Heart Rate Variations Explained

By: Dr. Bill Misner Ph.D.

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).

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.

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.

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]

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.

Reproducibility of this method has been shown to be good [12]. Using heart rate in exercise is difficult and confusing for many individuals, e.g. when participating aerobic classes, if they do not know their maximum heart rate. Adding beats/subtracting beats to the resting/pre-exercise heart rate helps them to better control the intensity [13]. This method is a new reading approach to the target heart rate charts [14]. In typical resistance training (targeting to muscle power and strength increase) heart rate does not play very important role during exercise bouts, but may be helpful in controlling the recovery time needed between the work out sessions. However, recently a heart rate guided low-resistance circuit training program has been shown to be beneficial for both aerobic and muscular fitness [15]. Heart rate recovery period (time) can be used to detect recovery after the exercise.

The time it takes for the heart to return to its resting rate is decreased as a consequence of regular endurance training [16, 17]. Heart rate can also be used as an indicator of overstrain. Comparison between the resting heart rate and “the standing up heart rate” (body posture and venous return change) is the idea in the orthostatic test [18]. Polar Overtraining Test in Polar Precision Performance SW2.1 is the latest application in overtraining detection and is based on HRV measure during orthostatic test.[4, 19] Most endurance athletes systematically use the Karvonen formula [20, 220-age = HRmax/100%] for determining HR response value for exercise training outcome. However, the Karvonen formula appears to overestimate heart rate intensity among those of low and average fitness and may be excessive for these groups.[21] To the degree of fitness in the athlete the greater differences in heart rate frequency.

Stroke volume does not plateau during graded exercise in elite athletes. Stroke volume (SV) responses during graded treadmill exercise were studied in 1) 5 ELITE MALE DISTANCE RUNNERS and 3 male NON-EL;ITE UNTRAINED UNIVERSITY STUDENTS. “Cardiac output (Q) and SV were determined by a modified acetylene rebreathing procedure.

There were no differences in SV responses among the three groups during the transition from rest to light exercise. However, the rates of change of SV during light to maximal exercise in untrained subjects (slope = -0.1544 mL x beat(-1)) and university distance runners (slope = 0.1041) did not change, whereas it dramatically increased in elite distant runners (slope = 0.6734). Moreover, the elite distance runners showed a further slope increase in SV when heart rate was above 160 bpm, which resulted in an average maximal SV of 187 +/- 14 mL x beat(-1) compared with 145 +/- 8 and 128 +/- 14 mL x beat(-1) in the university runners and untrained students, respectively. Similarly, max Q reached 33.8 +/- 2.3, 26.3 +/- 1.7, and 21.3 +/- 1.5 L x min(-1) in the three groups, respectively. On the other hand, THERE WAS A NONSIGNIFICANT TENDENCY FOR MAXIMAL ARTERIOVENOUS OXYGEN CONTENT DIFFERENCE TO BE LOWER IN THE ELITE ATHLETES COMPARED WITH THE OTHER GROUPS.

These university distance runners and untrained university students support the classic observation that SV plateaus at about 40% of maximal oxygen consumption despite increasing intensity of exercise. In contrast, stroke volume in the elite athletes does not plateau but increases continuously with increasing intensity of exercise over the full range of the incremental exercise test.” [22]

More specifically, athletes who exceed target and maximum heart rates, had poor heart rate recovery after exercise, and had episodes of nonsustained ventricular tachycardia and ST-segment depression of uncertain clinical significance.[24] PEAK HEART RATE DECREASES WITH INCREASING HYPOXIA OR ALTITUDE…At termination of exercise, maximal plasma lactate and norepinephrine concentrations were similar to those observed during maximal exercise in normobaric normoxia. One study clearly demonstrates that A PROGRESSIVE DECREASE IN PEAK HR WITH INCREASING ALTITUDE, despite evidence of similar exercise effort and unchanged sympathetic excitation. This corresponds to approximately 1-beat x min(-1) reduction in peak HR for every 7-mmHg decrease in barometric pressure below 530 mmHg (approximately 130 m of altitude gained above 3100 m).[25] DEHYDRATION MARKEDLY IMPAIRS CARDIOVASCULAR FUNCTION IN HYPERTHERMIC ENDURANCE ATHLETES DURING EXERCISE. Compared with control, hyperthermia (1 degrees C T(es) increase) and dehydration (4% body weight loss) each separately lowered SV 7-8% (11 +/- 3 ml/beat; and increased heart rate sufficiently to prevent significant declines in cardiac output. When dehydration was superimposed on hyperthermia, the reductions in SV were significantly greater (26 +/- 3 ml/beat), and cardiac output declined 13% (2.8 +/- 0.3 l/min).

Furthermore, mean arterial pressure declined 5 +/- 2%, and systemic vascular resistance increased 10 +/- 3%. When hyperthermia was prevented, all of the decline in SV with dehydration was due to reduced blood volume (approximately 200 ml). These results demonstrate that the superimposition of dehydration on hyperthermia during exercise in the heat causes an inability to maintain cardiac output and blood pressure that makes the dehydrated athlete less able to cope with hyperthermia. [26] ABNORMAL HEART RATE RECOVERY AFTER SUBMAXIMAL EXERCISE TESTING IS A PREDICTOR OF MORTALITY. Abnormal heart rate recovery after symptom-limited exercise predicts death. It is unknown whether this is also true among patients undergoing submaximal testing.

Researchers tested the prognostic implications of heart rate recovery in cardiovascularly healthy adults undergoing submaximal exercise testing. From 5234 adults without evidence of cardiovascular disease who were enrolled in the Lipid Research Clinics Prevalence Study. Heart rate recovery was defined as the change from peak heart rate to that measured 2 minutes later (heart rate recovery was defined as As the reader may have concluded, the origin and instigation of periodic measures of exercise-induced heart rate are complex. Rest, fluids, diet, balanced electrolyte replacement, moderation in training intensity, and stress-reduction responses are resolving protocols to consider when conscious concerns for heart rate variation are presented. If a variation is not resolved or cannot be explained, the athlete should submit to responsible cardiovascular diagnostic procedures without delay.[30]