European Journal of

Applied

Eur. J. AppL Physiol. 42, 61-69 (1979)

Physiology

and Occupational

Physiology @ Springer-Vertag 1979

Resting Heart Rate in Apparently Healthy Middle-aged Men Jan Erikssen 1 and Kaare Rodahi 1 Med. Dept. B, Rikshospitalet, Oslo, Norway, 2 Institute of Work Physiology,Norwegian College of Physical Education, Oslo, Norway

Summary. Resting heart rate (fCres0 was measured by a standardized technique in 2,014 men aged 4 0 - 5 9 years during a cardiovascular survey. All men were thought to be healthy prior to the survey examination. According to the survey findings, the material was subdivided into 5 clinical subgroups, according to survey findings of coronary heart disease (CHD), or suspect symptoms, or signs. Coronary angiography was performed in 105 subjects with particularly strong suspicions of CHD. FCrest varied between 6 1 - 6 3 among the 5 groups (p > 0.10). In 1832/2014 defined as "normals" the following findings were made: 1. Mean fC~st 61 (SD 9.7), and almost identical values obtained by auscultation and from resting ECGs in the same persons. 2. Linear drop in fewest by age (-0.126 beats/year, p < 0.001). 3. Increase in fcr~st with increasing systolic blood pressure. Since there is no generally accepted technique for measuring fCrest it is suggested that the wide variation in fCrest reported in the literature at least in part may be due to differences in techniques. Key words: Resting heart rate - Heart rate-pressure relationship - Standardized techniques -. Latent coronary heart disease - Resting heart rate and CHDrisk

Resting heart rate (= forest = for) is a parameter often used in connection with the discussion of a variety of physiological and clinical conditions. It has been claimed that for, both above and below normal, may be associated with an increased risk of coronary heart disease morbidity and mortality [1, 9, 16, 17]. Low fcr is generally considered to be an indication of a high level of physical fitness [19]. Fc r is sometimes used by the work physiologist when assessing cardiovascular strain in terms of "heart rate reserve" (HRR), i.e., the difference between maximal and resting heart rates in subjects exposed to work stress in the field [ 19]. While the term fc~ has been Offprint requests to: J. Erikssen, M.D. (address see above)

0301-5548/79/0042/0061/$ 01.80

62

J. Erikssen and K. Rodahl

widely used, little attention has been paid to the conditions under w h i c h the resting h e a r t rate has been m e a s u r e d . F u r t h e r m o r e , while it is well established t h a t the m a x i m a l h e a r t rate declines with age (19), c h a n g e s in fc r with age h a v e to a lesser degree been subject to s y s t e m a t i c studies. A large scale c a r d i o v a s c u l a r survey g a v e the o p p o r t u n i t y to investigate fcr in middle aged, a p p a r e n t l y h e a l t h y m e n b y m e a n s o f a s t a n d a r d i z e d t e c h n i q u e in o r d e r (1) to assess fcr in relation to age, (2) to assess if a n y relationship does exist b e t w e e n fc r and resting systolic b l o o d p r e s s u r e ( = Parest ) and (3) to assess if a high fc, is a s s o c i a t e d with a higher p r e v a l e n c e o f detectable, hitherto u n k n o w n and u n s u s p e c t e d c o r o n a r y heart disease ( C H D ) t h a n a n o r m a l or low fcr.

Material and Methods All males aged 40-59 years from 5 major companies or governmental institutions in Oslo, Norway were asked to participate in a cardiovascular survey. All were accepted provided none of the following diseases or disorders were present: Known (or suspected) CHD, other known heart disease, hypertension under treatment with drugs, diabetes mellitus, malignancy, disorders of the locomotor system preventing a near maximal bicycle exercise test, and miscellaneous disorders (advanced pulmonary disease, advanced renal disease, liver disease etc. The exclusions were decided upon by one of the authors (JE) and the local medical officers by reading and discussing available medical records from the factory health department. All men had had regular annual or biannual health checks for years. Men who on arrival for the survey examination said that they had had any of the above mentioned diagnoses made elsewhere since the last visit to the factory health department were also excluded. The study population, therefore, represent a sample of working, presumably healthy males aged 40-59 years. Of all eligible men 2,014 (= 86% of the eligible population) participated in the study. All subjects came for the examination at 07.30 a.m. after at least 12h fasting and non-smoking. The clinical examination, including measurement of fcr and Pa r took place between 08.30 a.m. and 11.00 a.m. in all cases. A diagnosis of possible latent CHD - previously unknown and unsuspected - was made in 140 individuals in the presence of one or more of the following criteria: 1. A positive World Health Organization Questionnaire on angina pectoris on personal interview [15] (= WHO-Q). 2. A positive exercise ECG during and/or post exercise during a near maximal bicycle exercise test. The details of the test, ECG-recording and interpretation of the test are presented elsewhere [6]. 3. Typical angina pectoris during the exercise test. 4. Signs of (silent) "very probably myocardial infarction" in the resting ECG [15]. 5. A positive Greater New York Health Insurance Plan Survey questionnaire on angina pectoris (= NY-Q) 7. In the 115 individuals who fulfilled any of the criteria 1-4 coronary angiography was proposed, and performed in the 109 who gave their informed consent. The details of this validational study are presented elsewhere [6]. The material was subdivided according to the clinical and angiographicai findings as follows: 1. Group of "normals" = 1,832 individuals with no apparent symptoms/signs of CHD irrespective of other clinicai/biochemical findings. 2. "Atypical chest pain group" = 35 individuals with recurrent chest pain, thought not to be angina pectoris (negative NY-Q). 3. "Angina pectoris group" (not angiographied) = 35 individuals with angina pectoris according to a positive NY-Q (in 32 of these the sole sign of CHD, in the remaining 3 other signs were present as well, but they refused coronary angiography). 4. Angionegative group = 36 individuals with suspect CHD according to criteria 1-4, but with normal coronary angiograms [6].

Resting Heart Rate in Man

63

5. Angiopositive group = 69 individuals with a suspect CHD according to criteria 1-4, and with pathological angiograms. Four angiographed individuals were excluded for various reasons, as were 3 with suspect CHD (without angina) who refused coronary angiography. Blood pressure was measured according to Rose and Blackburn [15] with the individuals sitting. Thereafter, fc~ was measured after exactly 5 min rest supine. The fcr was measured by auscultation for exactly 1 min, time being measured with a stopwatch. The watch was started immediately after one beat, and the next beat was counted as the first beat. After a complete physical examination a standard 12-lead ECG was taken supine after another 5-min rest in another laboratory. After finishing the survey, fc~ was estimated from the ECGs in a consecutive series of 200 individuals with sinus rhythm by measuring the time taken for 10 ECG-beats, and afterwards extrapolating to the number of beats/min. This was done in order to assess the comparability of measuring fcr by auscultation and from the ECG. The data were put on magnetic tape and analyzed by computerized programs [4]. The statistical analyses performed were one-way analysis of variance, linear regression analysis, linear correlation analysis and multiple t-tests, using conventional limits of statistical significance.

Results

The fcr data from the 200 subjects in whom measurements were made both by auscultation and from the ECGs are presented in Fig. 1. It is easily seen that the two parameters are highly correlated (r = 0.89, i.e., p < 0.001). Mean fc r was 61.15 beats/min according to auscultation and 6 I. 19 according to the ECGs (SD 9.57 and 9.76, respectively). Although the mean fcr values obtained by the two methods were O

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Fig. 1. Correlation between resting heart rate measured by auscultation and from ECG in 200 middle aged men with sinus rhythm. (Regression line + / - 2 SD.) (r = 0.89)

64

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and K. Rodahl

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I n T a b l e 2 similar d a t a o n P a r in the 5 groups are seen. M a r g i n a l l y higher P a r is seen in group 5 t h a n in group 1. Otherwise, n o differences in P a r are f o u n d a m o n g groups. Regression analysis of P a r with regard to age changes in group 1 indicates a n increase in Par b y 0.75 m m H g / y e a r (p < 0.001). T a b l e 3 presents the m e a n values, s t a n d a r d deviations a n d range of fcr in relation to four arbitrarily c h o s e n Par-subgroups. It is seen that m e a n fcr increases with increasing Par, a n d several of the differences a m o n g the g r o u p s are highly statisti-

66

J. Erikssen and K. Rodahl

Table 3. Resting heart rate in relation to systolic blood pressure in presumably healthy middle aged men Systolic blood pressure (A) (< 120 m m Hg)

(B) (C) (O) (120--138 m m Hg) ( 1 4 0 - 1 5 8 m m Hg) (160 m m Hg)

58.6 8.4 584 38-93

61.0 8.7 904 37-97

64.9 10.9 389 43-113

66.3 12.6 137 36-103

2. Group I a Mean heart rate 58.5 Standard deviation 8.4 No. of individuals 544 Range 38-93

61.0 8.8 826 37-97

64.8 11.0 347 43-113

66.5 12.7 115 36-103

1. Total material Mean heart rate Standard deviation No. of individuals Range

a For definition of group I: See Material and Methods PA-c-differcnce < 0.001 ; P A D-diererencc< 0.01 ; PB-c-di~rerence< 0.05. All other differences in mean heart rate among blood-pressure subgroups not significant (i. e., p < 0.05) Table 4a. Systolic blood pressure in relation to resting heart rate in presumably healthy middle aged men

1. 2. 3. 4. 5. 6. 7. 8.

Heart rate (beats/rain)

Mean blood pressure (mm Hg)

Standard deviation (mm Hg)

Highest blood pressure

Lowest blood pressure

< 40 40-49 50-59 60-69 70-79 80-89 90-99 ~ 100

128.5 123.5 125.9 130.7 136.8 139.6 148.7 162.0

23.6 15.1 15.9 17.3 18.1 18.2 23.3 14.2

162 168 182 206 220 186 186 188

1 I0 88 88 94 100 102 102 146

Totals

130.1

17.9

220

88

No. of individuals

4 165 649 698 236 56 17 7

(0.2%) (9.0%) (35.6%) (38.0%) (12.9%) (3.1%) (0.9%) (0.4%)

1832

(100.1%)

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Resting Heart Rate in Man

67

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Fig. 2. Correlation between reating heart rate and mean resting systolic blood pressure among 1,832 apparently healthy middle aged men

cally significant. Still there is a considerable overlapping in fc r among the groups. Table 4 and Fig. 2 present Pa r in relation to subgroups of fc e Except for the 4 individuals with an fc r below 40 all groups show an increase in Pa r with increasing fcr. The association between Pa r and fcr can be expressed by means of the linear equation Pa r = (98.8 + 0.50- fcr) mm Hg. This equation was revealed by polynomial regression analysis to obtain the best curve-fit between Pa~ and fce Thus, the apparent curvilinear association in Fig. 2 is spurious. Most group differences in Table 4 are highly significant.

Discussion

Valid comparisons of various experimental, clinical, and epidemiological data can only be made when strictly standardized techniques of measurement are applied [15]. In the case of fcr, many of the reported studies lack the necessary standardization. Hence, comparisons between various surveys may be unwarranted and give rise to misleading conclusions. The study of Grimby et al. [8] demonstrates convincingly how differences in techniques may give totally different results in the same population. Thus, 4 years prior to the study of Grimby et al. the fcr was found to be approximately 90/min in a group of 793 men [18], whereas Grimby and his colleagues found an for of 67/rain [8]. The difference between the data of Grimby et al. and ours (6 beats/min) may be explained by differences in the time of the exami-

68

J. Erikssen and K. Rodahl

nations. Their subjects were examined in the afternoon whereas our subjects were examined in the morning, and it is well known that fcr increases in the afternoon when compared with the morning fcr [9, 13]. Fcr's of similar magnitudes to ours are reported by Robinson [12], Hinkle et al. [9], Cooper et al. [2], and Grimby et al. [8]. Cumming et al. [3], Paul et al. [11], Kasser and Bruce [10] and Berkson et al. [1] all report for above 75-80 in apparently healthy middle-aged men. In 104 Eskimos examined by Rodahl [14] the mean fcr was 67. It is thus apparent that there is a wide variation in the reported fCr'S in the recent literature, but it is not clear whether these differences are real or are due to differences in the way fc~ was counted and the conditions under which the method was employed, (e.g., time of the day, sitting/supine, etc.). As indicated by the present study and the study of Grimby et al. [8] and Cooper et al. [2], it seems reasonable to assume that resting, supine heart rate in healthy middle-aged men is approximately 60 in the morning and 65-70 in the afternoon. These figures are far lower than those commonly reported. The actual method of recording fcr seems to be unimportant. Thus, the mean values obtained by the two methods (ECG-tracing and by auscultation) were identical, and the r-value of the two methods was 0.89. However, fcr measured with the aid of a stethoscope and from ECG may differ considerably when assessed in the same subjects within a few minutes under seemingly similar conditions. Hinkle et al. [9] suggested that their cases with bradycardia might be suffering from disease and/or advanced age changes of the pacemaker system. It is well known that the rate of depolarization decreases considerably from childhood into adulthood, whereas Robinson [12] states that FCr remains stable from age 25-30 years. In our group of "normals" we have found a small but statistically significant drop in mean fcr between the ages of 40 and 59. The drop of 0.126 beats/year approximates 2 - 3 beats/min during 20 years. Since Pa r increases by age and fc~ is higher the higher the Pa r, this age-dependent drop in fcr is even greater if we correct for increasing Par by age (data not shown). Whereas Berkson et al. [1] claim that high for in apparently healthy subjects increases the risk of future CHD considerably, high fcr was not associated with a high prevalence of CHD in the present material. However, long-term follow-up is necessary to determine the possible impact of high fcr on future CHD in the present material. Stehbens [16] and Texon [17] state on the basis of their experimental data and mathematic models that atheromatosis may - at least in part - be caused by repeated stress on the vessel wall by each pulse wave, each heart beat repeating the stress. Thus there is some theoretical support for the notion that increased heart rate may promote the development of CHD. These theories further show the importance of studying the relation between CHD and fee To obtain valid and comparable data it is highly desirable that standardized techniques are used for measuring fee Since we have shown a strong positive correlation between for and Par it is possible that the association between fc~ and CHD noted by Berkson et al. [1] may be explained in part by this association. However, this does not exclude a role of high fc, and a hypothetically increased "wear and tear" of the hemodynamic system by an increased frequency of pulse wave microtrauma [16, 17].

Resting Heart Rate in Man

69

References 1. Berkson, D. M., Stamler, J., Lindberg, H. A., Miller, W. A., Stevens, E. L., Soyugenc, R., Tikich, T. J., Stamler, R.: Heart rate: An important risk factor for coronary mortality. - Ten year experience of the Peoples Gas Co. In: Atherosclerosis: Proceedings of the second international symposium. R. J. Jones, (ed.), p. 382. New York: Springer 1970 2. Cooper, K. H., Plllock, M. L., Martin. R. P., White, S. R., Linnerud, A. C., Jackson, A.: Physical fitness levels vs. selected coronary risk factors. A cross-sectional study. JAMA 236, 166 (1976) 3. Cumming, G. R., Borysuk, L., Dufresne, C.: The maximal exercise ECG in asymptomatic men. Can. Med. Ass. J. 18, 649 (1972) 4. Dixon, W. J.: Biomedical computer programs (Revision 1975). Developed at the Health Sciences Computing Facility, UCLA, sponsored by NIH Special Research Grant RR-3. Berkely: University of California Press 1975 5. Erikssen, J., Jervell, J.: A trial of a new adrenergic beta-receptor blocker, ICI 66082, in the treatment of hypertension. Acta Med. Scand. 198, 49 (1975) 6. Erikssen, J., Enge, I., Forfang, K., Storstein, O.: False positive diagnostic tests and coronary angiographic findings in 105 presumably healthy males. Circulation 54, 371 (1976) 7. Frank, C. W., Weinblatt, E., Shapiro, S.: Angina peetoris in men. Prognostic significance of selected medical factors. Circulation 47, 509 (1973) 8. Grimby, G., Bjure, J., Aurell, M., Ekstr~m-Jodal, B., Tibblin, G., Wilhelmsen, L.: Work capacity and physiological responses to work. Men born in 1913. Am. J. Cardiol. 30, 37 (1972) 9. Hinkle, L. E., Carver, S. T., Plakun, A.: Slow heart rates and increased risk of cardiac death in middle-aged men. Arch. Intern. Med. 129, 732 (1972) 10. Kasser, I. S., Bruce, R. A.: Comparative effects of aging and coronary heart disease on submaximal and maximal exercise. Circulation 39, 759 (1969) 11. Paul, O., Lepper, M. H., Phelan, W. H., Dupertuis, G. W., MacMillan, A., McKean, H., Park, H.: A longitudinal study of coronary heart disease. Circulation 28, 20 (1963) 12. Robinson, S.: Experimental studies of physical fitness in relation to age. Arbeitsphysiologie 10, 251 (1938) 13. Rodahl, K.: Unpublished data 14. Rodahl, K.: Observations on blood pressure in Eskimos. Norsk Polarinstitutt, Skrifter Nr. 102, 53--65 (1954) 15. Rose, G., Blackburn, H.: Cardiovascular survey methods. Wrld. Hlth Org. Monograph Series 56, 1968 (Geneva) 16. Stehbens, W. E.: The role of hemodynamics in the pathogenesis of atherosclerosis. Prog. Cardiovasc. Dis. 18, 89 (1975) 17. Texon, M.: Atherosclerosis: Its hemodynamic basis and implications. Med. Clin. N. Am. 58, 257 (1974) 18. Tibblin, G., Wilhelmsen, L., Werko, L.: Risk factors for myocardial infarction and death due to ischemic heart disease and other causes. Am. J. Cardiol. 35, 514 (1975) 19. Astrand, P.-O., Rodahl, K.: Textbook of work physiology. 2. Edition. New York: McGrawHill Accepted April 11, 1979