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HEART RATE: FREQUENCY FACTORS FOR ENDURANCE PERFORMANCE OUTCOME

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. ACSMīs 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:

%HRmax = (%VO2max + 28.12) / 1.28.

Typically, 50-60% of the maximum heart rate represents light, 60-70% light to moderate, 70-80% moderate to heavy, 80-90% heavy and 90-100% very heavy intensity. Combining the rating of perceived exertion, e.g. Borg-scale [7] with heart rate, makes the intensity to better meet the individual target intensity. For the most accurate exercise intensity (heart rate) determination (also Karvonen-formula) the measured maximum heart rate is needed. Heart rate variability (HRV) has been shown to provide an individual method for target heart rate determination. Polar OwnZone[4] (in Polar SmartEdge and M-series HR monitors) is based on a decrease in HRV during incremental exercise [8, 9]. The target heart rate determination by the OwnZone results limits corresponding to 62-84% HRmax on healthy men and women [10] and 68-86% HRmax in obese adults [11]. 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]

 

 

HEART RATE VARIATIONS: THE EXPLAINED AND UNEXPLAINED

Endurance athletes subject their bodies to a variety of metabolic demands that are known to impose stress on stroke volume and heart rate frequency. Some of the heart rate variations are explainable from science research while some are unknown. Exercise-induced ventricular tachocardia in apparently healthy subjects occurs almost exclusively in the ELDERLY and is limited to short, asymptomatic runs of 3 to 6 beats usually near peak exercise, and does not portend increased cardiovascular morbidity or mortality rates over a 2-year period of observation.[23] The physical activity pattern that occurred during RECREATIONAL SPORTS caused cardiac responses that might be dangerous to health. 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 < or =42 beats/min). During 12 years of follow-up, 312 participants died. After adjustment for standard risk factors, fitness, and resting and exercise heart rates, abnormal heart rate recovery remained predictive (adjusted relative risk, 1.55 [CI, 1.22 to 1.98]). Even after submaximal exercise, abnormal heart rate recovery predicts death.[27] MAXIMAL HEART RATE AND TREADMILL PERFORMANCE IS RELATED TO AGE. Maximal treadmill exercise heart rate, work capacity and electrocardiographic response were studied in 95 asymptomatic, predominantly sedentary women between the ages of 19 and 69 years. Average MAXIMAL HEART RATE (MHR) WAS FOUND INVERSELY RELATED TO AGE, such that MHR = 216 -0.88 (years of age) +/- 10 beats/min (X +/- 1 SD). Treadmill exercise endurance was 7.64 min +/- 1.99. THE REDUCTION OF TREADMILL ENDURANCE WITH ADVANCING AGE WAS NOT STATISTICALLY SIGNIFICANT. Asymptomatic ST-segment depression occurred in 6% of subjects. In 5% the ST segment sloped upward, and in 1% it was flat. Mean age of women with ST depression was 52 years, compared with 39 years mean age of all subjects. Premature beats during exercise were found in 20 of 95 subjects, and were not related to age. Graded exercise testing of women employing target heart rates should use heart rate tables developed especially for women. These tables do not require correction for athletically trained for sedentary life-style.[28] WHAT THEN IS THE MOST EFFICIENT TARGET HEART RATE DURING EXERCISE? An exercise stress test with a semi-supine position bicycle ergometer was evaluated in 10 normal subjects and five cardiac patients to define the appropriate target heart rate for exercise echocardiography. The normal healthy subjects were aged between 24 and 30 years, while the five patients with artificial aortic valves were aged between 13 and 54 years. The workload was continuously increased from 0 W to the maximum achieved workload at 20 W/min for normal subjects and 10 W/min for patients. Echocardiography was recorded every minute during the test procedure. End-diastolic and end-systolic dimensions were measured and ejection fraction was calculated. The ejection fraction at heart rates 50, 60, 70 and 80% of predicted maximum heart rate and at maximum workload were compared. HEART RATES AT THE MAXIMUM WORKLOAD FOR NORMAL SUBJECTS WERE 76 TO 94% (86.3 +/- 6.3%) OF THE MAXIMUM HEART RATE PREDICTED FROM THE AGE of the subjects and 70 to 102% (84.0 +/- 12.6%) for the patients. THE LARGEST EJECTION FRACTION VALUES DURING EXERCISE STRESS WERE OBTAINED AT 70% OF THE MAXIMUM PREDICTED HEART RATE IN NORMAL SUBJECTS, AND AT 60% IN THE PATIENTS. THE TARGET HEART RATE FOR EXERCISE ECHOCARDIOGRAPHY IS 70% OF THE MAXIMUM CALCULATED HEART RATE.[29]

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]

 

REFERENCES

[1]-By permission courtesy of McGill University, Class 2003; Project Author: Francis Musyoki,

Project Mentor: Dr. Michael Guevera, McGill University, Physiology Dept., Montreal, QC @:

http://sprojects.mmi.mcgill.ca/cardiophysio/sinustachycardia.htm

[2]-By permission courtesy of Dr I Kestin, Consultant Anaesthetist, Derriford Hospital, Plymouth, UK; Control of Heart Rate @: http://www.nda.ox.ac.uk/wfsa/html/u03/u03_011.htm

[3]-The Merck Manual of Diagnosis and Therapy Section 16. Cardiovascular Disorders Chapter 213. Athletic Heart Syndrome @: http://www.merck.com/pubs/mmanual/section16/chapter213/213a.htm

[4]-Courtesy of POLAR ELECTRO INC., Personal Communication 3-13-2002,

370 Crossways Park Drive

Woodbury, NY 11797-2050

800-227-1314

Fax 516-364-5454

www.polarusa.com

EMAIL: customer.service.usa@polar.fi

http://www.polar.fi/research/articlelibrary/dId4r4E8GOGg.html

[5]-ACSM. Position stand. The Recommended Quantity and Quality of Exercise for Developing and Maintaining Cardiorespiratory and Muscular Fitness, and Flexibility in Healthy Adults. Med Sci Sports Exerc 30:975-991, 1998.

[6]-Armstrong N. et al. The peak oxygen uptake of British children with reference to age, sex and sexual maturity. Eur J Appl Physiol 62:369-375, 1991.

[7]-Borg G.A.V. Psychophysical bases on perceived exertion. Med Sci Sports Exerc 14:377-481, 1982.

[8]-Tulppo M. et al. Quantitative beat-to-beat analysis of heart rate dynamics during exercise. Am J Physiol 271:H244-252, 1996.

[9]-Tulppo M. et al. Vagal modulation of heart rate during exercise: effect of age and physical fitness. Am J Physiol 274:H424-429, 1998.

[10]-Laukkanen R. et al. Determination of heart rates for training using Polar SmartEdge heart rate monitor. Med Sci Sports Exerc 39 (Suppl 5):1430, 1998.

[11]-Byrne N. et al. Use of heart rate variability in prescribing exercise intensity thresholds in the obese. Int J Obes 23 (Suppl 5):567, 1999.

[12]-Kinnunen H. et al. Reproducibility of individual training heart rate determined by Polar SmartEdge heart rate monitor. Int. Puijo Symposium, Book of abstracts, Kuopio university publications D, Medical Sciences 149:63, 1998.

[13]-Laukkanen R. et al. Is intensity control possible during aerobics classes? Med Sci Sports Exerc 29(5, Suppl): 401, 1997.

[14]-Faigenbaum A.D. Target Heart Rates: A New View of an Old Chart. ACSM Certified News 6(1):8-9, 1996.

[15]-Kaikkonen H. et al. The effect of heart rate controlled low resistance circuit weight training and endurance training on maximal aerobic power in sedentary adults. Scand J Med Sci Sports, in press 1999.

[16]-Wilmore J.H. and Costill D.L. Physiology of Sport and Exercise. Human Kinetics, Champaign, Illinois, 1994, pp. 1-549.

[17]-Gilman M.B. The use of heart rate to monitor the intensity of endurance training. Sport Med 21(2):73-79, 1996.

[18]-Piha S.J. Cardiovascular Autonomic Function Tests. Publications of the Social Insurance Institution, Finland, ML:85, Turku, 1988.

[19]-Uusitalo A. Ability of non-invasive and invasive methods of autonomic function measurements and stress hormones to indicate endurance training-induced stress. Acta Universitatis Tamperensis 621, Doctoral dissertation, 1998.

[20]-Karvonen M. et al. The effect of training on heart rate. A longitudinal study. Ann Med Exp Biol Fenn 35:307-315, 1957.

[21]-Goldberg L, Elliot DL, Kuehl KS. Assessment of exercise intensity formulas by use of ventilatory threshold. Chest. 1988 Jul;94(1):95-8.

[22]-Zhou B, Conlee RK, Jensen R, Fellingham GW, George JD, Fisher AG. Stroke volume does not plateau during graded exercise in elite male distance runners. Med Sci Sports Exerc. 2001 Nov;33(11):1849-54.

[23]-Fleg JL, Lakatta EG. Prevalence and prognosis of exercise-induced nonsustained ventricular tachycardia in apparently healthy volunteers. Am J Cardiol. 1984 Oct 1;54(7):762-4.

[24]-Atwal S, Porter J, MacDonald P. Cardiovascular effects of strenuous exercise in adult recreational hockey: the Hockey Heart Study. CMAJ. 2002 Feb 5;166(3):303-7.

[25]-Lundby C, Araoz M, van Hall G. Peak heart rate decreases with increasing severity of acute hypoxia. High Alt Med Biol. 2001 Fall;2(3):369-76.

[26]-Gonzalez-Alonso J, Mora-Rodriguez R, Below PR, Coyle EF. Dehydration markedly impairs cardiovascular function in hyperthermic endurance athletes during exercise. J Appl Physiol. 1997 Apr;82(4):1229-36.

[27]-Cole CR, Foody JM, Blackstone EH, Lauer MS. Heart rate recovery after submaximal exercise testing as a predictor of mortality in a cardiovascularly healthy cohort. Ann Intern Med. 2000 Apr 4;132(7):552-5.

[28]-Sheffield LT, Maloof JA, Sawyer JA, Roitman D. Maximal heart rate and treadmill performance of healthy women in relation to age. Circulation. 1978 Jan;57(1):79-84.

[29]-Morizuki O, Kawauchi M, Furuse A. [Target heart rate for exercise echocardiography] J Cardiol. 1994 May-Jun;24(3):199-202.

[30]-The author wishes to further express his personal appreciation to McGill University's Dr. Francis Musyoki, Derriford Hospital's Dr. I. Kestin, Consultant Anaesthetist, and Polar Electro Inc.'s website for their combinate knowledged contribution to this article. The author* has no competing interests in products or equipment mentioned in this paper.

*Bill Misner Ph.D is the Director of Research & Product Development for E-CAPS Inc: 1-800-336-1977

E-MAIL: askdrbill@e-caps.com

OTHER ARTICLES @: http://www.e-caps.com/

 

 
 
 
 
 

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