other cardiac event, further training only causes further damage to the myocardium in these patients.
Increased myocardial oxygen demand most important physiological stimulus is exercise. An increase in cardiac output is the result of exercising muscle which in turn increases blood flow. Cardiac output increases the three main things that increase myocardial oxygen demand, heart rate, myocardial contractility and ventricular work.
The left ventricle demands oxygen which is six times more during heavy exercise. This demand is met by increasing the coronary blood flow usually due to haemoglobin concentration. The right ventricle demands less oxygen at rest and during exercise which is similar to the demands of the skeletal muscle. This shows that there is a difference in the regulation of blood flow between the right and left ventricles and hence a difference between the left ventricle and the skeletal muscle.
In recent years, cardiac rehabilitation has become one of the most important long term treatment options for chronic heart failure. The last few years have seen many documentations on the adaptations of the peripheral skeletal muscle to cardiac rehabilitation(training). The arteriovenous oxygen difference is increased. The other adaptations that are caused due to exercise and endurance training are increases in mitochondrial volume and density enhanced vasodilator capacity and reductions in systemic vascular resistance during exercise.( Dubach et al,1997).
Recent studies and observations show that the most important things that determines the capacity to exercise is the changes and adaptations in the periphery. There are many reasons for this. First of all, that the left ventricular function and the central hemodynamics are not properly researched. Though there have been many improvements due to medication there is no increase in the exercise capacity. Most patients with advanced cardiac disease or chronic hearts failure usually have peripheral muscle atrophy accompanying it. Finally, in the most recent studies it has been shown and proved that metabolic disturbances are present in the peripheral skeletal muscle of patients who have chronic heart failure. These metabolic responses are in relation to sub maximal exercise.(Minotti et al,1990)
Articles discussed in this review were identified by searches of the computerized PubMed database, using ''exercise,'' ''physical activity,'' and ''heart failure'' as the primary keywords. The search encompassed the entire database from 1966 through October 2006, and articles selected for review were restricted to those in English reporting results of RCTs in human adults aged 45 or older. The search yielded a total of 747 RCTs of potential interest. Inspection of those articles identified 14 duplicates. Studies were excluded from review if exercise was not included as an intervention (e.g., resynchronization, relaxation; n ¼ 109), if the study was a crossover design (n ¼ 28), if the target population was not patients with HF or left ventricular (LV) dysfunction (e.g., end-stage renal disease, pulmonary hypertension; n ¼ 56), if the study sample was restricted to patients with diastolic HF (n ¼ 2), or if the main objective was to evaluate pharmacologic therapy (n ¼ 469). In all, 69 trials met selection criteria for this review.
There is an increase in the systole due to the increase in heart rate. The microvasculature in the sub endocardial layers of the left ventricle has increases compressive forces. The cardiac response to exercise is mainly dependant on the vascular resistance of the vessels of the cardiac chambers. Neurohormones, endothelial and myocardial factors influence the vasodilator and vasoconstrictor effects which in turn influence the coronary vessel resistance. .( Duncker et al,2008)
The mechanisms that control the vasodilatation of the coronary vessels which happens due to exercise is tough. There are differences in the various species and also problems in the vasomotor control. In animals who have been trained to exercise, the coronary blood flow rates have been seen to increase. This is due to the fact that artery diameters(coronary vasculature) increase. This is the adaptation to exercise. There are new capillaries that are formed which increases the capillary density in larger animals that are trained more vigorously(on the treadmill). This is an exercise induced hypertrophy. Exercise causes the permeability of the capillaries to increase. There is usually no change in the number of capillaries. Due to this the coronary vascular resistance is distributed, altered and increased. In response to stretch, there is an increases myogenic tone. Local control of the coronary vessels is also altered by training and also increases the vasodilatation in all the microcirculation of the coronary capillaries. This vasodilatation is usually dependant on the endothelium. An increase in the physical activity decreases heart rate. This decrease in heart rate is due to the decrease in the extra vasculature compressive forces. .( Duncker et al,2008)
We still do not know whether there is central or peripheral limitations in the demand for oxygen.In recent studies it was proved that the major limiting factor in the ability to exercise is the ability of the heart to supply and meet the oxygen demands and not the skeletal muscle. The skeletal muscle was proved to be able to carry and accommodate 300ml of oxygen per minute.(Saltin , 1985)
When a coronary artery is stenosed, there is decrease of the inflow of blood. During exercise the blood is distributed away from the subendocardium to the subepicardium. In the past studies have showed that there is a dilation in the microvasculature which is caused by the damage to the myocardium(MI). But recent studies have proved otherwise. They show that in spite of the ischemia the capillaries have the ability to respond to the stimuli that causes vasoconstriction.
The majority of resistance is at the arteries. But there are some arteries that are not in the control of the metabolic system of the myocardium. But they remain sensitive to the effects of vasodilators(nitroglycerin).
There is a collateral system in the heart that is formed due to injury to the myocardium. This can help to modulate the blood flow to the heart as and when required or when the oxygen demand is high. In the acute phase, there is an active response in the collateral vessels which is vasomotor in origin. In the chronic phase, there is the growth of collateral vessels when the artery is stenosed or blocked. These help the injured myocardium during exercise due to the increased oxygen demand.
Vasoconstrictors (vasopressin, serotonin, thromboxane)and vasodilators (nitrogycerin, atrial natriurectic peptide) have an effect on the coronary collateral vessels. These vessels are responsive to them. An increasing production of vasoconstrictors locally or otherwise can influence the conduction of the blood flow across the collateral vessels. Hence they also influence the supply to the myocardium that is damaged. One other factor that can also influence the blood flow within the collateral vessels is the vasomotor activity that is present in them. When the resistance of the collateral vessels is changed, there is proof that the adaptations of the heart which has a occlusion, occurs generally and locally. It is proved here that endurance training does not increase the growth of collaterals. But in the case of long term exercise, when the ischemia is produced by exercise, which would not e present in normal conditions, the evidence states that the growth of the collateral bed can be increased. The stress on the vessels endothelium causes a pressure gradient between the vascular beds. This determines the rate with which the blood flows. This also may be an important factor to cause the growth of the collateral bed.( Duncker et al,2008)
The main importance that training increases the capillary bed is not to increase flow but to increase the mean transit time (MTT). This is the time in which the red blood cells pass through the capillaries. .(Saltin , 1985)
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Cardiol Clin. 2001 Aug;19(3):525-36.
Exercise rehabilitation of older patients with cardiovascular disease.
Aggarwal A, Ades PA.
Cardiovascular Disease Program, Medical Center Hospital of Vermont, Fletcher Allen Health Care, University of Vermont College of Medicine, Burlington, Vermont. [email protected]
As the population of elderly patients with cardiovascular disease continues to increase, much research needs to be done with the goal of maintaining physical functioning and personal independence in this population. It is of particular importance to determine whether training programs can improve physical functioning in the most severely disabled older coronary patients. Effects of cardiac rehabilitation programs on other outcome measures, including psychosocial outcomes, lipid levels, insulin levels, and body composition require better study. Finally, the economic benefits of cardiac rehabilitation in the older coronary patients has received little attention, although early reports are promising. In summary, the older population with coronary disease is characterized by high rates of disability. Exercise training has been demonstrated to be safe and to improve strength, aerobic fitness capacity, endurance and physical function. It remains to be seen whether exercise training can reverse or prevent disability in a broad population of older patients with cardiovascular disease. If successful, cardiac rehabilitation programs will pay great medical, social, and economic dividends in this population.
Journal of Cardiopulmonary Rehabilitation:
May/June 2002 - Volume 22 - Issue 3 - pp 170-177
Hemodynamic Responses During Aerobic and Resistance Exercise
Karlsdottir, Arna E. PT, MS; Foster, Carl PhD; Porcari, John P. PhD; Palmer-McLean, Karen PT, PhD; White-Kube, Roseanne MS; Backes, Richard C. MD
PURPOSE: Resistance training has become an accepted part of cardiac rehabilitation programs. Because of the potential for a high afterload to have a negative impact on left ventricular function, there has been concern regarding the safety of resistance training for patients with congestive heart failure.
METHODS: This study addressed this concern by studying 12 healthy volunteers, 12 patients with stable coronary artery disease, and 12 patients with stable congestive heart failure during upright cycling at 90% of ventilatory threshold, and during one set of 10 repeated leg presses, shoulder presses, and biceps curls at 60% to 70% of 1-repetition maximum. Left ventricular function was measured by echocardiography.
RESULTS: The pattern of changes in heart rate, blood pressure, left ventricular ejection fraction, wall thickness, and left ventricular internal diameters was similar across all three groups of subjects, although there were large differences in absolute values. Despite elevations in diastolic and mean arterial pressures during resistance exercise, there was no evidence of significant rest-to-exercise deterioration in left ventricular function during leg press (ejection fraction, 60%-59%, 56%-55%, and 38%-37%), shoulder press (66%-65%, 59%-53%, and 38%-35%), or biceps curls (63%-58%, 53%-54%, and 35%-36%), as compared with cycle ergometry (63%-69%, 51%-57%, and 35%-42%) in the healthy control subjects, the patients with coronary artery disease, and the patients with congestive heart failure, respectively.
CONCLUSIONS: Left ventricular function remains stable during moderate-intensity resistance exercise, even in patients with congestive heart failure, suggesting that this form of exercise therapy can be used safely in rehabilitation programs.