Echocardiography studies have been utilized in a variety of settings to evaluate left ventricular function and contractility. Left ventricular function indices measured previously have been shown to increase with aerobic exercise (6,11,13), primarily due to decreased after-load (8).
Although one would expect to obtain increases in left ventricular function with increase in adrenergic state produced by anaerobic exercise intervention, there are no data on the changes in left ventricular function at peak Wingate anaerobic test. This test is widely accepted and used in the evaluation of the human anaerobic performance capacity. Because this kind of effort is characterized by exposing the subjects to a very high degree of sudden strenuous all out exercise, it may alter the left ventricular contractility and function.
Thus, the present study was designed to provide information to better understand the effects of two considerably different modes of exercise and thus different stress-induced left ventricular function both at peak aerobic and all out anaerobic efforts in young healthy subjects.
Twenty-two aerobically well trained young healthy men (19 ± 1 yr) volunteered for this study. The subjects were recruited from the Military Academy of Physical Fitness student body. All subjects were judged free of coronary artery disease by clinical history, absence of major risk factors and by normal graded exercise stress test up to O2max. A written informed consent was obtained from each subject, which was approved by the Clinical Science Center Committee on Human Subjects.
Procedure and measurements.
Each subject reported three times to the laboratory. Sessions were spaced by at least 48 h and on average by intervals of no more than 1 wk. The first session was devoted to accustoming the subjects to the study’s procedures and to the general scope of the study. During the second session, subjects underwent a graded maximal bicycle exercise test. Subjects were tied by torso-straps to the wall while cycling (Fig. 1). This was done to minimize movement of the upper body and to facilitate auscultation of blood pressure and echocardiographic measurements at peak exercise. Oxygen uptake was determined breath by breath utilizing the Medical Graphics (St. Paul, MN) metabolic cart. The metabolic cart was calibrated before each test with known primary standard quality gases. A 12-lead electrocardiogram and heart rate were continuously monitored at rest, during exercise and recovery. Five-second recordings were obtained at rest and at peak exercise. After warm-up, subjects cranked against an initial workload of 125 W that was increased by 25 W every minute until the subject could no longer continue at the predetermined pace. Cardiac output was measured at peak exercise by means of echocardiographic measurements. Blood pressure was taken using a standard sphygmomanometer cuff and mercury manometer mounted at eye level, in the sitting position at rest and at peak exercise.
During the third session and after warm-up, subjects were asked to perform the 30 s all-out Wingate anaerobic test (4), utilizing a weight-adjusted Monark cycle-ergometer (Model 864, Varberg, Sweden). The subjects were seated on the ergometer with their feet fastened to the pedals by means of racing-type toe-clips, and seat height was adjusted. In addition, subjects’ backs were strapped to the wall, in order to minimize movement of the upper body and to facilitate auscultation of blood pressure and echocardiographic measurements at peak exercise. The anaerobic test consisted of 30-s supramaximal pedaling against a resistance determined relative to the subject’s body mass at 80 g·kg−1 body weight (4). At the command “start,” the subject commenced cranking as fast as he could against the ergometer’s inertial resistance only. The full, predetermined resistance load was applied within 3–4 s once the inertial resistance had been overcome. Pedal revolution count started at that instant by means of an electro-mechanical counter and subjects maintained an all-out effort throughout the test. Strong verbal encouragement was given to ensure maximal effort.
A 25-μL fingertip blood sample was taken at rest and during the 2nd min post exercise for the determination of lactic acid concentration at peak anaerobic effort. The sample was immediately transferred to a microtube containing 100 μL of 7% perchloric acid. The tubes were centrifuged after standing for at least 1 h. Twenty-microliter aliquots of the supernatant were subsequently used for lactic acid analysis on the Analox LM3 analyzer (Analox Instruments, England; Reagent Kit No. GMRD-071, London, U.K.).
Echocardiographic data processing.
Two-dimensional, echocardiographic and M-mode images were performed at rest and at peak exercise utilizing a Vingmed 725 Sonotron and Sony recorder equipped with 2- and 3-MHz transducers. The diameters of the aorta were determined by two-dimensionally directed M-mode. The left atrium was measured from the parasternal long-axis view. At rest, left ventricular end-diastolic and end-systolic diameters and intraventricular septum and left ventricular posterior wall thicknesses were measured from the parasternal long and short-axis views as well as from 4- and 5-chamber views, just below the mitral valve level, according to the recommendations of the American Society of Echocardiography (17). At peak exercise, due to the short time available for measurements, left ventricular volumes and ejection fraction were determined using Simpson’s rule from apical 4-chamber view.
All echocardiographic studies were performed with the subjects in the sitting position at rest, and at peak aerobic and anaerobic efforts. The probe was hand held and directed to a marked point from which the resting data were obtained. The beam was directed to the aortic valve outflow tract in the 5-chamber view, or from the supersternal approach for those subjects in whom adequate imaging of 5-chamber or parasternal long axis views was not obtained. To assess the objectivity of the echocardiographic readings, all recordings were evaluated by two independent experts. A high correlation (r = 0.89) was found for interobserver reliability.
At rest and peak exercise cardiovascular variables were computed as follows:
Stroke volume was the difference of left ventricular end diastolic volume − end systolic volume;
Cardiac output was determined as the product of heart rate and stroke volume;
TPR was calculated as: (mean arterial blood pressure × 80)/cardiac output;
Ejection fraction = [(end diastolic volume − end systolic volume)/end diastolic volume] × 100%;
Fraction shortening = [(end diastolic dimension − end systolic dimension)/end diastolic dimension] × 100%;
End-systolic pressure volume ratio = cuff-determined systolic blood pressure/left ventricular end-systolic volume (12,17); and
Mean arterial blood pressure = [(systolic pressure - diastolic pressure)/3 + diastolic pressure].
One-way ANOVA with repeated measures was employed for each of the variables measured in order to detect variations in the experimental parameters. In addition, the Students Newman-Keuls procedure was used for specific post hoc comparisons.
All subjects completed the exercise challenges without difficulties or abnormal symptoms, dysrhythmias, or electrocardiographic abnormality (e.g., S-T segment depression). Mean descriptive data are presented in Table 1. Data presented in this table indicates that subjects were well trained and that all variables measured were within normal values.
Hemodynamic responses and echocardiographic measurements at rest, and after maximal anaerobic and aerobic exercises are presented in Figure 2 and Table 2. All variables measured at peak aerobic and anaerobic efforts were significantly (P < 0.05) higher than resting values, across all conditions, except for diastolic blood pressure at peak aerobic test (Table 2), and stroke volume at peak all-out anaerobic exercise (Fig. 2). Values at peak anaerobic effort differed significantly from the respective values at peak aerobic exercise in the following variables: heart rate, stroke volume, cardiac output, left ventricular end systolic and diastolic volumes, systolic, diastolic and mean arterial blood pressures, oxygen uptake, TPR, and maximal load. The differences between the two exercise modes for peak blood lactate were not significant.
Although reliable measurements have been performed in multiple studies using conventional techniques, this study differs by its unique echocardiograph approach for measurements which were taken at peak exercise from 5-chamber view with the subjects seated and strapped to a wall. This helped to minimize movement of the upper body, thus enabling clear and reliable imaging and blood pressure measurement even at peak effort (2).
This study indicates that the left ventricular contractile state and function differs in normal subjects at peak all out anaerobic effort compared with maximal aerobic effort.
The mechanics of ventricular contraction include the concept of the inter-relationship between force, length, velocity, and time (20). The extent of myocardial fiber shortening is a reflection of the interaction between the initial fiber stretch (preload), the load opposing shortening (after-load), and the intrinsic contractile state (20). Based on this relationship, several researches have proposed the end-systolic pressure/volume relationship as a measure of left ventricular contractility which is independent of preload (15,16,20).
During the aerobic-type effort, contractility and left ventricular function were increased most likely due to the relatively lower after-load opposing the ejection of the left ventricle (1). This low after-load is known to be mediated through the peripheral autoregulation mechanism occurring in the active muscles. Such lower after-load allows cardiac output to increase as a result of increases in both stroke volume (18) and heart rate as previously reported when utilizing similar challenges (11,12). The increase in stroke volume during aerobic exercise is a result of left ventricular dilation suggesting higher preload and a decrease in end-systolic volume. Such responses may reflect both an increase in inotropism and a decrease in systemic vascular resistance (5,13,19).
All-out anaerobic effort did not produce the expected increases in the left ventricular volumes, ejection fraction, stroke volume, and cardiac output (7). Such unexpected responses could be the results of the known inverse relationship between left ventricular performance and after-load (1). This may suggest that the increase in left ventricular inotropic state was not adequate to increase left ventricular volumes and ejection fraction during the anaerobic bout (14).
It seems that in the present study, the observed lower left ventricular function at peak anaerobic (compared with the aerobic-type) effort is due, at least partially, to the greater elevation in systolic, diastolic, and mean blood pressures, and to the smaller reduction in TPR, due to greater concentrations of vasoactive substances owing to tissue hypoxia and acidosis.
The smaller reduction in TPR and the increased afterload associated with such exercise conditions (peak anaerobic effort) may force the ventricle to eject blood against a relatively higher pressure. This, coupled with lower peak heart rate and the relatively short duration (30 vs 330 s of the anaerobic and aerobic exercise, respectively) could result in a low overall cardiac output.
No electrocardiographic abnormalities were observed in the present study. Nonetheless, several previous studies of the effect of no warm-up before the performance of sudden strenuous exercise bout have evinced ischemia-like electrocardiographic abnormalities (3,9,10). The lack of electrocardiographic abnormalities in the present study may be explained by the fact that our subjects warmed up before the anaerobic exercise. This warm-up may ameliorate the ECG and enhance myocardial oxygen supply/demand balance (10).
In addition, the explanation for the presumed discrepancy could be found in the different protocols utilized and the known low sensitivity and/or specificity of the ECG for detecting true ischemia in supposedly healthy young subjects especially during brief explosive effort.
In conclusion, it is suggested that during all out anaerobic exercise, TPR and after-load values are lower than that at rest. However, these variables were not reduced to the level observed at peak aerobic exercise. Such inadequate reduction in peripheral resistance and after-load could be responsible for the lesser augmentation of left ventricular function found during the performance of the Wingate anaerobic test. This could imply that vascular autoregulation, although playing a crucial role during dynamic exercise, has an attenuated role in controlling hemodynamic responses during sudden strenuous effort. Therefore, it is suggested that anaerobic-type effort be performed with great caution.
1. Andersen, K., and H. Vik-Mo. Increased left ventricular
emptying at maximal exercise after reduction in afterload. Circulation 69:492–496, 1984.
2. Armstrong, W. F. Stress echocardiography for detection of coronary artery disease. Circulation 84(Suppl. I):I-430–I-449, 1991.
3. Barnard, R. J., R. Macalpin, A. A. Kattus, and G. D. Buckberg. Ischemic response to sudden strenuous exercise in healthy men. Circulation 48:936–942, 1973.
4. Bar-Or, O, R. Dotan, O. Inbar, A. Rotstein, J. Karlsson, and P. Tesch. Anaerobic capacity and muscle fiber type distribution in non-athletes and athletes. Int. J. Sports Med. 1:82–85, 1980.
5. Bar-Shlomo, B-Z., M. N. Druck, J. E. Morch, et al. Left ventricular
function in trained and untrained healthy subjects. Circulation 65:484–488, 1982.
6. Boucher, C. A., M. S. Anderson, and M. S. Schneider. Left ventricular
function before and after reaching the anaerobic threshold. Chest 87:145–150, 1985.
7. Daley, P. J., K. B. Sagar, and L. S. Wann. Doppler echocardiographic measurement of flow velocity in the ascending aorta during supine and upright exercise. Br. Heart J. 54:562–567, 1985.
8. Elkayam, U., J. M. Gardin, R. Berkley, C. A. Hughes, and W. L. Henry. The use of Doppler flow velocity measurement to assess the hemodynamic response to vasodilators in patients with heart failure. Circulation 67:377–383, 1983.
9. Foster, C., J. D. Antholm, C. K. Hellman, M. L. Pollock, and D. H. Schmidt. Left ventricular
function during sudden strenuous exercise. Circulation 63:592–596, 1981.
10. Foster, C., D. S. Dymond, J. Carpenter, and D. H. Schmidt. Effect of warm up on left ventricular
response to sudden strenuous exercise. J. Appl. Physiol. 53:380–383, 1982.
11. Foster, C., R. A. Gal, S. C. Port, and D. H. Schmidt. Left ventricular
ejection fraction during incremental and steady state exercise. Med. Sci. Sport Exerc. 27:1602–1606, 1995.
12. Grossman, W., E. E. Braunwald, T. Mann, L. P. Malaurin, and H. Green. Contractility state of the left ventricular
in man as evaluated from end-systolic pressure-volume relations. Circulation 56:845–852, 1977.
13. Higginbotham, M. B., K. G. Morris, and R. S. Williams. Regulation of stroke volume during submaximal upright exercise in normal men. Circ. Res. 58:281–291, 1986.
14. Poole, D. C., G. A. Gaesser, M. C. Hogan, D. R. Knight, and P. D. Wanger. Pulmonary and leg VO2
during submaximal exercise: implications for muscular efficiency J.
Appl. Physiol. 72:805–810, 1992.
15. Sagawa, K. The end-systolic pressure-volume relation of the ventricle: definition, modifications and clinical use (Editorial). Circulation 63:1223–1227, 1981.
16. Sagiv, M., P. Hanson, M. Besozzi, and F. Nagle. Left ventricular
responses to upright isometric handgrip and deadlift in men with coronary artery disease. Am. J. Cardiol. 55:1298–1304, 1985.
17. Shaw, D. J., A. Demaria, J. Kisslo, and A. Weyman. Recommendations regarding quantitation in M-mode echocardiography: results of survey of echocardiographic measurements. Circulation 58:1072–1083, 1978.
18. Sullivan, M. J., F. R. Cobb, and M. B. Higginbotham. Stroke volume increases by similar mechanisms during upright exercise in normal men and women. Am. J. Cardiol. 67:1405–1412, 1991.
19. Tarazi, R. C., and M. N. Levy. Cardiac responses to increased afterload: state-of-the-art review. Hypertension 4(Suppl. II):8–18, 1982.
20. Weber, K., and J. S. Janicki. The dynamics of ventricular contraction: force, length and shortening. Fed. Proc. 39:188–195, 1980.
Keywords:© 2000 Lippincott Williams & Wilkins, Inc.
CARDIAC OUTPUT; LEFT VENTRICULAR; ECHO-DOPPLER