MISCELLANEOUS
Effects of Exercise on Left Ventricular Diastolic Performance in Trained Athletes J. V. Nixon, MD, Alasdair R. Wright, BSC, Thomas R. Porter, MD, Valerie Roy, RN, and James A. Arrowood, MD
Dynamically trained athletes develop increased left ventricular (LV) wall mass. To determine whether this increased wall mass impaired characteristics of LV diastolic filling, serial Doppler echocardiograms were obtained from 10 trained athletes (mean age 21 years) at rest, during supine graded bicycle exercise and during recovery at heart rates of SO, 120 and 140 beats/min, respectively. Similar studies were obtained in 10 age-matched control subjects. Studies at rest showed significant increases in athletes in LV end-diastolic dimension and indexed LV wail mass. Differences in peak filling rates and in normalized peak lengthening rates between athletes and control subjects were seen at heart rates of 140 beats/min during exercise and recovery. Differences in Doppler-derived variables between athletes and control subjects were seen in total time-velocity integral, early peak filling velocity and E/A ratio. In athletes, time-velocity integral was increased during recovery at heart rates of 120 beats/min and SO beats/min, early peak filiing velocity was increased during exercise at 120 beats/min and during recovery at 120 beats/min and 80 beats/min, and E/A ratio was higher at ail heart rates during both exercise and recovery. Although no significant differences were found in LV diastolic filling indexes at rest, a significant enhancement was found in these parameters in dynamically trained athletes during exercise, partiilarly at higher levels of dynamic exercise. (Am J Cardiol 1991;68:94S-949)
From the Echocardiography Laboratories, Division of Cardiology, Medical College of Virginia, and the Athletic Department, Virginia Commonwealth University, Richmond, Virginia. This study was supported in part by National Research Service Awards HL-07580 and HL-07357 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland, by the A.D. Williams Foundation of the Medical College of Virginia, and by the National Collegiate Athletic Association. Manuscript received February 8, 1991; revised manuscript received May 30, 1991, and accepted May 31. Address for reprints: J.V. Nixon, MD, Division of Cardiology, Medical College of Virginia, MCV Box 128, Richmond, Virginia 23298.
he adaptation of cardiac structure and function to physical training depends on the type, intensity and duration of the training. Numerous studies have described the nature of adaptive cardiac structural changes.’ Dynamic exercise training is known to increase vagal tone, diminish resting heart rate and increase cardiac stroke volume.2 There is a resultant increase in left ventricular (LV) wall mass to maintain normal wall stress, which manifests as “physiological” LV hypertrophy.3-5 Several pathologic conditions are known to cause LV hypertrophy.6 Furthermore, the effects of LV hypertrophy on LV filling%haracteristics in these conditions have been6 documeq&d.7-10 However, little is known about the effects of physiologic LV hypertrophy on diastolic filling characteristics in trained athletes, particularly during dynamic exercise. The objective of this study was to determine the effects of physiologic LV hypertrophy in trained athletes on M-mode and Doppler echocardiographic LV filling characteristics during dynamic exercise,
T
METHODS Subjects: Ten trained athletes (6 men and 4 wom-
en, mean age 21 years, range 20 to 24) were studied. These trained athletes were recruited from our parent university National Collegiate Athletics Association Division IA basketball program; all were scholarship athletes. Ten normal age-matched control subjects (6 men and 4 women, mean age 22 years, range 19 to 24) were also recruited. All subjects were fully infotied of the procedures and protocol to be used, and gave written consent. Approval for the study was obtained from the Committee for the Conduct of Human Research at the Medical College of Virginia. All subjects underwent physical examinations before the studies and were found to be healthy. None were taking medication. Study protocol: Each subject underwent graded supine bicycle exercise. A standard exercise protocol with increasing work loads at 3-minute intervals was used to produce a smooth, gradual increase in heart rate to maximal exercise. Heart rate was continuously monitored by electrocardiogram, and blood pressures were recorded at l-minute intervals by sphygmomanometer throughout the exercise protocol and for 6 minutes of recovery, or until heart rate and blood pressure reEXERCISE
AND LEFT VENTRICULAR
DIASTOLE
945
TABLE I Resting Physiologic Athletes and Control Subjects
Characteristics
Mean age (yrs) Age range (yrs) Height (cm) Weight (kg) Body surface area (m2) Heart rate (beats/min) Mean blood pressure (mm Hg) LV end-diastolic dimension (cm) LV wall mass (81 LV wall mass indexed (g/m*)
of Trained
Athletes (n = 10)
Control subjects (n = 10)
21.2 + 0.3
22.3
20-23 189 75 2.07 59 89 5.4 226 107
19-24 2 2 f * f
f 0.5
5 10 0.08 1 4
175 i- 5* 74 f 6
1.90 f 0.09
2 0.1 * 19 + 11
164 + 12*
69 e 4* 91 + 4 5.0 + 0.1* 85 2 4*
*p ~0.05,
athletes versus control subjects. LV = left ventricular.
turned to basal resting values before exercise. Two-dimensionally guided M-mode and Doppler echocardiograms were obtained at rest, at heart rates of 80, 120 and 140 beats/min during exercise and at similar heart rates during recovery. Measurements were obtained at the same heart rates in all subjects to eliminate the influence of heart rate on LV filling. Measurements and analysis: Echocardiograms were obtained using a Hewlett-Packard 77020A Ultrasound System with a 2.5MHz phased array transducer. Studies were recorded on videotape for subsequent off-line analysis. The left ventricle was imaged in the standard parasternal short-axis and apical 4-chamber views. In the short-axis view, an optimal or almost circular image at the widest point of the left ventricle below the tips of the mitral valve leaflets was centralized within the display arc, and the M-mode cursor was directed across the left ventricle at its widest point. Mmode images were recorded. Use of the 2-dimensional image and the cursor ensured that M-mode echocardiographic images were obtained from the same point in the LV cavity despite any alterations in cardiac position produced by the exercise protocol.” Pulsed Doppler recordings of diastolic transmitral flow velocity profiles were recorded with the sample volume located at the tips of the mitral leaflets (from the apical 4-chamber view). Doppler sample volume size was set at its smallest limit (approximately 5 mm). Gain settings were optimized to enhance endocardial edge detection and spectral displays. Flow velocities were not corrected for angle deviation, but care was taken to align the sample volume as perpendicular to the mitral anulus as possible. Videorecordings of M-mode and Doppler echocardiograms were analyzed by an experienced echocardiographer on an off-line reviewing station incorporating an IBM Personal Computer and a Digisonics EC-500 Cardiology Analysis System. From M-mode recordings, LV septal and posterior wall endocardial surfaces 946
THE AMERICAN
JOURNAL
OF CARDIOLOGY
VOLUME
68
were digitized according to American Society of Echocardiography criteria. The following M-mode indexes of LV filling were then calculated: (1) Peak filling rate was determined as the peak rate of increase of the LV diameter (D) with respect to time, and calculated as the highest positive value of the instantaneous rate of diameter lengthening (dD/dt). (2) Normalized peak lengthening rate was identified as the maximal value of 1/D X dD/dt, which was derived by dividing dD/dt by instantaneous LV diameter during diastole. (3) Duration of rapid filling was defined as the time from minimum LV dimension to the time when the LV filling rate decreased to 20% of its maximal value. Mitral velocity profiles were digitized along the darkest lines of the velocity spectra. Peak early filling velocity (E) and atria1 filling velocity (A) were measured directly from the spectral display, and E/A ratio was calculated from these values. Total time velocity integral was determined as the area under the peak early and atria1 filling velocity profiles. To assess the reproducibility of the Doppler echocardiographic measurements, all recordings were analyzed on 2 separate occasions for intraobserver variability, as well as by a blinded investigator for interobserver variability. Both intra- and interobserver variabilities were minimal; correlations for the parameters measured ranged from 0.94 to 0.99 for intraobserver variability and from 0.92 to 0.98 for interobserver variability. Data obtained at specific heart rates were compared and significant differences were determined by analysis of variance for single factor experiments having repeated measures. l 2 RESULTS Table I compares the characteristics of the trained athletes with those of the control subjects, at rest. As expected in the trained athletes, significant differences were seen in height and in heart rate at rest. Furthermore, LV end-diastolic dimension, LV wall mass and indexed LV wall mass were significantly higher in the athletes. Table II shows the data generated from the digitized echocardiograms at different heart rates during supine exercise and during recovery in both athletes and control subjects. Significant differences between athletes and control subjects were seen at heart rates of 140 beats/min during both exercise and recovery in peak filling and normalized peak lengthening rates. Doppler echocardiographic variables of transmitral flow, obtained at different heart rates where possible, in athletes and in control subjects are listed in Table III. Significant differences in total time-velocity integral were seen in athletes during recovery at 120 and 80 OCTOBER
1, 1991
TABLE II Echocardiographic Variables Obtained (n = 10) and in Control Subjects (n = 10)
at Different
Heart
Rates During
Supine
Exercise
Exercise (beats/min)
Heart
rate (beats)
Peak filling
rate
km/s) Normalized peak lengthening rate (per set) Duration of rapid filling (ms) Mean blood pressure
(mm Hg)
Rest
80
A 59&l* C 6924 A 9.7 ? 0.5
10.6
C 9.7 f 0.6
10.2 f 0.9
A 2.3
f 0.2
C 2.5 r?~0.2 A 185 r 6 C 178 f 12 A 9529
c
97*9
140
14.5
r 0.7
12.1 ir 1.0
2.8 + 0.2 2.5 -+ 0.2 184 2 8 181 f 11
3.8 3.2 161 167
f e -tf
105
120
f 4
f 4
101 f 3
Recovery
in Athletes
Recovery (beatslmin)
120
f 0.7
and During
0.3 0.2 8 9
127 f 6
140
16.4
f 0.4*
12.9 2 1.0 4.2 3.4 144 158
f f 2 k
0.3* 0.2 8 7
124
2 4
131 f 6
15.0
120
r 0.7
13.4
11.8 rtr 0.7 4.1 2.8 142 159
* -t 2 2
0.4* 0.2 7 12
122
‘- 5
121 f 4
80
f 0.5
10.7
f 0.7
11.7 f 0.8
9.6 f 0.8
3.7 3.1 155 167
f 0.4 * 0.3
2.8 ziz 0.2 2.4 2 0.1
108
f 4
91 f 3
108 f 4
96 f 2
2 10
201
t 10
195 t 13
+ 16
*p 13 Documentation of increased myocardial stiffness due to increases in myocardial mass and interstitial connective tissue affecting diastolic filling at rest and during exercise has resulted in the suggestion that the same effects may result from LV hypertrophy occurring in endurance athletes.7,13-16 Only Granger et a1,t7 using resting radionuclide estimations of LV filling rate, have shown that this diastolic parameter is unchanged in endurance athletes in the presence of increased LV mass. Our study substantially extends these latter findings. It demonstrates that although LV diastolic filling in trained endurance athletes is unchanged at rest, it is significantly enhanced during dynamic exercise in the presence of increased LV mass, thus adding further credence to the concept of adaptive physiologic hypertrophy in normal subjects. Furthermore, the significant increases in echocardiographic peak filling rate, Doppler-derived peak filling velocity and E/A ratio in athletes during exercise suggest that this enhancement occurs in the active phase of diastole. Several mechanisms have been suggested for this adaptive mechanism. Although part of the increase in LV mass is a compensatory mechanism for the increased LV cavity size in these athletes maintaining a normal LV wall tension, Longhurst et al5 have suggested that true hypertrophy may occur in these elite endurance athletes.6 Penpargkul et al’* suggested that enhanced diastolic function may be due to improved calcium flux in the sarcoplasmic reticulum of the trained myocardium. Furthermore, it has also been shown that ventricular filling is a dynamic process with venous return augmented by both skeletal and cardiac muscle.19 Our data is consistent with the concept that dynamic exercise training, together with the development of adaptive ventricular hypertrophy, produces increased filling during the active phase of diastole. Although the mechanisms by which these adaptive changes occur are not apparent in a study of this nature, the data appear to provide further evidence supporting the value of dynamic exercise training in improving cardiac performance. However, it should be stated that these changes resulting in increased diastolic filling characteristics may be merely the result of the increase in LV volumes. Nevertheless, filling is enhanced in the presence of LV hypertrophy, and is a key finding irrespective of LV volume. There are a number of limitations to our study. The trained athletes do not serve as their own control subjects in regard to any adaptation to training. Thus, conclusions regarding the adaptative processes of endur-
948
THE AMERICAN
JOURNAL
OF CARDIOLOGY
VOLUME
68
ance training are implied by comparison to control subjects. Echocardiograms can only imply that adaptive changes in diastolic compliance have occurred.20 Furthermore, Doppler echocardiographic estimates of LV filling characteristics are altered by a number of hemodynamic variables. 21 Some of these limitations may be overcome by using the athletes as their own control subjects and by comparing LV filling characteristics at specific heart rates during exercise. However, the inability of these noninvasive techniques to measure LV pressures remains a limitation. Also, exercise was performed in the supine position, which is known to have a different sequence of hemodynamic responses compared with exercise in the upright position.22 Furthermore, a comparison of variables at different heart rates during dynamic exercise between trained athletes and normal subjects may be limited by the fact that the work load during exercise at any given heart rate may be different for athletes with a resting bradycardia than for control subjects. Thus, sympathetic activation and its effect on cardiac performance are likely to be different in trained athletes versus control subjects. Acknowledgment: We wish to acknowledge Jeanie Toombs for secretarial help, Cathy Guard and the Medical College of Virginia Echocardiographic Laboratory staff for assistance in obtaining the Doppler echocardiographic studies, and the Virginia Commonwealth University Athletic Director, the men’s and women’s teams’ basketball coaches, and the Sports Medicine Clinic staff for providing subjects.
REFERENCES 1. Longhurst JC, Kelly AR, Gonyea WJ, Mitchell JH. Chronic training with static and dynamic exercise: cardiovascular adaptation and response to exercise. Circ Res 1981;81(suppl 1):171-178. 2. Blomqvist CG, Saltin B. Cardiovascular adaptations to physical training. Ann Reu Physiol 1983;45:169-189. 3. Maron BJ. Structural features of the athlete heart as defined by echocardiography. J Am Coil Cardiol 1986;7:190-203. 4. Golan SD, Sanders SP, Borow KM. Physiological hypertrophy: effects on left ventricular systolic mechanics in humans. J Am Coil Cardiol 1987;9:776-783. 5. Longhurst JC, Kelly AR, Gonyea WJ, Mitchell JH. Echocardiographic left ventricular masses in distance runners and weight lifters. J Appl Physiol 1980;48:154-162. 6. Grossman W. Cardiac hypertrophy: useful adaptation or pathologic process. Am J Med 1980;69:576-583. 7. Lore11 BH, Grossman W. Cardiac hypertrophy: the consequences for diastole. J Am Coil Cmdiol 1987;9:1189-1193. 6. Stewart S, Mason DT, Braunwald E. Impaired rate of left ventricular filling in ideopathic hypertrophic subaortic stenosis and valvular aortic stenosis. Circulation 1968;37:8-14. 9. Petersen KL, Tsjui J, Johnson A, DiDonna J, LeWinter M. Diastolic left ventricular pressure-volume and stress-strain relations in patients with valvular aortic stenosis and left ventricular hypertrophy. Circulation 1978;58:77-90. 10. Fonad FM, Slominski JM, Tarazi RC. Left ventricular diastolic function in hypertension: relation to left ventricular mass and systolic function. J Am Coil Cardiol 1984;3:1500-1506. 11. Pietro DA, Voclkel AG, Ray BJ, Parisi AF. Reproducibility of echocardiog-
OCTOBER
1, 1991
raphy: a study evaluating the variability of serial echocardiographic measurements. Chest 1981;19:29-32. 12. Winer BJ. Statistical Principles in Experimental Design. 2nd ed. New York: McGraw-Hill, 1971:261-308. 13. Cuocolo A, Sax FL, Brush JE, Maron BJ, Bacharach SL, Bonow RO. Left ventricular hypertrophy and impaired diastolic filling in essential hypertension. Circulation 199&81:97X-986. 14. Buccino R, Harris AE, Spann JF Jr, Sonnenblick EH. Response of myocardial connective tissue to development of experimental hypertrophy. Am J Physiol 1974;226:1293-1297. 15. Hickson RC, Hammons GT, Holloszy JO. Development and regression of exercise-induced cardiac hypertrophy in rats. Am J PhysioI 1979;236:268-272. 16. Malhotra A, Penpargkul S, Schaible T, Shueuner J. Contractile proteins and sarcoplasmic reticulum in physiologic cardiac hypertrophy. Am J Physiol 1981;241:263-267. 17. Granger CB, Karimeddini MK, Smith V, Shapiro HR, Katz AM, Riba AL. Rapid ventricular filling in left ventricular hypertrophy: I. Physiologic hypertro-
phy. J Am Co11 Cardiol 1985;5:862-868. 18. Penpargkul S, Repke DI, Katz AM, Shueuer J. Effect of physical training on calcium transport by rat cardiac sarcoplasmic reticulum. Circ Res 1977;40: 134-138. 19. Sabbah HN, Stein PD. Pressure-diameter relation during early diastole in dogs. Circ Res 1981;48:357-365. 20. Stoddard MF, Pearson AC, Kern MJ, Ratcliff J, Mrosek DG, Labovitz AJ. Left ventricular diastolic function: comparison of pulsed Doppler echocardiographic and hemodynamic indexes in subjects with and without coronary artery disease. J Am CON Cardiol 1989;13:327-336. 21. Choong CY, Hermann HC, Weyman AE, Fifer M. Preload dependence of Doppler-derived indexes of left ventricular diastolic function in humans. J Am CON Cardiol 1987;10:800-808. 22. Poliner LR, Dehmer GJ, Lewis SE, Parkey RW, Blomqvist CG, Wilerson JT. Left ventricular performance in normal subjects: a comparison of the responses to exercise in the upright and supine positions. Circulation 1980; 62:528-534.
EXERCISE
AND LEFT VENTRICULAR
DIASTOLE
949
Effects of Exercise on Left Ventricular Diastolic Performance in Trained Athletes J. V. Nixon, MD, Alasdair R. Wright, BSC, Thomas R. Porter, MD, Valerie Roy, RN, and James A. Arrowood, MD
Dynamically trained athletes develop increased left ventricular (LV) wall mass. To determine whether this increased wall mass impaired characteristics of LV diastolic filling, serial Doppler echocardiograms were obtained from 10 trained athletes (mean age 21 years) at rest, during supine graded bicycle exercise and during recovery at heart rates of SO, 120 and 140 beats/min, respectively. Similar studies were obtained in 10 age-matched control subjects. Studies at rest showed significant increases in athletes in LV end-diastolic dimension and indexed LV wail mass. Differences in peak filling rates and in normalized peak lengthening rates between athletes and control subjects were seen at heart rates of 140 beats/min during exercise and recovery. Differences in Doppler-derived variables between athletes and control subjects were seen in total time-velocity integral, early peak filling velocity and E/A ratio. In athletes, time-velocity integral was increased during recovery at heart rates of 120 beats/min and SO beats/min, early peak filiing velocity was increased during exercise at 120 beats/min and during recovery at 120 beats/min and 80 beats/min, and E/A ratio was higher at ail heart rates during both exercise and recovery. Although no significant differences were found in LV diastolic filling indexes at rest, a significant enhancement was found in these parameters in dynamically trained athletes during exercise, partiilarly at higher levels of dynamic exercise. (Am J Cardiol 1991;68:94S-949)
From the Echocardiography Laboratories, Division of Cardiology, Medical College of Virginia, and the Athletic Department, Virginia Commonwealth University, Richmond, Virginia. This study was supported in part by National Research Service Awards HL-07580 and HL-07357 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland, by the A.D. Williams Foundation of the Medical College of Virginia, and by the National Collegiate Athletic Association. Manuscript received February 8, 1991; revised manuscript received May 30, 1991, and accepted May 31. Address for reprints: J.V. Nixon, MD, Division of Cardiology, Medical College of Virginia, MCV Box 128, Richmond, Virginia 23298.
he adaptation of cardiac structure and function to physical training depends on the type, intensity and duration of the training. Numerous studies have described the nature of adaptive cardiac structural changes.’ Dynamic exercise training is known to increase vagal tone, diminish resting heart rate and increase cardiac stroke volume.2 There is a resultant increase in left ventricular (LV) wall mass to maintain normal wall stress, which manifests as “physiological” LV hypertrophy.3-5 Several pathologic conditions are known to cause LV hypertrophy.6 Furthermore, the effects of LV hypertrophy on LV filling%haracteristics in these conditions have been6 documeq&d.7-10 However, little is known about the effects of physiologic LV hypertrophy on diastolic filling characteristics in trained athletes, particularly during dynamic exercise. The objective of this study was to determine the effects of physiologic LV hypertrophy in trained athletes on M-mode and Doppler echocardiographic LV filling characteristics during dynamic exercise,
T
METHODS Subjects: Ten trained athletes (6 men and 4 wom-
en, mean age 21 years, range 20 to 24) were studied. These trained athletes were recruited from our parent university National Collegiate Athletics Association Division IA basketball program; all were scholarship athletes. Ten normal age-matched control subjects (6 men and 4 women, mean age 22 years, range 19 to 24) were also recruited. All subjects were fully infotied of the procedures and protocol to be used, and gave written consent. Approval for the study was obtained from the Committee for the Conduct of Human Research at the Medical College of Virginia. All subjects underwent physical examinations before the studies and were found to be healthy. None were taking medication. Study protocol: Each subject underwent graded supine bicycle exercise. A standard exercise protocol with increasing work loads at 3-minute intervals was used to produce a smooth, gradual increase in heart rate to maximal exercise. Heart rate was continuously monitored by electrocardiogram, and blood pressures were recorded at l-minute intervals by sphygmomanometer throughout the exercise protocol and for 6 minutes of recovery, or until heart rate and blood pressure reEXERCISE
AND LEFT VENTRICULAR
DIASTOLE
945
TABLE I Resting Physiologic Athletes and Control Subjects
Characteristics
Mean age (yrs) Age range (yrs) Height (cm) Weight (kg) Body surface area (m2) Heart rate (beats/min) Mean blood pressure (mm Hg) LV end-diastolic dimension (cm) LV wall mass (81 LV wall mass indexed (g/m*)
of Trained
Athletes (n = 10)
Control subjects (n = 10)
21.2 + 0.3
22.3
20-23 189 75 2.07 59 89 5.4 226 107
19-24 2 2 f * f
f 0.5
5 10 0.08 1 4
175 i- 5* 74 f 6
1.90 f 0.09
2 0.1 * 19 + 11
164 + 12*
69 e 4* 91 + 4 5.0 + 0.1* 85 2 4*
*p ~0.05,
athletes versus control subjects. LV = left ventricular.
turned to basal resting values before exercise. Two-dimensionally guided M-mode and Doppler echocardiograms were obtained at rest, at heart rates of 80, 120 and 140 beats/min during exercise and at similar heart rates during recovery. Measurements were obtained at the same heart rates in all subjects to eliminate the influence of heart rate on LV filling. Measurements and analysis: Echocardiograms were obtained using a Hewlett-Packard 77020A Ultrasound System with a 2.5MHz phased array transducer. Studies were recorded on videotape for subsequent off-line analysis. The left ventricle was imaged in the standard parasternal short-axis and apical 4-chamber views. In the short-axis view, an optimal or almost circular image at the widest point of the left ventricle below the tips of the mitral valve leaflets was centralized within the display arc, and the M-mode cursor was directed across the left ventricle at its widest point. Mmode images were recorded. Use of the 2-dimensional image and the cursor ensured that M-mode echocardiographic images were obtained from the same point in the LV cavity despite any alterations in cardiac position produced by the exercise protocol.” Pulsed Doppler recordings of diastolic transmitral flow velocity profiles were recorded with the sample volume located at the tips of the mitral leaflets (from the apical 4-chamber view). Doppler sample volume size was set at its smallest limit (approximately 5 mm). Gain settings were optimized to enhance endocardial edge detection and spectral displays. Flow velocities were not corrected for angle deviation, but care was taken to align the sample volume as perpendicular to the mitral anulus as possible. Videorecordings of M-mode and Doppler echocardiograms were analyzed by an experienced echocardiographer on an off-line reviewing station incorporating an IBM Personal Computer and a Digisonics EC-500 Cardiology Analysis System. From M-mode recordings, LV septal and posterior wall endocardial surfaces 946
THE AMERICAN
JOURNAL
OF CARDIOLOGY
VOLUME
68
were digitized according to American Society of Echocardiography criteria. The following M-mode indexes of LV filling were then calculated: (1) Peak filling rate was determined as the peak rate of increase of the LV diameter (D) with respect to time, and calculated as the highest positive value of the instantaneous rate of diameter lengthening (dD/dt). (2) Normalized peak lengthening rate was identified as the maximal value of 1/D X dD/dt, which was derived by dividing dD/dt by instantaneous LV diameter during diastole. (3) Duration of rapid filling was defined as the time from minimum LV dimension to the time when the LV filling rate decreased to 20% of its maximal value. Mitral velocity profiles were digitized along the darkest lines of the velocity spectra. Peak early filling velocity (E) and atria1 filling velocity (A) were measured directly from the spectral display, and E/A ratio was calculated from these values. Total time velocity integral was determined as the area under the peak early and atria1 filling velocity profiles. To assess the reproducibility of the Doppler echocardiographic measurements, all recordings were analyzed on 2 separate occasions for intraobserver variability, as well as by a blinded investigator for interobserver variability. Both intra- and interobserver variabilities were minimal; correlations for the parameters measured ranged from 0.94 to 0.99 for intraobserver variability and from 0.92 to 0.98 for interobserver variability. Data obtained at specific heart rates were compared and significant differences were determined by analysis of variance for single factor experiments having repeated measures. l 2 RESULTS Table I compares the characteristics of the trained athletes with those of the control subjects, at rest. As expected in the trained athletes, significant differences were seen in height and in heart rate at rest. Furthermore, LV end-diastolic dimension, LV wall mass and indexed LV wall mass were significantly higher in the athletes. Table II shows the data generated from the digitized echocardiograms at different heart rates during supine exercise and during recovery in both athletes and control subjects. Significant differences between athletes and control subjects were seen at heart rates of 140 beats/min during both exercise and recovery in peak filling and normalized peak lengthening rates. Doppler echocardiographic variables of transmitral flow, obtained at different heart rates where possible, in athletes and in control subjects are listed in Table III. Significant differences in total time-velocity integral were seen in athletes during recovery at 120 and 80 OCTOBER
1, 1991
TABLE II Echocardiographic Variables Obtained (n = 10) and in Control Subjects (n = 10)
at Different
Heart
Rates During
Supine
Exercise
Exercise (beats/min)
Heart
rate (beats)
Peak filling
rate
km/s) Normalized peak lengthening rate (per set) Duration of rapid filling (ms) Mean blood pressure
(mm Hg)
Rest
80
A 59&l* C 6924 A 9.7 ? 0.5
10.6
C 9.7 f 0.6
10.2 f 0.9
A 2.3
f 0.2
C 2.5 r?~0.2 A 185 r 6 C 178 f 12 A 9529
c
97*9
140
14.5
r 0.7
12.1 ir 1.0
2.8 + 0.2 2.5 -+ 0.2 184 2 8 181 f 11
3.8 3.2 161 167
f e -tf
105
120
f 4
f 4
101 f 3
Recovery
in Athletes
Recovery (beatslmin)
120
f 0.7
and During
0.3 0.2 8 9
127 f 6
140
16.4
f 0.4*
12.9 2 1.0 4.2 3.4 144 158
f f 2 k
0.3* 0.2 8 7
124
2 4
131 f 6
15.0
120
r 0.7
13.4
11.8 rtr 0.7 4.1 2.8 142 159
* -t 2 2
0.4* 0.2 7 12
122
‘- 5
121 f 4
80
f 0.5
10.7
f 0.7
11.7 f 0.8
9.6 f 0.8
3.7 3.1 155 167
f 0.4 * 0.3
2.8 ziz 0.2 2.4 2 0.1
108
f 4
91 f 3
108 f 4
96 f 2
2 10
201
t 10
195 t 13
+ 16
*p 13 Documentation of increased myocardial stiffness due to increases in myocardial mass and interstitial connective tissue affecting diastolic filling at rest and during exercise has resulted in the suggestion that the same effects may result from LV hypertrophy occurring in endurance athletes.7,13-16 Only Granger et a1,t7 using resting radionuclide estimations of LV filling rate, have shown that this diastolic parameter is unchanged in endurance athletes in the presence of increased LV mass. Our study substantially extends these latter findings. It demonstrates that although LV diastolic filling in trained endurance athletes is unchanged at rest, it is significantly enhanced during dynamic exercise in the presence of increased LV mass, thus adding further credence to the concept of adaptive physiologic hypertrophy in normal subjects. Furthermore, the significant increases in echocardiographic peak filling rate, Doppler-derived peak filling velocity and E/A ratio in athletes during exercise suggest that this enhancement occurs in the active phase of diastole. Several mechanisms have been suggested for this adaptive mechanism. Although part of the increase in LV mass is a compensatory mechanism for the increased LV cavity size in these athletes maintaining a normal LV wall tension, Longhurst et al5 have suggested that true hypertrophy may occur in these elite endurance athletes.6 Penpargkul et al’* suggested that enhanced diastolic function may be due to improved calcium flux in the sarcoplasmic reticulum of the trained myocardium. Furthermore, it has also been shown that ventricular filling is a dynamic process with venous return augmented by both skeletal and cardiac muscle.19 Our data is consistent with the concept that dynamic exercise training, together with the development of adaptive ventricular hypertrophy, produces increased filling during the active phase of diastole. Although the mechanisms by which these adaptive changes occur are not apparent in a study of this nature, the data appear to provide further evidence supporting the value of dynamic exercise training in improving cardiac performance. However, it should be stated that these changes resulting in increased diastolic filling characteristics may be merely the result of the increase in LV volumes. Nevertheless, filling is enhanced in the presence of LV hypertrophy, and is a key finding irrespective of LV volume. There are a number of limitations to our study. The trained athletes do not serve as their own control subjects in regard to any adaptation to training. Thus, conclusions regarding the adaptative processes of endur-
948
THE AMERICAN
JOURNAL
OF CARDIOLOGY
VOLUME
68
ance training are implied by comparison to control subjects. Echocardiograms can only imply that adaptive changes in diastolic compliance have occurred.20 Furthermore, Doppler echocardiographic estimates of LV filling characteristics are altered by a number of hemodynamic variables. 21 Some of these limitations may be overcome by using the athletes as their own control subjects and by comparing LV filling characteristics at specific heart rates during exercise. However, the inability of these noninvasive techniques to measure LV pressures remains a limitation. Also, exercise was performed in the supine position, which is known to have a different sequence of hemodynamic responses compared with exercise in the upright position.22 Furthermore, a comparison of variables at different heart rates during dynamic exercise between trained athletes and normal subjects may be limited by the fact that the work load during exercise at any given heart rate may be different for athletes with a resting bradycardia than for control subjects. Thus, sympathetic activation and its effect on cardiac performance are likely to be different in trained athletes versus control subjects. Acknowledgment: We wish to acknowledge Jeanie Toombs for secretarial help, Cathy Guard and the Medical College of Virginia Echocardiographic Laboratory staff for assistance in obtaining the Doppler echocardiographic studies, and the Virginia Commonwealth University Athletic Director, the men’s and women’s teams’ basketball coaches, and the Sports Medicine Clinic staff for providing subjects.
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phy. J Am Co11 Cardiol 1985;5:862-868. 18. Penpargkul S, Repke DI, Katz AM, Shueuer J. Effect of physical training on calcium transport by rat cardiac sarcoplasmic reticulum. Circ Res 1977;40: 134-138. 19. Sabbah HN, Stein PD. Pressure-diameter relation during early diastole in dogs. Circ Res 1981;48:357-365. 20. Stoddard MF, Pearson AC, Kern MJ, Ratcliff J, Mrosek DG, Labovitz AJ. Left ventricular diastolic function: comparison of pulsed Doppler echocardiographic and hemodynamic indexes in subjects with and without coronary artery disease. J Am CON Cardiol 1989;13:327-336. 21. Choong CY, Hermann HC, Weyman AE, Fifer M. Preload dependence of Doppler-derived indexes of left ventricular diastolic function in humans. J Am CON Cardiol 1987;10:800-808. 22. Poliner LR, Dehmer GJ, Lewis SE, Parkey RW, Blomqvist CG, Wilerson JT. Left ventricular performance in normal subjects: a comparison of the responses to exercise in the upright and supine positions. Circulation 1980; 62:528-534.
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