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The goal of this work is to use inverse dynamics to estimate joint torques and muscle forces resulting from using the ARED, and thus more accurately prescribe exercise regimens for the astronauts. In general an exercise plan should consist of aerobics , exercises that increase the strength and endurance of various skeletal muscle groups, and flexibility exercises to maintain good joint function. The blood flowing through the heart does not directly serve the heart. Corrosion Debris Dust Weather. The 4 Parts of the Cardiovascular System. Physical movement creates supplemental oxygen and stimulates the lymphatic system.
Central nervous system
It is still not clear whether beta endorphin levels outside of the brain rise and fall in a parallel manner with those in the brain. At present, the hypothesis that exercise-produced endorphins result in mood alteration remains plausible, but not satisfactorily demonstrated in the literature. Allen's "detoxification" theory is another credible explanation. With this theory, it is hypothesized that exercise "detoxifies," or gets rid of the stress-related hormones quickly.
This could be a result of the increased metabolism from exercise or possible unknown hormones involved in this complex occurrence.
The efficacy of exercise to reduce stress and improve mental well-being is well-founded and supported even though the underlying mechanisms to these changes is speculative.
Yet there is plenty of reason to be optimistic that this mystery will unfold. A great deal of interest exists in the research community involving this phenomenon which will surely lead to a better understanding, development and application of theories underlying the relationship between physical activity and mental health.
The Effect of Exercise on Cardiac Risk It is important to emphasize that only individuals with underlying heart disease are at risk of a cardiac event i.
No evidence suggests that people with healthy cardiovascular systems are at risk of sudden cardiac death from exercise. It is the cardiovascular pathology, not the exercise, that establishes the likelihood of a cardiac event Franklin et al. The importance of the aerobic warm-up and cool-down cannot be minimized, as this is the time when cardiovascular events may occur. For instance, one theory regarding the risk of a cardiac event upon abrupt cessation of exercise involves the relation between blood pressure and the hormones, epinephrine and norepinephrine.
During exercise, epinephrine and norepinephrine stimulate the heart to beat faster. When exercise stops abruptly, the blood pressure begins to drop rapidly, but the hormone response continues to stay up, causing the heart to continue its fast pumping. The venous blood return to the heart also slows creating an imbalance in the body's circulatory system the heart is rapidly pumping with an inadequate blood supply.
This anomaly may mediate an irregular heart response. This is why exercisers need to be continually reminded of the importance of a progressive aerobic cool-down to their workout. There is an increase in caloric output through endurance-type exercise that provides a significant and desirable option for unbalancing the energy balance equation i.
The alterations in body composition most often attributed to aerobic exercise are a decrease in fat weight and a maintenance or slight increase in fat-free mass indicating the importance of aerobic exercise to burning calories and losing body fat Hoeger, Although resistance training does not usually create the caloric deficit that rhythmic aerobic activities do, it can increase the body's resting metabolic rate the amount of energy used by the body during rest due to the increase in muscle tissue.
Metabolic rate is directly proportional to lean body mass: Muscles expend calories much more than fat. For instance, a pound of muscle may burn as much as 40 to 50 more calories a day than a pound of fat Rosato, Therefore, an exercise program combining aerobic activities with resistance training appears to be the best combined approach of using exercise in weight management programs. Summary Understanding some of the underlying physiological mechanisms of how physical activity can affect bodily processes can help you better explain to your clients and students the overall value of a complete health and fitness program.
As fitness educators, our continued efforts will then be focused on developing various strategies to increase the commitment and motivation of our students towards lifetime enjoyment of physical activity.
Its nature and control. The effects of aerobic exercise on plasma catecholamines and blood pressure in patients with mild hypertension. Journal of the American Medical Association, , Core concepts and labs in physical fitness and wellness. Physical fitness training and mental health. American Psychologist, 36, Exercise and cardiac complications: Do the benefits outweigh the risks? Physician and Sportsmedicine, 22, Running through your mind.
Journal of Psychosomatic Research, 22, Training induced adaptation of skeletal muscle and metabolism during submaximal exercise. Journal of Physiology, , Sympathetic and parasympathetic cardiac control in athletes and nonathletes at rest. Journal of Applied Physiology, 52, Physiology of exercise 2nd ed. Beta-Endorphin and components of emotionality discriminate between physically active and sedentary men. Biological Psychiatry, 26, Energy, nutrition, and human performance 3rd ed.
Application of exercise for weight control: The trait psychology controversy. Research Quarterly for Exercise and Sport, 5 1 , Exercise and mental health. The fifth report of the joint national committee on detection, evaluation, and treatment of high blood pressure. Archives of Internal Medicine, , Fitness for wellness 3rd edition.
Medicine and Science in Sports and Exercise, 21, The most common gallop heart sound noted in dogs is a result of an accentuated S 3 and typically occurs secondary to a normal quantity of blood "dumping" into a stiff left ventricle eg, DCM , or a massive amount of blood "dumping" into a normal left ventricle in early diastole eg, mitral regurgitation and patent ductus arteriosis.
An S 4 gallop heart sound is caused by atrial contraction pushing blood into a stiff left ventricle. In cats with cardiomyopathy, especially hypertrophic cardiomyopathy, the left ventricle is stiff, so both third and fourth heart sounds can be heard. However, because the heart rate commonly exceeds — bpm in cats in an examination room, it is usually impossible via auscultation to determine whether the gallop sound is due to an S 3 or S 4 gallop; often, it is a summation of the two.
Gallop rhythms are not the only three-heart-sound rhythms that can be ausculted. Systolic clicks also occur in dogs and cats and are much more common than gallop rhythms in dogs. A systolic click is a short, sharp sound that occurs during mid to late systole. In dogs, they occur mostly in middle-aged to older small-breed dogs and are thought to be evidence of early myxomatous AV valve degeneration causing mitral valve prolapse as they are in people.
A systolic murmur may or may not also be present. Although systolic clicks are reasonably easy to distinguish from a gallop sound in a dog they are usually relatively loud and high pitched whereas a gallop sound is soft and low-pitched , they often sound identical to a gallop sound in a cat. Thoracic radiographs can be used to help make the distinction between the two. In cats, gallop sounds are heard only in those with severe heart disease. Systolic clicks are usually heard in cats with an otherwise normal heart.
So if the heart is not enlarged, the sound is more likely a systolic click. Systolic clicks usually are single but may be multiple and can vary in intensity even completely disappearing depending on cardiac loading conditions.
Rarely, a three-heart-sound rhythm can be caused by a bigeminal rhythm. Splitting of S 1 is caused by discordant closure of the mitral and tricuspid valves, which can occur when there is asynchronous contraction of the ventricles as in left or right bundle-branch block, cardiac pacing, and ectopic premature ventricular beats.
Splitting of S 1 can also occur in healthy, large-breed dogs and in large animals. Delayed closure of the pulmonic valve in relation to the aortic valve results in splitting of S 2. Splitting of S 2 can be a normal finding in horses during respiration.
Abnormal splitting of S 2 has been associated with pulmonary hypertension, as in pulmonary emphysema of horses and severe heartworm disease in dogs. Other possible causes include a large atrial septal defect, right bundle-branch block, or premature ventricular ectopic beats of left ventricular origin. Delayed closure of the aortic valve paradoxical splitting of S 2 might be heard with left bundle-branch block or premature ventricular ectopic beats of right ventricular origin.
A split second heart sound is a subtle finding that usually must be heard several times before it can be appreciated.
Heart murmurs are audible vibrations sound emanating from the heart or major blood vessels. The vast majority are due to turbulent blood flow brought on by high velocity blood flow that produces a mixed-frequency murmur. Much less commonly, they are due to vibrations of cardiac structures such as part of a valve leaflet or chordal structure that produces a single frequency musical murmur.
Murmurs are typically defined relative to timing systole, diastole, continuous , intensity grade I-VI , and location eg, left apex, left base but can also be characterized by frequency pitch , quality eg, musical , and configuration eg, crescendo-decrescendo.
A systolic murmur is classically described as either ejection crescendo-decrescendo or regurgitant holosystolic, plateau. However, making this distinction is often difficult, even for an experienced examiner, especially when the heart rate is fast. Ejection-quality systolic murmurs typically demonstrate the greatest intensity during mid-systole and appear diamond-shaped on phonocardiography.
They are most commonly produced by stenotic lesions at the semilunar valves eg, pulmonic stenosis or subaortic stenosis. A classic regurgitant systolic murmur demonstrates a constant intensity throughout systole and is commonly caused by mitral or tricuspid regurgitation eg, myxomatous degeneration of the mitral valve or a ventricular septal defect.
However, these murmurs may also change intensity during systole. Diastolic murmurs are typically decrescendo decreasing in intensity through diastole and usually the result of aortic insufficiency such as that caused by aortic valve infective endocarditis in dogs or degenerative disease in horses.
In horses, the murmur of aortic insufficiency is most commonly musical, although "musical" in this context is a technical term single frequency. They may sound like a dive-bomber or grunting. A continuous murmur is most commonly the result of patent ductus arteriosus and occurs throughout systole and diastole.
A continuous murmur varies in intensity over time, typically being most intense at the end of ventricular ejection second heart sound and then decreasing in intensity through diastole. A to-and-fro murmur describes a murmur that occurs both in systole and in diastole eg, in an animal with subaortic stenosis and aortic insufficiency. In horses, early systolic and diastolic murmurs can be noted in the absence of heart disease or anemia.
The point of maximal intensity is typically located over the left heart base. A short, high-pitched, squeaking, early diastolic cardiac murmur is sometimes heard in healthy, young horses. Often, a systolic heart murmur is heard in a cat without cardiac disease.
Some of these systolic murmurs are due to an increase in right outflow tract flow velocity dynamic right ventricular outflow tract obstruction. Innocent cardiac murmurs are also sometimes noted in immature cats and dogs Heart murmur intensity is classified as follows: Grade I—the lowest intensity murmur that can be heard, typically detected only while auscultation is performed in a quiet room; Grade II—a faint murmur, easily audible, and restricted to a localized area; Grade III—a murmur immediately audible when auscultation begins; Grade IV—a loud murmur immediately heard at the beginning of auscultation but not accompanied by a thrill; Grade V—a very loud murmur with a palpable thrill; and Grade VI—an extremely loud murmur with a thrill and that can be heard when the stethoscope is just removed from the chest wall.
Arrhythmias are abnormalities of the rate, regularity, or site of cardiac impulse formation and are noted during auscultation. Other terms such as dysrhythmia and ectopic rhythm are also used to describe arrhythmias.
The presence of a cardiac arrhythmia does not necessarily indicate the presence of heart disease; some arrhythmias are normal, such as sinus arrhythmia in a dog and second-degree AV block in a horse; many cardiac arrhythmias are clinically insignificant and require no specific therapy.
Some arrhythmias, however, may cause severe clinical signs, such as syncope, or lead to sudden death. Numerous systemic disorders may be associated with abnormal cardiac rhythms. For discussion of specific arrhythmias, see Common Tachyarrhythmias.
Common auscultatory findings in animals with an arrhythmia are a rate that is too slow bradycardia , a rate that is too fast tachycardia , premature beats a beat is heard too early , an irregular rhythm, and pauses in the rhythm. Whenever an abnormal rhythm is heard, an ECG should be performed. The arterial pulse is the rhythmic expansion of an artery that can be digitally palpated or visualized during physical examination.
Physiologically, the pulse pressure is the systolic pressure minus the diastolic pressure. The arterial pulse can be felt best in several different locations.
For example, in dogs and cats, the arterial pulse is typically palpated at the femoral artery. In horses, the facial artery is usually used. To feel the maximum pulse, an examiner must first occlude the artery with his or her fingers and then gradually decrease the digital pressure until the maximum pulse is felt. A weak pulse a reduction in pulse pressure is usually caused by a decrease in systolic pressure and can be noted with decreased stroke volume in animals in heart failure, hypovolemic shock, or cardiac tamponade, as well as with subaortic stenosis.
However, a weak pulse can also be felt in a healthy animal if the artery is not palpated appropriately or in an obese or heavily muscled animal. A bounding pulse an increase in pulse pressure is usually caused primarily by a reduced diastolic pressure and can be noted with aortic insufficiency and patent ductus arteriosus.
However, the pulse in a thin, athletic dog may also feel stronger than expected. The pulse felt with mitral regurgitation is often normal but at times may be termed "brisk. This often occurs as the result of a premature beat that occurs so early that the ventricles are unable to fill sufficiently, resulting in a reduced stroke volume that produces either a weak pulse or no pulse.
Atrial fibrillation also produces pulse deficits as well as alternating pulse strength. Dogs with severe subaortic stenosis may have a pulse pressure that slowly increases during ventricular systole and reaches a peak pressure late in systole called pulsus parvus et tardus. Pulsus paradoxus is a decrease in pulse pressure during inspiration and an increase in pulse pressure during expiration.
This is a normal occurrence in animals, but it is too subtle to observe on physical examination. Animals with cardiac tamponade severe pericardial effusion , however, demonstrate an exaggeration of this finding, so it becomes detectable. Pulsus alternans is an alternating strong and weak pulse while the animal is in sinus rhythm; it can be noted albeit rarely in animals with severe usually terminal myocardial failure or tachyarrhythmias.
Pulsus bigeminus is an alternating strong and weak pulse caused by an arrhythmia such as ventricular bigeminy. The weaker pulse during the ventricular premature contraction typically follows a shorter time interval than the stronger pulse. Jugular venous pulsation can be noted in normal animals but typically does not extend beyond the thoracic inlet. Pulmonary edema may develop as a result of congestive heart failure CHF. Animals with pulmonary edema will be hyperpneic increased rate and depth of respiration and may be dyspneic.
The increased depth of respiration may increase bronchovesicular sounds. Fine, and less commonly, coarse crackles might be ausculted in animals with pulmonary edema, but fine crackles are usually heard only at the end of a deep inspiration. Coarse crackles in dogs are most commonly heard with chronic bronchitis. Pulmonary edema is often silent no auscultatory abnormality. Respiratory sounds may be absent in animals with pleural effusion, especially ventrally. Abdominal distention may occur as a result of gas, soft tissue, or fluid accumulation.
Animals with right heart failure eg, due to severe heartworm disease, severe tricuspid valve dysplasia, cardiac tamponade can develop ascites. Because there are many causes of ascites, it is important to evaluate the jugular veins in every case in which ascites is present.
If right heart failure is the cause of the ascites, the jugular veins may be distended but often are not in dogs and cats by the increase in right atrial pressure. If the jugular veins are not distended in a dog or cat with ascites, a hepatojugular reflux test should be performed.
To do this, one person examines the jugular veins with the animal standing or sitting, while another places firm and steady pressure on the abdomen. In a dog or cat in right heart failure, the jugular veins should distend well up the neck with this maneuver. If ascites is present without jugular venous distension and with a negative hepatojugular reflux test, then extracardiac causes of the ascites should be considered.
The diaphragm may contract synchronously with the heart to produce loud thumping noises on auscultation and usually visible contraction in the flank area. The syndrome results from stimulation of the phrenic nerve by atrial depolarization and occurs primarily when there is a marked electrolyte or acid-base imbalance, particularly with hypocalcemia. It is most common in horses and dogs. It is seen most commonly in dogs in association with hypocalcemia and electrolyte disturbances induced by GI disease.
Similarly, in horses it is seen with hypocalcemia and in endurance horses that are dehydrated and electrolyte depleted. Thoracic radiographs frequently provide valuable information in the assessment of animals with or suspected of having heart disease.
However, thoracic radiography is rarely performed in horses or cows to evaluate heart disease because of the animal's large size and body conformation, which reduces the quality of the images. In dogs, in which numerous different body types must be dealt with, chest conformation must always be assessed before attempting to evaluate cardiac size. On the lateral view, dogs can be normal, shallow-chested, or deep-chested.
On the dorsoventral DV or ventrodorsal VD views, they can be normal, narrow-chested, or barrel-chested. Many small breeds of dogs are shallow-chested. This makes the cardiac silhouette appear to be enlarged on the lateral view and often necessitates relying on the DV view to obtain an accurate assessment of size and shape. In deep-chested breeds, even severe cardiomegaly can look normal on the lateral view and, because the heart sits more upright in the chest, can also mask its presence on the DV view eg, in Doberman Pinschers with DCM.
Obesity also interferes with accurate reading of cardiac size by the presence of intrapericardial fat or by pushing the diaphragm forward, reducing the size of the thoracic space and pushing the heart into the cranial and narrower aspect of the thoracic cavity. Because of the marked variation in chest conformation, the changes seen between inspiration and expiration, and the changes seen between systole and diastole, only relatively dramatic changes in overall cardiac size can be identified in most dogs.
Consequently, conditions such as mild generalized cardiomegaly cannot be identified on thoracic radiographs. The one chamber where mild, moderate, and severe enlargement can be relatively accurately identified is the left atrium. Finding enlargement of specific cardiac chambers and great vessels makes the presence of heart disease more likely and may also provide clues as to the specific disease present.
Cardiogenic pulmonary edema is a common finding in animals with CHF and may be associated with pulmonary venous congestion. However, the identification of pulmonary edema is often difficult and may not be possible in some dogs and even some cats. Cardiogenic pulmonary edema in dogs is typically found in the caudodorsal aspects of the lungs. In many cases, this region has an interstitial density that is enhanced by age and by expiration, giving a false impression that pulmonary edema is present or masking the presence of pulmonary edema.
Digital radiography units, especially if not set up perfectly to match analog units , have made the diagnosis even harder in many cases. In animals with chronic left heart failure, the left atrium is usually severely and always at least moderately enlarged.
In acute heart failure eg, chorda tendineae rupture , the left atrium may not be enlarged. Pleural effusion can usually be readily identified radiographically. In most species, this is seen with right or biventricular heart failure. However, in cats it is seen most commonly with left heart failure. Resolution of these abnormalities on subsequent thoracic radiographs can be used as one indication of efficacy of therapy.
The presence of pulmonary edema or pleural effusion does not definitively confirm a cardiogenic origin or exclude another origin. Overall cardiac size can be assessed using the vertebral heart scale or score. This is most commonly done using the lateral projection. The maximal diameter of the cardiac silhouette from cranial to caudal is measured, as well as the distance from the carina to the apex of the cardiac silhouette dorsal to ventral. These lengths are added together and measured in terms of thoracic vertebral bodies, so they are normalized for the size of the animal.
The vertebral bodies are measured from the fourth thoracic vertebra caudally. The normal range is 8. In many cases, it is more important to try to accurately assess the size of the left atrium than the overall size of the cardiac silhouette. Electrocardiography is the recording of cardiac electrical activity from the body surface surface ECG.
It should primarily be used to identify cardiac arrhythmias. It can also identify conduction disturbances that do not alter rhythm and has been used to identify chamber enlargement in dogs and cats.
However, its inaccuracy in identifying chamber enlargement and the advent of diagnostic ultrasound have diminished this role. Consequently, there is no relationship between complex height on a surface ECG and chamber enlargement. The most common ECG lead used in large animals is a base-apex that produces large deflections and is used for rhythm analysis.
ECGs should be used only to characterize an arrhythmia in an animal with an auscultatory arrhythmia and to monitor rhythm during anesthesia; they should never be used as screening tools, as they are in human medicine primarily for changes secondary to coronary artery disease.
Chamber enlargement can be indicated by waveform abnormalities in dogs and cats, but these abnormalities are commonly absent when there is chamber enlargement and are sometimes present when the heart is normal. In lead II in dogs and cats, wide or notched P waves suggest left atrial enlargement, whereas tall P waves suggest right atrial enlargement.
Deep S waves in the same leads in which the positive electrode is on the left side of the heart or the presence of a right-axis deviation suggest right ventricular enlargement. Wide QRS complexes can be seen in animals with either right or left ventricular enlargement; however, they can also be due to conduction disturbances see AV Conduction Disturbances. The ECG is very insensitive at identifying mild to moderate changes in chamber size and unacceptably insensitive for detecting severe enlargement.
Although false-positive findings are less frequent than false-negative findings, they do occur. Consequently, the accuracy is unacceptable, especially when compared with echocardiography and even with thoracic radiography. The sinus node initiates depolarization of the rest of the heart in a healthy animal, sets the normal rate and rhythm, and is called the normal pacemaker of the heart.
It functions as the pacemaker because it is automatic depolarizes on its own and does so at a rate faster than the other automatic sites in the heart AV node and Purkinje fibers. Normal sinus rhythm is regular and originates at the sinus node, indicated on the ECG by a P wave that precedes each normal QRS complex. The rate at which the sinus node fires varies tremendously from species to species and situation to situation.
For example, a healthy horse can have a heart rate of 30 bpm at rest and bpm during maximal exercise. A healthy cat can have a heart rate of bpm at rest in an examination room.
Sinus bradycardia is a regular sinus rhythm that is slower than expected for that species and for the situation the animal is in. Treatment for sinus bradycardia is typically not needed unless clinical signs associated with the bradycardia, such as exercise intolerance, weakness, or collapse, are noted. In dogs and cats, atropine 0.
The initiating cause should also be corrected. Sinus tachycardia is the finding of a regular sinus rhythm at a rate faster than normal but generally appropriate for the situation the animal is in eg, stress, exercise, heart failure. If the rate is inappropriately high eg, bpm in an otherwise healthy dog at rest at home , another form of tachycardia eg, atrial or ventricular should be considered.
Causes include stress resulting in high sympathetic drive , exercise, hyperthyroidism, fever, pain, hypovolemia, cardiac tamponade, heart failure, or administration of agents that can increase the rate of sinus node discharge eg, catecholamines.
Treatment involves resolving the underlying cause. Sinus arrhythmia occurs as a result of irregular discharge of the sinus node most commonly associated with the respiratory cycle. The site of impulse formation remains the sinus node; however, the frequency of the discharge varies. Sinus arrhythmia is a normal finding in dogs and horses; it is abnormal in cats in the hospital setting, although it appears to be more common in cats in their home environment.
Respiratory sinus arrhythmia is characterized by an increase in heart rate with inspiration and a decrease with expiration. In dogs, sinus arrhythmia can also be seen that is not in sync with respiration. The variation in heart rate is associated with variation in the intensity of vagal tone. It is abolished by reduced vagal tone resulting from excitement, exercise, or administration of vagolytic drugs such as atropine.
It may be associated with a wandering pacemaker, which is characterized on the ECG by taller P waves during faster rates and smaller P waves during slower rates. Sinoatrial SA block occurs when the impulse from the SA node fails to be conducted through the surrounding tissue to the atria and ventricles. This is often difficult to diagnose in dogs because sinus arrhythmia is common, resulting in a variable normal P-P interval.
Sinus arrest sinoatrial arrest, sinus pause is the absence of P waves on the ECG for a short period typically accepted as a pause exceeding twice the normal P-P interval. Sinus arrest is caused by excessive vagal tone, inherent sinus node disease, or both. This is usually due to some form of sick sinus syndrome see below. Atrial standstill is characterized as the complete absence of P waves on the ECG and occurs as a result of the atria being unable to be depolarized from the SA node discharge.
This occurs either because the atrial myocardium is functionally unable to be depolarized usually due to hyperkalemia , or because it has been destroyed by a cardiomyopathy or myocarditis persistent atrial standstill. In hyperkalemia, the sinus node continues to depolarize, and the electrical tracts from the sinus node to the AV node internodal tracts continue to function, so the sinus node controls the rate albeit at a slower rate.
With persistent atrial standstill, the sinus node is destroyed, so the animal usually has an AV nodal junctional escape rhythm with a heart rate in the 40—65 bpm range dog. Sick sinus syndrome is a constellation of abnormalities, including ECG changes sinus arrest, junctional or ventricular escape complexes, and possibly supraventricular tachycardia and possible weakness or syncope from the bradycardia usual or tachycardia rare.
With this clinical syndrome, the principal problem either lies within the SA node or perinodal tissue, or is due to increased vagal tone, or both. In some instances, other portions of the specialized conduction tissue of the myocardium, including the AV node, can also be affected. Therefore, evidence for AV block may also be seen see below. This condition is commonly noted in geriatric dogs, including Miniature Schnauzers and American Cocker Spaniels.
Medical therapy consisting of parasympatholytics eg, propantheline bromide, 0. These drugs may also worsen supraventricular tachyarrhythmias that can occur with sick sinus syndrome.
The most effective treatment for the bradycardia is pacemaker implantation. Atrioventricular AV block refers to alteration of impulse conduction through the AV node from the atria to the ventricles.
In first-degree AV block prolonged conduction , the conduction time is increased and is recognized on an ECG as an increased PR interval. This is clinically silent. In second-degree AV block intermittent conduction , occasional impulses fail to be conducted through the AV node, bundle of His, or both bundle branches and is characterized by occasional P waves not followed by QRS complexes.
During the block, there is no S 1 or S 2 and no arterial pulse.