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HEART RATE: FREQUENCY FACTORS FOR ENDURANCE

By: Bill Misner Ph.D. INTRODUCTION One common question from endurance athletes is why is my heart rate so high, so low, or varying in such-and-such a manner. Even experienced Cardiologists are not always able to define heart rate variations. When a heart rate is slowed, speeds up, or varies inexplicably, there are a number of mechanisms to consider. This article considers only a few of them as it would take volumes to describe every instance in which the heart is called to vary its rate in response to specific life-support demands. This paper reviews the science of slow heart rate, fast heart rate, the athletic heart syndrome, differences in between athletes and non-athletes, and a few of the numerous changes in heart rate frequency response. HEART RATE VARIATIONS FROM SLOW TO FAST SINUS BRADYCARDIA (brady - slow) occurs when the hearts rate is SLOWER than 60 beats per minute. The sinus bradycardia rhythm is similar to normal sinus rhythm, except that the RR interval is longer. Each P wave is followed by a QRS complex in a ratio of 1:1. The PR interval is often slightly prolonged and occasionally, the P-waves might be abnormally wide. The symptoms of sinus bradycardia may include dyspnea, dizziness, and extreme fatigue. Bradycardia may be accompanied by an increase in stroke volume due to greater end diastolic pressure (preload). The pulse volume may be greater due to a greater stroke volume and an increased diastolic run-off time (longer time for blood to flow away from the heart). SINUS BRADYCARDIA (brady - slow) MAY OCCUR DUE TO: A-Increase in parasympathetic (vagal) tone, for instance, DUE TO TRAINING IN ATHLETES. This is a normal response. The heart rate increases with exercise or atropine. B-Parasympathetic (vagal) stimulation, for instance, with carotid sinus stimulation. Stimulation of carotid sinus baroreceptors results in increased parasympathetic stimulation that decreases the heart rate. C-Sick sinus syndrome or sinoatrial (SA) node disease. These are rhythm disorders that occur if the SA node loses its ability to initiate or increase the heart rate. If the SA node is unable to properly function due to sick sinus syndrome, the AV node (or ventricular tissue if the AV node is also not functioning) take over the initiation of the heart beat, but at a rate that is slower than the sinus rhythm. D-Heart block which occurs when the signal from the SA node is slowed or stopped at the AV node or in the ventricular conducting system. Heart block is described as first, second, or third degree. The decrease in the heart rate depends on the degree of heart block. E-Acute myocardial infarctions. F-Drugs like digitalis and beta-blockers.

SINUS TACHYCARDIA (tachy = fast) occurs when the sinus rhythm is faster than 100 beats per minute. The rhythm is similar to normal sinus rhythm with the exception that the RR interval is shorter, less than 0.6 seconds. P waves are present and regular and each P-wave is followed by a QRS complex in a ratio of 1:1. At very rapid rates, the P-waves might become superimposed on the preceding T waves such that the P waves are obscured by T waves. Sinus tachycardia may be accompanied by a decrease in stroke volume because the ventricles do not have enough time to fill (after atrial systole) before ventricular contraction.. The pulse pressure may decrease due to a lower stroke volume and decreased time for diastolic run-off. Sinus tachycardia results from increased automaticity of the SA node, for instance, due to increased sympathetic stimulation of the heart, fever or cardiac toxicity.[1] The heart will beat independently of any nervous or hormonal influences. This spontaneous rhythm of the heart (called intrinsic automaticity) can be altered by nervous impulses or by CIRCULATORY SUBSTANCES, LIKE ADRENALINE. The muscle fibers of the heart are excitable cells like other muscle or nerve cells, but have a unique property. Each cell in the heart will spontaneously contract at a regular rate because the electrical properties of the cell membrane spontaneously alter with time and regularly depolarize. This means the reversal of the electrical gradient across the cell membrane that causes muscle contraction or passage of a nervous impulse. Muscle fibers from different parts of the heart have different rates of spontaneous depolarization; the CELLS FROM THE VENTRICLE ARE THE SLOWEST, AND THOSE FROM THE ATRIA ARE FASTER. The coordinated contraction of the heart is produced because the cells with the fastest rate of depolarization capture the rest of the heart muscle cells. These cells with the fastest rate of depolarization are in the sinoatrial node (SA node), the pacemaker of the heart, found in the right atrium. As the SA node depolarizes, a wave of electrical activity spreads out across the atria to produce atrial contraction. Electrical activity then passes through the atrioventricular node (AV node) and through into the ventricles via the Purkinje fibers in the Bundle of His to produce a ventricular contraction. If there is any disease of the conducting system of the heart, then this process may be interfered with and the heart rate altered. If, for example, there is disease of the AV node, then there is an electrical block between the atria and the ventricles. The ventricles will beat with their own inherent rhythm, which is much slower, usually 30-50 beats per minute. Anaesthetic drugs, like halothane, may depress the rate of depolarization of the SA node, and the AV node may become the pacemaker of the heart. When this occurs it is frequently termed nodal or junctional rhythm. This automatic rhythm of the heart can be altered by the autonomic nervous system. The sympathetic nervous system supply to the heart leaves the spinal cord at the first four thoracic vertebra, and supplies most of the muscle of the heart. Stimulation via the cardiac beta-1 receptors causes the heart rate to increase and beat more forcefully. The vagus nerve also supplies the atria, and stimulation causes the heart rate to DECREASE (BRADYCARDIA). Surgical procedures can cause vagal stimulation and produce SEVERE BRADYCARDIA(brady - slow). EXAMPLES include pulling on the mesentery of the bowel, anal dilatation or pulling on the external muscles of the eye. Under normal conditions the

VAGUS NERVE is the more important influence on the heart. THIS IS ESPECIALLY NOTICEABLE IN ATHLETES WHO HAVE SLOW HEART RATES. THERE ARE NERVOUS REFLEXES THAT EFFECT HEART RATE. The afferent are nerves in the wall of the atria or aorta that RESPOND TO STRETCH. The aorta contains high pressure receptors. When the blood pressure is high these cause reflex slowing of the heart to reduce the cardiac output and the blood pressure. Similarly, when the blood pressure is low, the heart rate increases, as in shock. Similar pressure receptors are found in the atria. When the atria distend, as in heart failure or overtransfusion, there is a reflex increase in the heart rate to pump the extra blood returning to the heart. When there is a sudden reduction in the pressure in the atria the heart slows. This is called the BAINBRIDGE REFLEX and is the cause for the marked bradycardia sometimes seen during spinal anaesthesia. It is best treated by raising the legs to increase the venous return. CIRCULATORY SUBSTANCES can also affect the heart rate. CATECHOLAMINES, like ADRENALINE, are RELEASED DURING STRESS, CAUSING AN INCREASE IN HEART RATE. DRUGS are another common cause of change in the heart rate and most anaesthetic drugs can do this. HALOTHANE affects the SA node and will also depress the force of contraction of the heart. ISOFLURANE, by contrast has little direct affect on the heart, but causes peripheral vasodilation of the blood vessels. This will then decrease the blood pressure, and hence produce a reflex tachycardia as explained above. KETAMINE causes stimulation of the sympathetic nervous system, and therefore produces a tachycardia. Other circulating substances may also affect the heart rate, acting indirectly through the autonomic nervous system. For example INCREASED BLOOD CONCENTRATIONS OF CARBON DIOXIDE will cause stimulation of the sympathetic nervous system and tachycardia, and is an important sign of respiratory failure.[2] ATHLETIC HEART SYNDROME The constellation of normal anatomic and physiologic adaptations in persons who regularly perform strenuous dynamic exercise (ENDURANCE-TRAINED ATHLETES). Resting sinus bradycardia, third and fourth heart sounds, systolic murmurs, a variety of ECG abnormalities, and cardiac enlargement on chest x-ray are characteristic. This syndrome, which would be considered abnormal in an untrained person, IS A SUCCESSFUL ADAPTATION TO ENDURANCE EXERCISE and should not be misdiagnosed as heart disease. THE PHYSIOLOGY OF INCREASED CARDIAC VOLUME AND MASS OCCUR CHARACTERISTICALLY WITH ENDURANCE TRAINING, whereas skeletal muscle and myocardial hypertrophy occur with strength (isometric) training. In the endurance-trained athlete, dilation of all four cardiac chambers and increased left ventricular wall thickness increase the pumping capability of the heart. Cardiac chamber dimensions rarely exceed the upper limits of normal. The increase in cardiac output results from a substantial increase in maximal stroke volume. In untrained persons, cardiac output increases in response to exercise primarily by an increase in heart rate. The endurance-trained athlete does so mainly by an INCREASE IN STROKE VOLUME.

Intracardiac pressures at rest are normal in endurance-trained athletes, and intracardiac, pulmonary, and peripheral vascular pressures respond normally to exercise. Ventricular work per minute is also normal.Increased cardiac output and O2 delivery to the tissues, both at rest and at all levels of exercise, are DUE PRIMARILY TO AN INCREASE IN STROKE VOLUME. Increased diastolic filling time with bradycardia further augments the stroke volume and the coronary blood flow, which is predominantly a diastolic event. The total Hb and blood volume of the endurance-trained athlete are also increased, further enhancing O2 transport. The heart rate both at rest and at all levels of submaximal exercise decreases progressively with endurance training, primarily reflecting augmented vagal tone. However, decreased sympathetic activation and possibly other nonautonomic factors that decrease the intrinsic rate of the sinus node also play a role. Despite the increase in left ventricular stroke work due to the increased ventricular volume, the O2-sparing effect of the bradycardia predominates, such that myocardial O2 demand decreases for the same absolute levels of external work. CARDIAC ENLARGEMENT AND BRADYCARDIA CHARACTERISTICALLY REGRESS WHEN ENDURANCE TRAINING IS DISCONTINUED. SYMPTOMS AND SIGNS OF SINUS BRADYCARDIA, often with sinus arrhythmia, or, occasionally, wandering supraventricular pacemaker is characteristic. FIRST-DEGREE ATRIOVENTRICULAR BLOCK CAN OCCUR IN UP TO 1/3 OF ATHLETES. Wenckebach (type 1) 2nd-degree atrioventricular block, occasionally present at rest, characteristically resolves with exercise. Ectopic atrial and junctional rhythms may occur. The arrhythmias are typically asymptomatic and characteristically decrease or disappear as the heart rate increases with exercise. QRS and T voltages are increased on the ECG, often with a prominent U wave, which may be related to the bradycardia. Repolarization (ST-T) abnormalities are common and usually normalize with exercise-induced sinus tachycardia. ACTUAL SYSTEMIC BP DIFFERS LITTLE BETWEEN ENDURANCE-TRAINED ATHLETES AND NORMAL UNTRAINED PERSONS. The carotid pulses are hyperdynamic. The left ventricular impulse is displaced, enlarged, and hyperdynamic. A third heart sound (due to early diastolic rapid ventricular filling) is frequently present; a fourth heart sound (more easily heard with increased diastolic filling time and a thin chest wall) is less common. A left sternal border ejection systolic murmur (likely reflecting nonlaminar flow across the aortic and pulmonic valves secondary to the increased stroke volume) often decreases in intensity with change from a supine to an upright posture. The cardiac silhouette is globular and enlarged on chest x-ray; at fluoroscopy, cardiac pulsations are brisk and prominent. At echocardiography, atrial and ventricular cavity dimensions and left ventricular wall thickness are increased. THE EXTENT OF BRADYCARDIA[slowing HR], CARDIAC ENLARGEMENT, OR ECG ABNORMALITY DOES NOT DIRECTLY CORRELATE WITH THE LEVEL OF TRAINING OR CARDIOVASCULAR PERFORMANCE. There is no evidence that even the most strenuous physical activity is deleterious to the cardiovascular function of a person with a normal heart or predisposes to cardiovascular disease later in life. However, sudden death, both at rest and with exertion, occurs occasionally in apparently healthy young athletes, probably due to a cardiac arrhythmia; characteristically,

undetected cardiac disease is the substrate. Although the increased ventricular refractory period with bradycardia theoretically favors the occurrence of ventricular ectopic rhythms, sudden death related to arrhythmia in athletes is most frequently due to previously undetected atherosclerotic coronary heart disease, hypertrophic cardiomyopathy, myocarditis, or congenital coronary artery or aortic valve anomalies.[3] Being an endurance athlete does not make the subject invulnerable to cardiovascular disease. EXERCISE HEART RATE FREQUENCY VARIATIONS[4, 5] Exercise heart rate is regulated by increased sympathetic activity. It varies within an individual according to: [A]-HEREDITY (size of the left ventricle in heart) [B]-FITNESS LEVEL [C]-EXERCISE MODE [D]-SKILL (economy of exercise) [E]-BODY POSTURE [F]-ENVIRONMENTAL VARIABLES (temperature, humidity, altitude) [G]-STATE OF MOOD [H]-HORMONAL STATUS [I]-DRUGS [J]-STIMULANTS [K]-EATING HABITS According to the goal of the exercise, however, the target heart rate and heart rate zones can be calculated as a percentage of the maximum aerobic power or heart rate. ACSM s latest recommendation [6] for developing and maintaining cardiorespiratory fitness in healthy adults gives 55/65%-90% of maximum heart rate (HRmax) or 40/50%-85% of oxygen uptake reserve (VO2R) as the intensity limits. Percentages of VO2max (being about 10% less than %HRmax at the same intensity) can be changed to the %HRmax with the following formula:

The Three Emanations of Pema Lingpa


The first speech incarnation of Pema Lingpa was Gyalwa Tendzin Drakpa, the first mind emanation Dawa Gyaltsen, and the first body incarnation Pema Thinley. Although, these three emanations are popularly known as the body, speech and mind emanations; later, it was common to refer to the emanations as the Peling Yab S Sum or Pema Lingpa father and sons which included Pema Lingpa himself, the mind emanation Dawa Gyaltsen and the body emanation Pema Thinley. The Peling Yab S Sum were blessed as heart-emanations of Guru Rinpoche and confirmed as the benefactors of multitude of sentient beings. The three emanations often reincarnated as teacher and pupil amongst themselves, thereby enabling the transmission and reception of the ripening and liberation teachings from one to another. This has ensured the transmission of the

lineage teachings in their entirety through an unbroken pure lineage without losing any precious blessings of the teachings in the process. Over the course of lifetimes these incarnations have benefited sentient beings greatly through their Buddha activities of blessing, empowerments and transmission of the authentic lineage teachings.

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