(Circulation. 1996;94:359-367.)
© 1996 American Heart Association, Inc.
Articles |
Continuum of Cardiovascular Performance Across a Broad Range of Fitness Levels in Healthy Older Men
the Gerontology Research Center (J.L.F., F.C.O., E.G.L.), National Institute on Aging, and the Division of Gerontology (A.P.G., L.I.K., J.M.H., L.E.L.), University of Maryland School of Medicine and Geriatrics Research, Education and Clinical Center, Veterans Administration Medical Center, Baltimore; the Divisions of Geriatric Medicine and Gerontology (J.B.-W.) and Cardiology (S.P.S., G.G., L.C.B.), The Johns Hopkins Medical Institutions; and the Center on Aging (J.M.H.), University of Maryland, College Park, Md.
Correspondence to Edward G. Lakatta, MD, Gerontology Research Center, Laboratory of Cardiovascular Science, 4940 Eastern Ave, Baltimore, MD 21224.
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Abstract |
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Background Although it has become clear that habitual exercise in older individuals can partially offset age-associated cardiovascular declines, it is not known whether the beneficial effects of exercise training in older individuals depend on their prior fitness level.
Methods and Results Ten sedentary men (S), age 60.0±1.6 years (mean±SEM), who were carefully screened to exclude cardiac disease underwent exercise training for 24 to 32 weeks, and eight age-matched endurance-trained men (ET) stopped their exercise training for 12 weeks. All underwent treadmill exercise and rest and maximal cycle exercise upright gated blood pool scans at baseline and after the lifestyle intervention. Before the intervention, the treadmill maximum rate of oxygen consumption (
O2max) was 49.9±1.9 and 32.1±1.4 mL·kg-1·min-1 in ET and S, respectively. During upright cycle exercise at exhaustion, although heart rate did not differ between groups, cardiac index, stroke volume index, ejection fraction, and left ventricular contractility index (systolic blood pressure/end-systolic volume index) all were significantly higher, and end-systolic volume index, diastolic blood pressure, and total systemic vascular resistance all were significantly lower in ET versus S. After the partial deconditioning of ET men, O2max fell to 42±2.2 mL·kg-1·min-1, and training of S increased O2max to 36.2±1.6 mL·kg-1·min-1. Training of S had effects on cardiovascular function that were similar in magnitude but directionally opposite those of detraining ET. All initial differences in cardiovascular performance at peak work rate between S and ET were abolished with the intervention. Across the broad range of fitness levels encountered before and after change in training status (O2max of 26 to 58 mL·kg-1·min-1), cardiac index, stroke volume index, end-systolic volume index, ejection fraction, and the left ventricular contractility index were all linearly correlated with O2max.
Conclusions Exercise training or detraining of older men results in changes in left ventricular performance that are qualitatively and quantitatively similar, regardless of the initial level of fitness before the intervention.
Key Words: aging • exercise • cardiac volume
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Introduction |
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Aging in healthy, sedentary individuals is accompanied by a decline in several aspects of cardiovascular reserve function. Although declines occur in the maximum HR during upright exercise with advancing age, SV has been reported to be maintained by LV end-diastolic dilatation in some but not all studies (see Reference 1 for review). The ability to reduce the LV ESV and to increase the EF from resting levels also declines with age. Recent studies indicated that some age-associated changes in cardiovascular function can be partially offset with aerobic exercise training.2 3 4 Although the intensity and duration of the exercise training protocol are known to affect the resultant
O2max,4 whether the cardiovascular benefits derived from exercise training in older individuals depend qualitatively or quantitatively on the baseline status of an individual before a training intervention or on the level of fitness achieved after a training intervention is not well defined. Longitudinal measurements of cardiovascular function across a broad spectrum of fitness levels are required to address this issue. One way to achieve a broad spectrum of fitness among older individuals would be to incrementally exercise train sedentary subjects until they achieve endurance athlete status. However, rarely has endurance athlete status been achieved in this manner within an experimental study. Another approach to achieve a broad spectrum of fitness among older individuals would be to start with two groups of individuals at opposite ends of the fitness spectrum and to inversely vary their training status, ie, to discontinue exercise in endurance-trained individuals and to train sedentary individuals. This was the approach that we took in the present study. We hypothesized that the marked differences in cardiovascular function between endurance-trained and sedentary older men before the study would diminish after detraining of the former and training of the latter, ie, we predicted that qualitatively and quantitatively similar (but directionally opposite) cardiovascular adaptations would occur after training and detraining in these two groups of individuals. If this were the case, a continuum of cardiovascular function would be identified across the broad range of fitness levels encountered in the study panel before and after intervention. This indicates that the level of fitness before intervention would not be a determinant of the relative resultant cardiovascular adaptations.
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Methods |
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Study Population
The study population consisted of 18 healthy men ranging in age from 53 to 76 years. Eight of the subjects were endurance-trained men who agreed to undergo detraining. Because endurance-trained older women could not be identified as potential volunteers, the study was limited to men. Each of the endurance-trained men used running as his primary form of exercise. Monthly mileage for the group ranged from 50 to 250 miles (median, 100 miles). In addition to running, 3 athletes cycled 70 to 375 miles per month, and 3 swam 5 to 12 miles per month. The men had been training regularly for 4 to 42 years (median, 16 years). Only 2 athletes had trained continuously since high school. Ten sedentary older men agreed to undergo endurance training, and they provided written informed consent to participate in the study. All subjects were recruited from the Fitness After Fifty Program. All subjects were free of cardiovascular disease as determined with detailed history and physical examination, and a negative exercise ECG and thallium scan were performed according to standard methods.5 In addition to the absence of cardiovascular disease, entry criteria for inclusion into the endurance-trained group included normal blood lipids and normal fasting and 2-hour postprandial glucose determinations. Furthermore, as evidence of the endurance-trained state,
O2max measurements with subjects subjected to two treadmill exercise tests had to be >1 SD above age-matched control O2max determinations for untrained participants from a reference population, the Baltimore Longitudinal Study on Aging.6 7 Expired gas volumes during treadmill exercise were measured with a Parkinson Cowan gas meter. Expired O2 and CO2 concentrations were measured with a medical mass spectrometer (Perkin Elmer MGA-1100), and O2 was calculated every 30 seconds. O2max was defined by achievement of at least two of the following three criteria: leveling off of O2, a peak HR of 
90% of the age-predicted rate, and a respiratory exchange ratio of 1.10 at maximal effort. Percent body fat was determined through underwater weighing and corrected for residual volume.8 All subjects had a resting blood pressure of <160/95 mm Hg, and none were receiving cardiovascular medication. Subjects were counseled to follow an American Heart Association Step I diet9 and were stabilized on this diet before the onset of the study. The relative composition of the diets was maintained throughout the study, but calories were adjusted upward in an attempt to prevent weight loss during training or downward to prevent weight gain during detraining. Body weight was monitored weekly, and 24-hour diet recalls were reviewed with participants to ensure compliance.
Detraining of Older Endurance-Trained Men
Before detraining, subjects underwent a baseline gated blood pool scan to assess LV volumes and systolic performance at rest and during maximal cycle exercise (see below). Subjects then ceased all endurance activity, even walking moderate distances, for 4 weeks to achieve a reduction in O2max. They were contacted weekly to assess compliance and any weight changes. After 4 weeks of inactivity, subjects underwent repeat treadmill testing to determine O2max. If their O2max had not decreased by 10%, they continued this sedentary phase for another 4 weeks when their O2max was reassessed and were then placed on a low-intensity exercise program to stabilize their O2max at this reduced level. On average, this deconditioning protocol took 12 weeks to complete. This design permitted a focus on the effects of a change in O2max on cardiovascular function rather than the acute effects of detraining. Once subjects stabilized at the detrained O2max, a repeat cycle exercise gated blood pool study was performed, and O2max and percent body fat were remeasured.
Training Protocol for Sedentary Older Men
An aerobic exercise program was prescribed based on the subject's cardiovascular responses during the treadmill exercise tests. Initial training began at a target HR of 60% of HRR calculated as: Target HR=0.60(HRmax-HR rest)+HR rest. Subjects were taught to palpate their pulse at rest and during exercise; these measurements were recorded with resting and exercise blood pressure measurements at each exercise session. All training sessions began with 10 minutes of low-intensity warm-up and flexibility exercises. Subjects then exercised on treadmills (walk/jogging) and cycle ergometers three times a week under supervision of study personnel at an exercise facility. Exercise gradually increased in intensity from 60% of HRR to 75% to 80% of HRR and in duration from 30 to 45 minutes of continuous exercise. Exercise tests performed at 3-month intervals were used to adjust the exercise prescription. By 4 months, most subjects were exercising at 75% to 80% of HRR continuously for 30 minutes. At 6 months, most were training three or four times a week at 75% to 85% of HRR continuously for 30 to 45 minutes. Exercise session attendance was >80% for these subjects during the 2 months before final cardiovascular testing.
Rest and Exercise Gated Blood Pool Scan Protocol
All subjects underwent two upright rest and maximal cycle exercise gated blood pool studies to assess cardiac volumes (EDV, ESV, and SV) and systolic performance (cardiac output and EF) at baseline and after either detraining (of endurance-trained individuals) or training (of sedentary individuals). Upright graded exercise on a cycle ergometer began at a 25-W work rate and was increased by 25 W every 3 minutes until exhaustion; pedal speed was maintained at 60 rpm. All subjects exercised to exhaustion without cardiac symptoms.
Resting and exercise gated blood pool scans were obtained in an 
40° left anterior oblique position to best define the ventricular septum after in vivo labeling of red blood cells with 25 to 30 mCi 99mTc. Images were acquired in a 64x64-byte matrix with 1.9 zoom using a high-sensitivity, parallel-hole collimator attached to a standard Anger camera and interfaced with a commercial nuclear medicine computer system. Twenty frames were acquired per RR interval. Acquisitions were obtained at rest and during the last 2.5 minutes of each 3-minute exercise workload.
Calculation of LV volumes was performed with validated methods described in detail previously.10 In brief, time-activity curves were constructed with the use of a semiautomated commercial program in which edges were placed around the LV in each frame with a combined second derivative and threshold algorithm. Background was automatically determined with a region of interest drawn inferior and lateral to the LV in the end-systolic frame. From these LV regions of interest, a background-subtracted time-activity curve was generated. All participants had normal regional LV wall motion, both at rest and throughout exercise.
Absolute LV volumes were computed based on the ratio of the attenuation-corrected end-diastolic count rate from the gated study to the count rate per milliliter of a sample of venous blood. Sphygmomanometric brachial artery blood pressure was measured during the last minute of each exercise workload.
Derived Measurements
Cardiac volumes and cardiac output were expressed as indexes (per body surface area). Mean arterial pressure was calculated as [SBP+(2 DBP)]/3; TSVR was calculated as mean arterial pressure/cardiac output; SWI was calculated as SVIxSBP; and LV contractility index was calculated as SBP/ESVI.
Statistical Analysis
The present study design permits both cross-sectional and longitudinal comparisons. Cross-sectional comparisons measure the diversity of cardiovascular performance encountered among the healthy older community-dwelling individuals, who differed markedly in lifestyle (training habits) before the study. Longitudinal assessment of the effects of the exercise intervention was made within each group. A cross-sectional comparison of the measured variables can also be made after the lifestyle intervention. Comparison of this second cross-sectional analysis with the former determines the extent to which any significant variation between the groups before study is attenuated as a result of the change in training status. The study design also permits an assessment of the relations between measured variables and O2max across the broad spectrum of the latter (26 to 58 mL·kg-1·min-1) encountered in the study.
Measured variables before and after the intervention (longitudinal design) were compared within a group with paired t test. The effect of the intervention (change in training status) between the two groups was compared with a two-factor repeated-measures ANOVA. ANCOVA was used to compare the slopes of the relations for the change in SWI or SVI versus EDVI between the training states at maximum work rate. Between-group comparisons (cross-sectional design) before or after intervention were made with Student's unpaired t test. Least-squares linear regressions of cardiovascular variables on O2max or between cardiovascular variables included data from both groups at each training status. All data are reported as mean±SEM. A two-tailed P<.05 value was considered significant; all values of P<.10 are reported.11
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Results |
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Each table of data (Tables 1
through 3 and 5) has four columns. Columns 1 and 4 compare the absolute values of parameters in the two groups at the start of the study, ie, the untrained sedentary and endurance-trained men in the highly conditioned state, respectively (unpaired t test). A longitudinal assessment of the change in training status within each group is made by comparing columns 1 and 2 and columns 3 and 4 (paired t test). A comparison of the effects of the intervention between groups is made with an unpaired t test of the change between columns 1 and 2 and columns 3 and 4 or with a repeated-measures ANOVA. A cross-sectional assessment of absolute parameters following the intervention is gleaned by comparing columns 2 and 3 with an unpaired t test.
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Anthropometry and Aerobic Capacity
The mean age of the two study groups did not differ (Table 1
). Before the study, treadmill O2max averaged >55% higher in the endurance-trained than in the sedentary men (Table 1). Peak cycle work rate was higher in the former than in the latter. Body weight was higher in the sedentary than in the endurance-trained group. Percent body fat tended to be higher (P<.08) in the sedentary group, but fat-free mass did not differ between groups (Table 1). The training/detraining intervention significantly altered O2max in both groups. Body weight tended to decrease in the sedentary group after training (P<.07) but did not change with detraining in the endurance-trained group. Percent body fat decreased in the sedentary men after training but did not change with deconditioning in endurance-trained men (Table 1). Fat-free mass did not differ with the lifestyle intervention in either group. After the intervention, the intergroup difference in O2max was reduced from 40% to 15%, but the latter difference remained statistically significant (P<.04).
Resting Cardiovascular Function
Before the intervention, the only cardiovascular parameter at rest that significantly differed between groups was SBP, which was higher in the sedentary than in the endurance-trained group (Table 2). Neither detraining of the endurance-trained men nor conditioning of the sedentary men significantly affected the cardiovascular parameters measured at rest in the seated positions (Table 2). However, in the more conditioned state, there was a trend (P<.1) for HR to be lower in both groups, and there was a trend (P<.1) toward lower SBP and DBP after conditioning in the sedentary men. When analyzed across the broad range of fitness, resting HR, as expected, was highly and inversely linearly correlated with O2max (see Table 4 and Fig 1). Trends for positive correlations between O2max and resting SVI, EF, and SBP were also observed, but these did not reach statistical significance (see Table 4).
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Indicates endurance-trained conditioned; 
, endurance-trained deconditioned; 
, sedentary conditioned; 
, sedentary unconditioned.
Cardiovascular Function During Submaximal Exercise
Similarities, differences, and trends for differences in cardiovascular measurements between the two study groups or within each group between relative conditioning states in general persisted when measured at a fixed submaximal work rate (100 W) and at the relative work rate of 50% of maximum (data not shown).
Cardiovascular Function at Maximal Exercise
The effects of relative conditioning status on cardiovascular measures at the maximum work rate are presented in Table 3. Average values for training effects and average absolute values in the trained relative to untrained or detrained states are graphically depicted in Figs 2 and 3, respectively. Before the intervention, CI, SVI, and EF at the maximum work rate were significantly higher and SWI (P<.06) and the LV contractility index tended to be higher (P<.07) in the endurance-trained men in the highly conditioned state than in the untrained sedentary men (Table 3, column 1 versus 4). ESVI (P<.006), DBP (P<.05), and TSVR (P<.01) at maximal work rate were significantly lower in the former than in the latter (Table 3).
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The partial deconditioning of endurance athletes significantly reduced the EDVI, SVI, CI, and SWI and tended to decrease EF (P<.07) at the maximal work rate but did not change HR (Table 3, paired t test, column 3 versus 4). Similar effects (but opposite in direction) occurred in sedentary men after conditioning. SVI (P<.06), EF (P<.09), and SWI (P<.05) increased, and DBP (P<.07) decreased (Table 3). The average change in O2max and all cardiovascular measures at maximal work rate affected by the change in training status were the same in both groups (unpaired t test of the differences in columns 1 and 2 versus differences in columns 3 and 4). The similar training effects in both groups for selected parameters are illustrated in Fig 2. The effect of the training/detraining intervention between the two groups was assessed with a two-factor (group and training status) ANOVA for repeated measures (training status is repeated factor). No significant interactions (or trends, ie, .05<P<.1) occurred between groups, indicating that the training/detraining intervention had quantitatively similar effects in sedentary and endurance-trained men. As expected based on data in Table 1, significant interaction was observed between groups for O2max (P<.009); a trend (P<.07) for a differential training/detraining effect between groups was also observed for percent body fat.
The similarity of the pattern of the effects on O2max and selected cardiovascular measures resulting from the intervention in each group can also be assessed by expressing the data for a given parameter as a ratio of the values in the relatively more trained to the values in the relatively detrained or untrained state (Fig 3). The higher O2max in the trained state was accompanied by a higher peak CI, produced by an increased SVI but not an increased HR (Figs 1 and 3A). Higher SVI in the relatively trained state was mediated by both an increase in EDVI and a reduction in ESVI. EF and SWI were also increased in the trained state in both groups (Fig 3). None of the ratios of the variables in the trained to untrained or detrained state depicted in Fig 3 differed between groups (unpaired t test). Also, the ratio for LV contractility index at maximal work rate in the trained versus the untrained state was 110.5±16.2 and 129.4±16 in endurance-trained and sedentary groups, respectively (P<.10 between groups, data not shown). Fig 4 illustrates that the slope of the relation of the change in SWI between the conditioned and deconditioned or unconditioned state was linearly correlated with the change in EDVI at maximum work rate for all individuals studied. The slope of this function was also the same for both groups by ANCOVA. The change in SVI versus the change in EDVI between training states (not shown) was also linearly correlated (r=.66, P<.01). The slopes of these relations did not differ statistically between groups by ANCOVA.
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Because the changes elicited by the conditioning and deconditioning interventions in the two study groups were similar in magnitude but opposite in direction, group differences in the absolute values of cardiovascular measures at maximum work rate between endurance-trained men in the highly conditioned state and sedentary men in the unconditioned state before study (Table 3, column 1 versus 4) were no longer present after the lifestyle intervention (Table 3, column 2 versus 3). The similar pattern of many aspects of cardiovascular performance in the conditioned relative to the deconditioned or unconditioned state in both groups (Figs 2 and 3) implies that a performance continuum at maximum work rate exists across the wide range of conditioning states encountered in the present study. Table 4 and Fig 5 indicate that this continuum is linear: CI, SVI, ESVI, EF, and LV contractility index at maximal effort were linearly correlated with O2max. A trend (P<.08) for an inverse relation between TSVR and O2max was also observed (Table 4). In contrast, neither HR nor EDVI at maximum work rate correlated with the fitness level in these older healthy individuals.
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Cardiovascular reserve function, defined as the difference in a hemodynamic parameter between maximal exercise work rate and seated rest, is shown in Table 5. Before the intervention, the CI, SVI, ESVI, EF, SWI, and LV contractility index reserves significantly differed between the groups, and HR reserve tended (P<.10) to differ (Table 5, column 1 versus 4 by unpaired t test). Training of sedentary men significantly increased the CI, SVI, and SWI reserve function and tended to increase the reserve EF (P<.1), LV contractility index (P<.07), and SBP (P<.07). Detraining of endurance-conditioned men significantly reduced the reserve CI and SWI (Table 5, column 1 versus 2 or 3 versus 4 by paired t test). After the intervention, only the EDVI reserve differed between groups (Table 5, column 2 versus 3). The SVI reserve (Fig 6) and reserve SWI (not shown) were significantly correlated with the EDVI reserve. The reserve CI, HR, ESVI, and LV contractility index values were significantly and linearly correlated with O2max across the broad range of the latter (Table 6).
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Discussion |
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It is well documented that maximal aerobic capacity declines with age.7 12 13 The increasingly sedentary lifestyle with advancing age may be in part responsible for this decline. Alternatively, the effects of exercise training to augment aerobic capacity in older individuals1 3 4 7 14 15 16 may be construed as partially offsetting a reduction in aerobic capacity caused by an "aging process." Both cross-sectional and longitudinal studies have indicated that the increase in aerobic capacity through exercise training in older individuals is accompanied by an augmentation of some aspects of cardiovascular performance (see Reference 1 for a review).
In the present study, we compared the cardiovascular changes that accompany detraining of endurance-trained older men and training of sedentary older men. This combined cross-sectional study and longitudinal design allowed us to assess whether and to what extent cardiovascular changes occurring with an exercise intervention in older individuals depend on the preintervention aerobic capacity. The study design also permits identification of which aspects of cardiovascular function in older individuals might vary as a continuum across a broad range of aerobic fitness levels. There were differences in several cardiovascular measures between the sedentary and endurance-trained (master athlete) individuals as assessed with the use of cross-sectional group comparison before the intervention, thus confirming results of prior studies.15 17 18 The longitudinal results of the present study show that changes in cardiovascular function of similar magnitude, but directionally opposite, occur in healthy older men after partial deconditioning from the endurance-trained state and after conditioning from the sedentary state. Specifically, physical conditioning of sedentary older men results in significant increases in O2max, peak work rate, and reserve CI, SVI, and SWI. These results are similar to those of prior longitudinal studies of the effects of exercise training of sedentary older men.2 3 Detraining of endurance-trained older men resulted in significant decreases in O2max, peak EDVI, SVI, CI, and reserve CI and SWI.
To our knowledge, this is the first study in which cardiac volumes were measured after detraining of older endurance-trained individuals. It is of interest that a significant change in body fat did not accompany this deconditioning intervention; this was due to a unique aspect of the study design that reduced caloric intake with cessation of endurance training. Thus, changes in aerobic capacity and cardiovascular performance that accompany a change in conditioning status of older individuals are dissociated for the first time from concomitant changes in body composition. Thus, within the limits of the present study design, the pattern of beneficial cardiovascular effects attributed to the conditioned state did not necessarily depend on a change in body fat.
The present results show that differences in cardiovascular performance between endurance-trained men in the highly conditioned state and untrained sedentary men are abolished after detraining of the former and training of the latter (Table 3, column 2 versus 3). It is noteworthy that although the difference in CI at maximal work rate between the two groups was no longer present after the deconditioning/conditioning intervention (Table 3, column 2 versus 3), the O2max in deconditioned endurance-trained men was still significantly greater than in the conditioned sedentary men (Table 1, column 2 versus 3). This apparent dissociation between maximal CI and O2max can be accounted for by an effect of conditioning on peripheral O2 utilization. However, the effect of conditioning on total body (A-V)O2 in the present study cannot be determined as O2 consumption was not measured during cycle exercise, ie, simultaneous with cardiac volumes. Therefore, to address this important issue, we estimated peak cycle O2 with a conversion factor of 12 mL of oxygen consumption for each watt of cycle power and derived (A-V)O2 from the quotient of this estimated peak O2max and measured peak cardiac output. Calculated in this manner, the peak (A-V)O2 before the intervention was 13.1 and 12.2 mL O2/dL in the athletes and sedentary men, respectively, with minimal change after the intervention to 13.4 and 12.5 mL O2/dL, respectively. Ehsani et al3 also failed to demonstrate an effect of training on peak cycle (A-V)O2 in older men, although Seals et al4 observed a training-induced increase in this variable during maximal treadmill exercise. Recent data by Spina et al19 indicate that older women rely on an increase in (A-V)O2 to a greater extent than do older men to augment O2max with aerobic training.
The present results indicate that the improved pattern of training effects on cardiovascular performance is similar in both groups, despite differences in the starting or final fitness level (Figs 2 and 3). The beneficial cardiovascular effects of exercise training include an increase in peak CI and an increase in SVI but no change in peak HR (Fig 3A). The increase in peak SVI is due to both an increase in EDVI and a reduction in ESVI (Fig 3B). The SVI is highly correlated to the EDVI, as shown in several previous studies.3 15 16 The change in SVI or SWI within individuals after a change in training status is correlated with the change in EDVI (Fig 4). This relation is the same, regardless of the prior conditioning status. Thus, the present results strongly suggest that similar increments in cardiovascular performance can be achieved through physical conditioning in older men, regardless of their baseline or preconditioning level. The cardiac pump performance variables at maximal work rate that are most closely linearly related to fitness level are the ESVI and EF.
The greater ability to reduce end-systolic size and to increase EF as fitness increases is not likely to be due to enhanced myocardial ß-adrenergic responses with conditioning, as the diminished cardiovascular ß-adrenergic responsiveness with aging1 20 21 is not altered by chronic conditioning.22 Alternatively, the improved ability of the LV to empty as fitness increases may relate to a reduction in arterial stiffness in the conditioned state23 and thus to a reduction in afterload. Although an index of resting arterial stiffness was not measured in the present study, aortic stiffness is closely related to resting SBP. The latter was greater in sedentary than in endurance-trained men (Table 2), and at maximal work rate, SBP also showed a tendency (P<.15) to vary with training in sedentary men (Table 3). Thus, it is possible that aortic stiffness varied inversely with fitness. Neither arterial stiffness nor impedance has been measured during exercise in older humans of any fitness level. Prior studies in beagles, however, have shown that the age-associated increase in aortic impedance during exercise was abolished when the exercise was conducted in the presence of ß-adrenergic blockade.24 Additional studies are required to clarify this issue. The fact that the LV contractility index, which controls for the arterial blood pressure component of afterload, also varies with fitness (Fig 5D) suggests that intrinsic myocardial contractile function varies with fitness. This interpretation is in accord with the interpretation of other estimates of myocardial function in prior studies.3 15 16
At peak work rate, LV or myocardial performance indexes varied linearly with O2max (Table 4 and Fig 5). It is noteworthy that significant cardiac effects of training in older men, in addition to improved LV contractility index and EF, include the extent to which the Frank-Starling mechanism is used. Demonstration of the latter requires measurement of the change in the SWI or SVI-EDVI relations across conditioning states within individuals at maximal exercise (Figs 3 and 6), as the absolute EDVI at peak work rate during upright cycle exercise increases with age, even in sedentary older men (see Reference 1 for a review). Thus, regardless of whether exercise training influences the age-associated reduction in LV filling rate,21 25 26 27 LV EDVI does not vary with fitness when the latter is measured over a broad range of fitness in healthy older men. Further study is required to determine whether changes in LV EDVI within an individual (as in Fig 4) after conditioning or deconditioning are associated with a change in the LV early diastolic filling rate.
Potential limitations of the present study include the relatively small number of subjects evaluated and moderate changes in O2max with conditioning within each of the two groups. The moderate changes in O2max with the exercise interventions probably resulted in smaller changes in some aspects of cardiovascular performance than previously reported. Observed nonsignificant trends for some of the measured parameters to vary with the relative level of conditioning would probably reach statistical significance if it were possible to study a larger number of subjects. However, this limitation is (partially) offset by the combined use of cross-sectional and longitudinal analyses between and within the two diverse study panels that span a broad range of O2max and cardiovascular performance, permitting the highly conditioned and deconditioned states to be considered as a continuum. Also, an ANOVA for repeated measures indicated that the training/detraining intervention had quantitatively similar effects in both study groups. Although the majority of statisticians believe that an analysis of this sort is valid, even if the change in many of within-group parameters after the intervention is nonsignificant, its robustness may be questioned. A second limitation of the present study may be that the durations of the conditioning versus deconditioning protocols differed. For example, it might be argued that a deconditioning period of >12 weeks would elicit further and differential changes in O2max or measured cardiovascular variables in the endurance-trained men.
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Acknowledgments |
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This study was supported in part by Johns Hopkins Teaching Nursing Home Award (P01-AG-04402); grants R01-AG-07660 (Dr Goldberg), 5K08-AG-00497 (Dr Katzel), and 5K08-AG-00383 (Dr Busby-Whitehead); GCRC grant MOI-RR-02719; and the NIA Intramural Research Program.
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Footnotes |
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Dr Hagberg's present address: Preventive Cardiology Department, University of Pittsburgh Medical Center, Pa.
Dr Busby-Whitehead's present address: Division of General Internal Medicine/Program on Aging, University of North Carolina at Chapel Hill.
Received November 13, 1995; revision received January 30, 1996; accepted February 1, 1996.
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References |
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1. Lakatta EG. Cardiovascular regulatory mechanisms in advanced age. Physiol Rev.. 1993;73:413-467.
2.
Stratton JR, Levy WC, Cerqueira MD, Schwartz RS, Abrass IB. Cardiovascular responses to exercise: effects of aging and exercise training in healthy men. Circulation.. 1994;89:1648-1655.
3.
Ehsani AA, Ogawa T, Miller TR, Spina RJ, Jilka SM. Exercise training improves left ventricular systolic function in older men. Circulation.. 1991;83:96-103.
4.
Seals DR, Hagberg JM, Hurley BF, Ehsani AA, Holloszy JO. Endurance training in older men and women, I: cardiovascular responses to exercise. J Appl Physiol.. 1984;57:1024-1029.
5.
Fleg JL, Gerstenblith G, Zonderman AB, Becker LC, Weisfeldt ML, Costa PT, Lakatta EG. Prevalence and prognostic significance of exercise-induced silent myocardial ischemia detected by thallium scintigraphy and electrocardiography in asymptomatic volunteers. Circulation.. 1990;81:428-436.
6. Shock NW, Greulich RC, Andres R, Arenberg D, Costa PT, Lakatta EG, Tobin JD. Normal Human Aging: The Baltimore Longitudinal Study of Aging. Washington, DC: US Government Printing Office; NIH Publication No. 84-2450, 1984:45-57.
7.
Fleg JL, Lakatta EG. Role of muscle loss in the age-associated reduction in O2max. J Appl Physiol.. 1988;65:1147-1151.
8. Behnke AR, Wilmore JH. Evaluation and regulation of body build and composition. In: International Research Monograph Series in Physical Education. Englewood Cliffs, NJ: Prentice-Hall; 1974:228-236.
9. American Heart Association Steering Committee for Medical and Community Programs. Phase I diet. Circulation.. 1985;62:449A-455A.
10.
Links AJ, Becker LC, Shindledecker JG, Guzman P, Burow RD, Nickoloff EL, Alderson PO, Wagner HN. Measurement of absolute left ventricular volume from gated blood pool studies. Circulation.. 1982;65:82-91.
11. SAS Institute. SAS/STAT User's Guide: Version 6. 4th ed. Cary, NC: SAS Institute; 1989.
12.
Dehn MM, Bruce RA. Longitudinal variations in maximal oxygen intake with age and activity. J Appl Physiol.. 1972;33:805-807.
13. Astrand I. Aerobic work capacity in men and women with special reference to age. Acta Physiol Scand Suppl.. 1960;169:1-92.
14.
Rogers MA, Hagberg JM, Martin WH III, Ehsani AA, Holloszy JO. Decline in VO2max with aging in master athletes and sedentary men. J Appl Physiol.. 1990;68:2195-2199.
15.
Fleg JL, Schulman SP, O'Connor FC, Gerstenblith G, Becker LC, Fortney S, Goldberg AP, Lakatta EG. Central and peripheral cardiovascular adaptations in highly trained older men. J Appl Physiol.. 1994;77:1500-1506.
16.
Seals DR, Hagberg JM, Spina RJ, Rogers MA, Schechtman KB, Ehsani AA. Enhanced left ventricular performance in endurance trained older men. Circulation.. 1994;89:198-205.
17.
Heath GW, Hagberg JM, Ehsani AA, Holloszy JO. A physiological comparison of young and older endurance athletes. J Appl Physiol.. 1981;51:634-640.
18.
Ogawa T, Spina RJ, Martin WH III, Kohrt WM, Schechtman KB, Holloszy JO, Ehsani AA. Effects of aging, sex, and physical training on cardiovascular responses to exercise. Circulation.. 1992;86:494-503.
19.
Spina RJ, Ogawa T, Kohrt WM, Martin WH III, Holloszy JO, Ehsani AA. Differences in cardiovascular adaptations to endurance exercise training between older men and women. J Appl Physiol.. 1993;75:849-855.
20.
Fleg JL, Schulman SP, O'Connor F, Becker LC, Gerstenblith G, Clulow JF, Renlund DG, Lakatta EG. Effects of acute ß-adrenergic receptor blockade on age-associated changes in cardiovascular performance during dynamic exercise. Circulation.. 1994;90:2333-2341.
21. Schulman SP, Lakatta EG, Fleg JL, Lakatta L, Becker LC, Gerstenblith G. Age-related decline in left ventricular filling at rest and exercise. Am J Physiol. 1992;263(Heart Circ Physiol 32):H1932-H1938.
22.
Stratton JR, Cerqueira MD, Schwartz RS, Levy WC, Veith RC, Kahn SE, Abrass IB. Differences in cardiovascular responses to isoproterenol in relation to age and exercise training in healthy men. Circulation.. 1992;86:504-512.
23.
Vaitkevicius PV, Fleg JL, Engel JH, O'Connor FC, Wright JG, Lakatta LE, Yin FCP, Lakatta EG. Effects of age and aerobic capacity on arterial stiffness in healthy adults. Circulation.. 1993;88:1456-1462.
24. Yin FCP, Weisfeldt ML, Milnor WB. Role of aortic input impedance in the decreased cardiovascular response to exercise with aging in dogs. J Clin Invest.. 1981;68:28-38.
25.
Douglas PS, O'Toole M. Aging and physical activity determine cardiac structure and function in the older athlete. J Appl Physiol.. 1992;72:1969-1973.
26.
Levy WC, Cerqueira MD, Abrass IB, Schwartz RS, Stratton JR. Endurance exercise training augments diastolic filling at rest and during exercise in healthy young and older men. Circulation.. 1993;88:116-126.
27.
Fleg JL, Shapiro EP, O'Connor F, Taube J, Goldberg AP, Lakatta EG. Left ventricular diastolic filling performance in older male athletes. JAMA.. 1995;273:1371-1375.
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