Aging and physical activity determine cardiac structure and function in the older athlete PAMELA S. DOUGLAS AND MARY O’TOOLE Charles A. Dana Research Institute and Harvard-Thorndike Laboratory of Beth Israel Hospital; Cardiovascular Division, Department of Medicine, Beth Israel Hospital and Harvard Medical School, Boston, Massachusetts 02215; and Department of Orthopedic Surgery, University of Tennessee,Memphis, Tennessee38163 DOUGLAS,PAMELAS.,ANDMARYO'TOOLE. Agingandphysical activity determine cardiac structure and function in the older athlete. J. Appl. Physiol. 72(5): 1969-1973, 1992.-To evaluate the effects of age and physical activity on cardiac structure and function, 45 ultraendurance athletes were compared with 24 sedentary control subjects. Two-dimensionally guided M-mode echocardiograms and pulsed Doppler studies of left ventricular inflow velocity were obtained. Both older and younger athletes differed from age-similar sedentary control subjects in having lower heart rates (56 vs. 72 beats/min, younger; 53 vs. 74 beats/ min, older), larger left ventricular cavities at end diastole (5.4 vs. 4.9 cm younger; 5.4 vs. 4.9 cm, older), and higher ratios of early to atria1 inflow velocities (2.14 vs. 1.37, younger; 1.32 vs. 0.83, older; all P < 0.05). Older athletes differed from younger athletes in having higher systolic and diastolic blood pressures (131/79 vs. 122/71 mmHg), greater posterior wall thickness (1.1 vs. 0.9 cm), lower rapid filling velocity (52 vs. 70 cm/s), higher atria1 systolic velocity (41 vs. 34 cm/s), and lower earlyto-atria1 inflow velocity ratios (1.32 vs. 2.14, all P < 0.05). Thus the aging heart manifests structural and functional changes in response to physical activity that are similar but not identical to those seen in younger subjects. The expected pattern of cardiac alterations normally seen in response to age is modified in the older athlete, suggesting that exercise training, as well as aging, is an effective stimulus in shaping left ventricular structure and function in the older heart. exercise; hypertrophy;
diastolic
function
have documented increased left ventricular size and wall thickness and normal systolic and diastolic performance in athletes (9, 12, 19, 20, 28, 30, 32). However, investigations of the effects of exercise training on the human heart have largely been performed in young subjects. Whether such exercise-induced changes occur in the older heart, and to the same extent, is unclear (11). Some studies suggest that improvements in aerobic capacity in the aging individual in response to conditioning may be solely due to peripheral changes rather than central adaptation (30, 31). If so, then the cardiac adaptation to physiological as well as pathological stressors may be limited by advancing age. Several cardiac changes accompany the normal aging process, including prolongation of excitation-contraction and relaxation, increased afterload, increased vascular and myocardial stiffness, and decreased catecholamine sensitivity (21-23). These changes are manifest echocarMANY STUDIES
0161-7567/92
$2.00 Copyright
diographically as increased left ventricular wall thickness without dilation or concentric hypertrophy, prolonged relaxation time, and an altered left ventricular filling pattern (2-4, 10, 14, 26, 33). The purpose of the present study was to evaluate the interaction of these two distinct processes of cardiac remodeling: aging and exercise training. Because some of the “normal” effects of aging, such as reduced maximal aerobic capacity, can be partially reversed by exercise training, it is reasonable to hypothesize that these structural and functional cardiac changes might be modified as well. In particular we sought to examine how the heart of the older athlete might differ from that of an older sedentary individual or a younger active individual and thereby to determine whether cardiac aging can be modified by physical activity. METHODS
The study population consisted of 69 subjects, including 45 ultraendurance athletes who trained vigorously 220 h/wk, including swimming (10 miles/wk), biking (250 miles/wk), and running (50 miles/wk) for >2 yr and successfully completed the Hawaii Ironman Triathlon (2.4-mile swim, 112-mile bike, 26.2-mile run). There were 24 young athletes (mean age 23 t 2 yr, range 19-25 yr; 19 men, 5 women) and 21 older athletes (mean age 58 t 6 yr, range 50-71 yr; 18 men, 3 women). Twenty-four healthy sedentary control subjects engaged in aerobic activities (including walking or weight training) for 100 I 52 80 . I
60
0 0
r!?
W
1
Z
. - . - . - . - . - . - . - . - . - 1
o 2.5 i= a 2 CT 5 1.5
I
40
&
1971
HEART
4
1
601
20
THE
- ’ - . - 1 0 Athletes { 0 Controls 1
t
80
AND
- - - - - - -
0
lo
20
30
40 50 60 AGE (yrs)
70
80
90
100
FIG. 4. Early-to-atria1 flow velocity (E/A) ratio vs. age. Both older and younger athletes had a higher E/A ratio than similarly aged controls. In addition, both younger groups had a higher E/A ratio than their older counterparts.
2. Correlation coefficient of heart rate and left ventricular size and filling
TABLE
Controls
Athletes
O 0
LV diastolic diameter Rapid filling velocity Atria1 systolic velocity E/A ratio
0.232
0.049
0.487*
0.043
0.276
0.242
0.113
0.134
* P = 0.016. l.L J
somewhat different in the athlete and sedentary groups. Unlike the control subjects, rapid filling velocity was reduced in older compared with younger athletes (49 vs. 51 a 01 - a - * - m - m - a - m - a - a - a - I cm/s in young vs. old control subjects, 70 vs. 52 cm/s in 0 10 20 30 40 50 60 70 80 90 100 young vs. old athletes), although this may in part be reAGE (yrs) lated to the increased rapid filling velocity in the younger FIG. 3. Atria1 filling velocity vs. age. Both older groups had higher athletes. Although A was higher in both older groups atria1 filling velocities than their younger counterparts, and older aththan in their younger counterparts, this difference was letes had lower atria1 filling velocities than older control subjects. much more marked in the sedentary group. Similarly, larly aged controls (53 vs. 74 beats/min, P < 0.01; Table although both older groups had lower E/A ratios, the 1). Blood pressures did not differ within the older age reduction seen in the older athletes caused them to have group. Older athletes also demonstrated left ventricular a mean value similar to young control subjects, rather dilation, with cavity sizes similar to their younger coun- than to age-matched control subjects. Thus the E/A ratio terparts. There were no differences in posterior wall remained higher in older as well as younger athletes than thickness, left ventricular mass, mass index, or relative in their age-matched groups. wall thickness between sedentary and active older subBecause heart rate may affect cardiac size and left venjects. Fractional shortening was higher in control sub- tricular inflow pattern (16, 24), its relationships to these jects. E values were similar in the two older groups, al- variables were examined in each of the two subject though the sedentary subjects had a higher A, resulting groups (Table 2). In sedentary control subjects, heart in a lower E/A ratio (0.83 vs. 1.32, P < 0.01). rate was weakly related only to rapid filling velocity (r = Effects of age: comparison of older and younger subjects 0.487, P = 0.016) and not to A, E/A ratio, or left ventricuwithin activity groups. Comparison of sedentary subjects lar dimension. In athletes, heart rate was not related to of different age groups showed that older control subjects any of these measures. had higher systolic blood pressures and greater posterior Similarly, because left ventricular mass has been rewall thickness and relative wall thickness than their lated to inflow pattern, it was compared with each filling younger counterparts (Table 1). A was higher, and E/A variable in all subjects and in control subjects and athratio was lower. Many of these age-related structural letes separately. There were no significant relationships changes were also observed in athletes, with higher sys(all r < 0.40). tolic and diastolic blood pressures, increased wall thickness, and increased relative wall thickness seen in older compared with younger athletes. Left ventricular mass DISCUSSION Alterations in left ventricular structure and function and mass index both tended to be higher, but neither are a well-described and accepted component of the rereached statistical significance. In contrast, the age-related changes in left ventricular filling pattern were sponse to physical conditioning (1,9,12,13,18-20,25,28, 2 I-
20
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1972
AGING, ACTIVITY,
AND THE
HEART
increased reliance on atria1 systole. Because the interperformed using younger subjects. In those in which pretation of inflow velocities as indexes of diastolic older subjects are employed, athletes generally engage in function is problematic because of the many factors inless intense exercise training than their younger coun- fluencing these variables (especially transmitral filling terparts, such that the responses to exercise may be lim- pressures, in addition to diastolic left ventricular performance), our data cannot definitively describe diastolic ited in these older subjects, and comparisons with younger more highly trained individuals may be problemfunction in the older athlete. Nevertheless, they do provide insight into the interaction of aging and exercise atic (11,30). In the present study, older and younger athtraining as a factor affecting cardiac function. letes engaged in similar ultraendurance training. Both Both athlete and control groups showed changes in left groups demonstrated cardiac changes previously documented to occur with exercise training, including lower ventricular inflow pattern associated with aging in the heart rates, larger left ventricular cavities, lower wall normal population. However, because the amount of the stresses, and higher E/A ratios. increase in atria1 systolic velocity was much larger in The plasticity of the older heart in response to both older sedentary subjects (from 37 to 62, or 25 cm/s) than physiological and pathological stimuli has been ques- in older athletes (from 34 to 41, or 7 cm/s), older athletes demonstrated a “younger” pattern of left ventricular filltioned (6, 11, 29, 30), in part on the basis of observations ing. This finding is not entirely unexpected in light of of limited hypertrophy in elderly patients with hypertension or aortic stenosis, but supported by exercise data as reports of “supra-normal” diastolic function in young well. Several studies suggest that the increased exercise athletes (1,9, 13,18, 25). These results also suggest that the diastolic dysfunction is not inevitably associated with capacity achieved in the elderly by physical conditioning aging and may even be partially reversable by physical may be due to peripheral rather than central adaptation (30, 31). Furthermore, older individuals are believed to conditioning. The extent to which the cardiac response to exercise is have a different response to single bouts of exercise, with declines in peak heart rate, peak stroke volume, and re- altered by the level of function before training is undertaken is difficult to determine but likely to be important. sponsiveness to P-adrenergic stimulation (5). Although the acute response to exercise was not examined, our In particular, the influence of baseline values is the most data suggest that the older individual can indeed respond plausible explanation as to why variables were altered in centrally to exercise training, and that aging alone does younger but not older athletes and why there was some not eliminate the possibility of structural adaptation to overlap of values in individual groups. Thus the lack of a physical conditioning. Our findings confirm those of higher left ventricular mass or rapid filling velocity in Heath et al. (19), who found larger left ventricular cavi- older athletes compared with sedentary subjects suggests ties and higher mass in master as well as younger athan impaired ability of the aging heart to adapt to exerletes, and are similar to those of Ehsani et al. (II), who cise. The higher left venticular mass and much higher atria1 systolic velocity and lower E/A ratio that occur as noted increases in left ventricular diameter, wall thickness, and mass after 1 yr of vigorous training in middle- part of normal aging may affect the ability of exercise training to alter these parameters, suggesting an imporaged (45 t 2 yr) men with coronary disease. In contrast, Schocken et al. (30) found no changes in left ventricular tant interaction between these two processes. Exercise training appears to alter and even eliminate size after exercise training in a truly elderly group with a mean age of 72 t 6 yr (30). These disparate results may in some of the cardiovascular changes generally considered part be due to the mild intensity of exercise employed in to be age related, suggesting that what has been attributed to normal aging alone may instead represent contrithe study of Schocken et al. (1.5 h/wk for 12 wk), in that the stimulus may have been inadequate. butions from both advancing years and increasingly sedDespite the occurrence of structural and functional entary habits. Perhaps the definition of normal aging changes in response to exercise in the older hearts, the may be somewhat clouded by an interaction between lifeolder athletes’ hearts were significantly different in some style and senescence. Our results may be affected by several factors. Inrespects from those of their younger counterparts, suggesting that some aspects of normal aging were unaltered creased heart rate can alter left ventricular size as well as by exercise training. Systolic blood pressure, posterior the left ventricular filling pattern, usually by increasing wall thickness, and relative wall thickness were increased atria1 systolic velocity (13, 16, 18, 24). In the present in both older groups, regardless of activity level. These study, atria1 velocity was increased in older controls; howchanges have been widely noted in studies of normal ag- ever, their heart rate was similar to that of the younger ing and generally have been attributed to increased vas- sedentary subjects, in whom atria1 velocity was not incular stiffness, increased impedance, and hence in- creased. Furthermore, in our subjects, there was no correlation between heart rate and atria1 systolic velocity creased resistance to ejection with compensatory hypertrophy (21-23). or E/A ratio in either group. Although none of our subjects had any historic or echocardiographic evidence of One of the most striking changes in cardiac structure cardiac disease, we cannot definitely exclude the presand function with advancing age is an alteration in left ventricular diastolic function (2-4, 10, 22, 23, 26, 33). ence of underlying asymptomatic coronary disease as a Relaxation is prolonged, as are the indexes that measure contributor to our findings. Although a long-term longiit: isovolumic relaxation time and the pressure delay tudinal study might offer advantages in examining the constant 7. The left ventricle becomes stiffer, presum- effects of physical conditioning in the elderly, our incluably because of hypertrophy, and indexes that measure sion of a younger athlete group with two appropriately left ventricular filling, such as peak filling rate and aged control groups allowed study of the interaction of Doppler inflow velocities and their ratio, document an aging and exercise training by comparison of agins ath-
30, 32). However, most studies in this area have been
Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (161.023.084.010) on August 23, 2018. Copyright © 1992 American Physiological Society. All rights reserved.
AGING,
ACTIVITY
letes with younger athletes as well as with similarly aged sedentary controls. Both groups of athletes had trained vigorously for 22 yr, following regimens far beyond the intensity and training duration of most aerobically fit athletes. However, because of their age, the older athletes had had the opportunity to be physically active for a much longer period. Although we cannot exclude the possibility that the cumulative effects of many years of physical activity may be different from those of a shorter time period, we purposefully selected subjects who had undergone rigorous training for 22 yr. Similarly, we cannot eliminate the possibility of intrinsic differences between sedentary and control groups in each age range in addition to the effects of activity. Our results suggest that, given an adequate exercise stimulus, the aging heart can manifest physiological structural and functional changes in response to physical conditioning. Although some of these changes are similar to those seen in younger subjects, they are not identical, suggesting that aging does modify the cardiac adaptation to exercise. Concomitantly, the expected “age-related” pattern of alterations in left ventricular structure and function are altered in the aging athlete. These findings suggest that both aging and exercise training are effective stimuli in shaping cardiac structure and function in the active older individual. The authors thank Iris Wasserman for excellent secretarial support. Address for reprint requests: P. S. Douglas, Cardiovascular Div., Beth Israel Hospital, 330 Brookline Ave., Boston, MA 02215. Received
14 June
1991; accepted
in final
form
19 November
1991.
REFERENCES 1. APPLETON, C. P., M. J. CARUCCI, C. P. HENRY, AND M. OLAJOS. Influence of incremental changes in heart rate on mitral flow velocity: assessment in lightly sedated, conscious dogs. J. Am. Coil. Cardiol. 17: 227-236, 1991. 2. ARORA, R. R., J. MACHAC, M. E. GOLDMAN, R. N. BUTLER, R. GORLIN, AND S. F. HOROWITZ. Atria1 kinetics and left ventricular diastolic filling in the healthy elderly. J. Am. Coil. Cardiol. 9: 125% 1260, 1987. 3. BERMAN, G. O., N. REICHEK, D. BROWNSON, AND P. S. DOUGLAS. Effects of sample volume location, imaging view, heart rate and age on tricuspid velocimetry in normal subjects. Am. J. Cardiol. 65: 1026-1030, 1990. 4. BRYG, R. J., G. A. WILLIAMS, AND A. J. LABOVITZ. Effect of aging on left ventricular diastolic filling in normal subjects. Am. J. Cardiol. 59: 971-974, 1987. 5. CAPASSO, J. M., A. MALHOTRA, J. SCHEUER, AND E. M. SONNENBLICK. Myocardial biochemical, contractile and electrical performance after imposition of hypertension in young and old rats. Circ. Res. 58: 445-460, 1986. 6. COLAN, S. D., S. P. SANDERS, D. MACPHERSON, AND K. M. BOROW. Left ventricular diastolic function in elite athletes with physiologic cardiac hypertrophy. J. Am. Coil. Curdiol. 6: 545-549,
1985. 7. DEMARIA, A. N., A. NEUMANN, P. J. SCHUBART, G. LEE, AND D. T. MASON. Systematic correlation of cardiac chamber size and ventricular performance determined with echocardiography and alterations in heart rate in normal persons. Am. J. Curdiol. 43: l-9,1979. 8. DEVEREUX, R. B., D. R. ALONSO, E. M. LUTAS, G. J. GOTTLIEB, E. CAMPO, I. SACHS, AND N. REICHEK. Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings. -4,. J. Curdiol. 57: 450-458, 1986. 9. DO~JGLAS, P. S., M. L. O’TOOLE, W. D. B. HILLER, AND N. REICHEK. Left ventricular structure and function by echocardiography in ultraamdurance athletes. Am. J. Curdiol. 58: 805-809, 1986. 10. Dow~%s, T. R., A. M. NOMEIR, K. M. SMITH, K. P. STEWART, AND W. C. LITTLE. Mechanism of altered pattern of left ventricular
AND
THE filling
1973
HEART with
aging
in subjects
without
cardiac
disease.
Am. J. Cur-
diol. 64: 523-527, 1989. 11. EHSANI, A. A. Cardiovascular adaptations to exercise training in the elderly. Federation Proc. 46: 1840-1843, 1987. 12. EHSANI, A. A., W. H. MARTIN, G. W. HEATH, AND E. F. COYLE. Cardiac effects of prolonged and intense exercise training in patients with coronary artery disease. Am. J. Curdiol. 50: 246-254, 1982. 13. FINKELHOR, R. S., L. J. HANAK, AND R. C. BAHLER. Left ventricular filling in endurance-trained subjects. J. Am. Coil. Curdiol. 8: 289-293, 1986. 14. GERSTENBLITH, G., J. FREDERIKSEN, F. C. P. YIN, N. J. FORTUIN, E. G. LAKATTA, AND M. L. WEISFELDT. Echocardiographic assessment of a normal adult aging population. Circulation 56: 273-278, 1977. 15. GERSTENBLITH, G., D. S. RENLUND, AND E. G. LAKATTA. Cardiovascular response to exercise in younger and older men. Federation Proc. 46: 1834-1839, 1987. 16. GILLEBERT, T., F. RADEMAKERS, AND D. BRUTSAERT. Left ventricular function in athletes: analysis of relaxation. In: Sports Curdiology, edited by R. H. Fagard and I. E. Bekaert. Dordrecht, The Netherlands: Nijhoff, 1986, p. 70-84. 17. HAGBERG, J. M. Effect of training on the decline of VOW,,, with aging. Federation Proc. 46: 1830-1833, 1987. 18. HARRISON, M. R., G. D. CLIFTON, A. T. PENNELL, A. N. DEMARIA, AND A. CATER. Effect of heart rate on left ventricular diastolic transmitral flow velocity patterns assessed by Doppler echocardiography in normal subjects. Am. J. Curdiol. 67: 622-627, 1991. 19. HEATH, G. W., J. M. HAGBERG, A. A. EHSANI, AND J. 0. HOLLOSZY. A physiological comparison of young and older endurance athletes. J. Appl. Physiol. 51: 634-640, 1981. 20. HUSTON, T. P., J. C. PUFFER, AND W. M. RODNEY. The athletic heart syndrome. N. Engl. J. Med. 113: 24-32, 1985. 21. KENNEDY, R. D., AND F. I. CAIRD. Physiology of’aging of the heart. In: Geriatric Cardiology, edit,ed by R. J. Noble and D. A. Rothbaum. New York: Davis, 1981, p. l-8. 22. LAKATTA, E. G., J. H. MITCHELL, A. POMERANCE, AND G. G. ROWE. Human aging: changes in structure and function. J. Am. Coil. Curdiol. Suppl. 10: 42A-47A, 1987. 23. LAKATTA, E. G., AND F. C. P. YIN. Myocardial aging: functional alterations and related cellular mechanisms. Am. J. Physiol. 242 (Heart Circ. Physiol. 11): H927-H941, 1982. 24. LAVINE, S. J., V. KRISHNASWAMI, N. LEVINSON, AND J. A. SHAVER. Effect of heart rate alterations produced by atria1 pacing on the pattern of diastolic filling in normal subjects. Am. J. Curdiol. 62: 1098-1102, 1988. 25. MATSUDA, M., Y. SUGISHITA, S. KOSEKI, I. ITO, T. AKATSUKA, AND K. TAKAMATSU. Effect of exercise on left ventricular diastolic filling in athletes and non-athletes. J. Appl. Physiol. 55: 323-328, 1983. 26. MILLER, T. R., S. J. GROSSMAN, K. B. SCHECTMAN, D. R. BIELLO, P. A. LUDBROOK, AND A. A. EHSANI. Left ventricular diastolic filling and its association with age. Am. J. Curdiol. 58: 531-535, 1986. 27. SAHN, D. J., A. DEMARIA, J. KISSLO, AND A. WEYMAN. The Committee on M-mode Standardization of the American Society of Echocardiography: recommendations regarding quantitation in Mmode echocardiography: results of a survey of echocardiographic measurements. Circulation 58: 1072-1081, 1978. 28. SCHAIBLE, T. F., AND J. SCHEUER. Cardiac adaptations of chronic exercise. Prog. Curdiovusc. Lb. 27: 297-324, 1985. 29. SCHEUER, J., AND P. BUTTRICK. The cardiac hypertrophic responses to pathologic and physiologic loads. Circulation 75: 163165, 1987. 30. SCHOCKEN, D. D., J. A. BLUMENTHAL, S. PORT, P. HINDLE, AND R. E. COLEMAN. Physical conditioning and left ventricular performance in the elderly: assessment by radionuclide angiocardiography. Am. J. Curdiol. 52: 359-364, 1983. 31. SEALS, D. R., B. F. HURLEY, J. M. HAGBERG, J. M. SCHULTZ, B. J. J. LINDER, L. NATTER, AND A. A. EHSANI. Effects of training on systolic time intervals at rest and during isometric exercise in men and women 61-64 years old. Am. J. Curdiol. 55: 797-800, 1985. 32. SHAPIRO, L. M. Physiological left ventricular hypertrophy. Br. Heart J. 52: 130-135, 1984. 33. SPIRITO, P., AND B. J. MARON. Influence of aging on Doppler echocardiographic indices of left ventricular diastolic function. Br. Heart J. 59: 672-679, 1988.
Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (161.023.084.010) on August 23, 2018. Copyright © 1992 American Physiological Society. All rights reserved.
diastolic
function
have documented increased left ventricular size and wall thickness and normal systolic and diastolic performance in athletes (9, 12, 19, 20, 28, 30, 32). However, investigations of the effects of exercise training on the human heart have largely been performed in young subjects. Whether such exercise-induced changes occur in the older heart, and to the same extent, is unclear (11). Some studies suggest that improvements in aerobic capacity in the aging individual in response to conditioning may be solely due to peripheral changes rather than central adaptation (30, 31). If so, then the cardiac adaptation to physiological as well as pathological stressors may be limited by advancing age. Several cardiac changes accompany the normal aging process, including prolongation of excitation-contraction and relaxation, increased afterload, increased vascular and myocardial stiffness, and decreased catecholamine sensitivity (21-23). These changes are manifest echocarMANY STUDIES
0161-7567/92
$2.00 Copyright
diographically as increased left ventricular wall thickness without dilation or concentric hypertrophy, prolonged relaxation time, and an altered left ventricular filling pattern (2-4, 10, 14, 26, 33). The purpose of the present study was to evaluate the interaction of these two distinct processes of cardiac remodeling: aging and exercise training. Because some of the “normal” effects of aging, such as reduced maximal aerobic capacity, can be partially reversed by exercise training, it is reasonable to hypothesize that these structural and functional cardiac changes might be modified as well. In particular we sought to examine how the heart of the older athlete might differ from that of an older sedentary individual or a younger active individual and thereby to determine whether cardiac aging can be modified by physical activity. METHODS
The study population consisted of 69 subjects, including 45 ultraendurance athletes who trained vigorously 220 h/wk, including swimming (10 miles/wk), biking (250 miles/wk), and running (50 miles/wk) for >2 yr and successfully completed the Hawaii Ironman Triathlon (2.4-mile swim, 112-mile bike, 26.2-mile run). There were 24 young athletes (mean age 23 t 2 yr, range 19-25 yr; 19 men, 5 women) and 21 older athletes (mean age 58 t 6 yr, range 50-71 yr; 18 men, 3 women). Twenty-four healthy sedentary control subjects engaged in aerobic activities (including walking or weight training) for 100 I 52 80 . I
60
0 0
r!?
W
1
Z
. - . - . - . - . - . - . - . - . - 1
o 2.5 i= a 2 CT 5 1.5
I
40
&
1971
HEART
4
1
601
20
THE
- ’ - . - 1 0 Athletes { 0 Controls 1
t
80
AND
- - - - - - -
0
lo
20
30
40 50 60 AGE (yrs)
70
80
90
100
FIG. 4. Early-to-atria1 flow velocity (E/A) ratio vs. age. Both older and younger athletes had a higher E/A ratio than similarly aged controls. In addition, both younger groups had a higher E/A ratio than their older counterparts.
2. Correlation coefficient of heart rate and left ventricular size and filling
TABLE
Controls
Athletes
O 0
LV diastolic diameter Rapid filling velocity Atria1 systolic velocity E/A ratio
0.232
0.049
0.487*
0.043
0.276
0.242
0.113
0.134
* P = 0.016. l.L J
somewhat different in the athlete and sedentary groups. Unlike the control subjects, rapid filling velocity was reduced in older compared with younger athletes (49 vs. 51 a 01 - a - * - m - m - a - m - a - a - a - I cm/s in young vs. old control subjects, 70 vs. 52 cm/s in 0 10 20 30 40 50 60 70 80 90 100 young vs. old athletes), although this may in part be reAGE (yrs) lated to the increased rapid filling velocity in the younger FIG. 3. Atria1 filling velocity vs. age. Both older groups had higher athletes. Although A was higher in both older groups atria1 filling velocities than their younger counterparts, and older aththan in their younger counterparts, this difference was letes had lower atria1 filling velocities than older control subjects. much more marked in the sedentary group. Similarly, larly aged controls (53 vs. 74 beats/min, P < 0.01; Table although both older groups had lower E/A ratios, the 1). Blood pressures did not differ within the older age reduction seen in the older athletes caused them to have group. Older athletes also demonstrated left ventricular a mean value similar to young control subjects, rather dilation, with cavity sizes similar to their younger coun- than to age-matched control subjects. Thus the E/A ratio terparts. There were no differences in posterior wall remained higher in older as well as younger athletes than thickness, left ventricular mass, mass index, or relative in their age-matched groups. wall thickness between sedentary and active older subBecause heart rate may affect cardiac size and left venjects. Fractional shortening was higher in control sub- tricular inflow pattern (16, 24), its relationships to these jects. E values were similar in the two older groups, al- variables were examined in each of the two subject though the sedentary subjects had a higher A, resulting groups (Table 2). In sedentary control subjects, heart in a lower E/A ratio (0.83 vs. 1.32, P < 0.01). rate was weakly related only to rapid filling velocity (r = Effects of age: comparison of older and younger subjects 0.487, P = 0.016) and not to A, E/A ratio, or left ventricuwithin activity groups. Comparison of sedentary subjects lar dimension. In athletes, heart rate was not related to of different age groups showed that older control subjects any of these measures. had higher systolic blood pressures and greater posterior Similarly, because left ventricular mass has been rewall thickness and relative wall thickness than their lated to inflow pattern, it was compared with each filling younger counterparts (Table 1). A was higher, and E/A variable in all subjects and in control subjects and athratio was lower. Many of these age-related structural letes separately. There were no significant relationships changes were also observed in athletes, with higher sys(all r < 0.40). tolic and diastolic blood pressures, increased wall thickness, and increased relative wall thickness seen in older compared with younger athletes. Left ventricular mass DISCUSSION Alterations in left ventricular structure and function and mass index both tended to be higher, but neither are a well-described and accepted component of the rereached statistical significance. In contrast, the age-related changes in left ventricular filling pattern were sponse to physical conditioning (1,9,12,13,18-20,25,28, 2 I-
20
Downloaded from www.physiology.org/journal/jappl by ${individualUser.givenNames} ${individualUser.surname} (161.023.084.010) on August 23, 2018. Copyright © 1992 American Physiological Society. All rights reserved.
1972
AGING, ACTIVITY,
AND THE
HEART
increased reliance on atria1 systole. Because the interperformed using younger subjects. In those in which pretation of inflow velocities as indexes of diastolic older subjects are employed, athletes generally engage in function is problematic because of the many factors inless intense exercise training than their younger coun- fluencing these variables (especially transmitral filling terparts, such that the responses to exercise may be lim- pressures, in addition to diastolic left ventricular performance), our data cannot definitively describe diastolic ited in these older subjects, and comparisons with younger more highly trained individuals may be problemfunction in the older athlete. Nevertheless, they do provide insight into the interaction of aging and exercise atic (11,30). In the present study, older and younger athtraining as a factor affecting cardiac function. letes engaged in similar ultraendurance training. Both Both athlete and control groups showed changes in left groups demonstrated cardiac changes previously documented to occur with exercise training, including lower ventricular inflow pattern associated with aging in the heart rates, larger left ventricular cavities, lower wall normal population. However, because the amount of the stresses, and higher E/A ratios. increase in atria1 systolic velocity was much larger in The plasticity of the older heart in response to both older sedentary subjects (from 37 to 62, or 25 cm/s) than physiological and pathological stimuli has been ques- in older athletes (from 34 to 41, or 7 cm/s), older athletes demonstrated a “younger” pattern of left ventricular filltioned (6, 11, 29, 30), in part on the basis of observations ing. This finding is not entirely unexpected in light of of limited hypertrophy in elderly patients with hypertension or aortic stenosis, but supported by exercise data as reports of “supra-normal” diastolic function in young well. Several studies suggest that the increased exercise athletes (1,9, 13,18, 25). These results also suggest that the diastolic dysfunction is not inevitably associated with capacity achieved in the elderly by physical conditioning aging and may even be partially reversable by physical may be due to peripheral rather than central adaptation (30, 31). Furthermore, older individuals are believed to conditioning. The extent to which the cardiac response to exercise is have a different response to single bouts of exercise, with declines in peak heart rate, peak stroke volume, and re- altered by the level of function before training is undertaken is difficult to determine but likely to be important. sponsiveness to P-adrenergic stimulation (5). Although the acute response to exercise was not examined, our In particular, the influence of baseline values is the most data suggest that the older individual can indeed respond plausible explanation as to why variables were altered in centrally to exercise training, and that aging alone does younger but not older athletes and why there was some not eliminate the possibility of structural adaptation to overlap of values in individual groups. Thus the lack of a physical conditioning. Our findings confirm those of higher left ventricular mass or rapid filling velocity in Heath et al. (19), who found larger left ventricular cavi- older athletes compared with sedentary subjects suggests ties and higher mass in master as well as younger athan impaired ability of the aging heart to adapt to exerletes, and are similar to those of Ehsani et al. (II), who cise. The higher left venticular mass and much higher atria1 systolic velocity and lower E/A ratio that occur as noted increases in left ventricular diameter, wall thickness, and mass after 1 yr of vigorous training in middle- part of normal aging may affect the ability of exercise training to alter these parameters, suggesting an imporaged (45 t 2 yr) men with coronary disease. In contrast, Schocken et al. (30) found no changes in left ventricular tant interaction between these two processes. Exercise training appears to alter and even eliminate size after exercise training in a truly elderly group with a mean age of 72 t 6 yr (30). These disparate results may in some of the cardiovascular changes generally considered part be due to the mild intensity of exercise employed in to be age related, suggesting that what has been attributed to normal aging alone may instead represent contrithe study of Schocken et al. (1.5 h/wk for 12 wk), in that the stimulus may have been inadequate. butions from both advancing years and increasingly sedDespite the occurrence of structural and functional entary habits. Perhaps the definition of normal aging changes in response to exercise in the older hearts, the may be somewhat clouded by an interaction between lifeolder athletes’ hearts were significantly different in some style and senescence. Our results may be affected by several factors. Inrespects from those of their younger counterparts, suggesting that some aspects of normal aging were unaltered creased heart rate can alter left ventricular size as well as by exercise training. Systolic blood pressure, posterior the left ventricular filling pattern, usually by increasing wall thickness, and relative wall thickness were increased atria1 systolic velocity (13, 16, 18, 24). In the present in both older groups, regardless of activity level. These study, atria1 velocity was increased in older controls; howchanges have been widely noted in studies of normal ag- ever, their heart rate was similar to that of the younger ing and generally have been attributed to increased vas- sedentary subjects, in whom atria1 velocity was not incular stiffness, increased impedance, and hence in- creased. Furthermore, in our subjects, there was no correlation between heart rate and atria1 systolic velocity creased resistance to ejection with compensatory hypertrophy (21-23). or E/A ratio in either group. Although none of our subjects had any historic or echocardiographic evidence of One of the most striking changes in cardiac structure cardiac disease, we cannot definitely exclude the presand function with advancing age is an alteration in left ventricular diastolic function (2-4, 10, 22, 23, 26, 33). ence of underlying asymptomatic coronary disease as a Relaxation is prolonged, as are the indexes that measure contributor to our findings. Although a long-term longiit: isovolumic relaxation time and the pressure delay tudinal study might offer advantages in examining the constant 7. The left ventricle becomes stiffer, presum- effects of physical conditioning in the elderly, our incluably because of hypertrophy, and indexes that measure sion of a younger athlete group with two appropriately left ventricular filling, such as peak filling rate and aged control groups allowed study of the interaction of Doppler inflow velocities and their ratio, document an aging and exercise training by comparison of agins ath-
30, 32). However, most studies in this area have been
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AGING,
ACTIVITY
letes with younger athletes as well as with similarly aged sedentary controls. Both groups of athletes had trained vigorously for 22 yr, following regimens far beyond the intensity and training duration of most aerobically fit athletes. However, because of their age, the older athletes had had the opportunity to be physically active for a much longer period. Although we cannot exclude the possibility that the cumulative effects of many years of physical activity may be different from those of a shorter time period, we purposefully selected subjects who had undergone rigorous training for 22 yr. Similarly, we cannot eliminate the possibility of intrinsic differences between sedentary and control groups in each age range in addition to the effects of activity. Our results suggest that, given an adequate exercise stimulus, the aging heart can manifest physiological structural and functional changes in response to physical conditioning. Although some of these changes are similar to those seen in younger subjects, they are not identical, suggesting that aging does modify the cardiac adaptation to exercise. Concomitantly, the expected “age-related” pattern of alterations in left ventricular structure and function are altered in the aging athlete. These findings suggest that both aging and exercise training are effective stimuli in shaping cardiac structure and function in the active older individual. The authors thank Iris Wasserman for excellent secretarial support. Address for reprint requests: P. S. Douglas, Cardiovascular Div., Beth Israel Hospital, 330 Brookline Ave., Boston, MA 02215. Received
14 June
1991; accepted
in final
form
19 November
1991.
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