Can age-related decline in left ventricular compliance be slowed by habitual endurance exercise?

Abstract

To answer this question, 13 competitive endurance athletes (mean age 69) and 13 age matched healthy non-athletic men underwent an echo/Doppler treadmill exercise stress test using Balke protocol. Left ventricular (LV) diastolic indices at rest and immediately after maximal stress were not different between the groups. Significant mean differences (P<0.001) between athletes and non-athletes were in exercise duration (24 vs. 12 minutes), peak V02 (27 vs 44 ml/kg/min), VO2 at anaerobic threshold (24 vs 35 ml/kg/min), BMI (26 vs 22 kg/m2). Diastolic pressure rose during stress in non-athletes (82 to 89 mmHg; P<0.016)).

Conclusions: This study failed to demonstrate significant differences in LV diastolic indices between elderly athletes and healthy non-athletes. Implications are that the superior cardiac fitness in elderly athletes is achieved through mechanisms other than LV diastolic compliance, possibly by preservation of high arterial vasoreactivity and oxygen consumption in the myocardium.

Keywords: aging, exercise, cardiac function

I. Introduction

Left ventricular (LV) contractile function is not affected by aging to the same extent as LV diastolic compliance(l). Most investigators agree that LV contractility is preserved at older age and can be augmented by exercise(2,3). The role of exercise in preserving normal diastolic function into an old age, however, remains controversial. While several authors have observed exercise-related improvement of diastolic compliance both in younger and older athletes (4-6), their findings have not been duplicated in a more recent report(7).

Our access to a group of highly competitive elderly male endurance athletes gave us the opportunity to assess whether a high level of aerobic exercise augments LV diastolic function above that seen in physically inactive senior men in good cardiovascular health. The focus of this investigation was on the effect of intensive aerobic athletic activity on myocardial aging process.

II. Material and Methods

A. Study populations. The athletic subjects consisted of 13 male distance runners (mean age 69 years) who consistently placed at the top of their age groups in road races ranging from 5 kilometers to the marathon. On the average, these men ranked in the 75th percentile of age related standards for long distance running established by the World Association of Veteran Athletes (now World Masters Athletics). Participants included a 75-year-old age-group world record holder in several running distances, and a 70-year-old US triathlon age-group champion. The men averaged 40 miles of training per week prior to enrolling in the study.

The controls consisted of 13 men (mean age 69 years) categorized as non-athletic, although not truly sedentary. We were unable to recruit a large enough cohort of elderly males who were averse to any form of physical exercise and who met our study entry criteria. Men whose physical activities were infrequent (weekend) and categorized as "fun" were accepted.

Men in both groups fulfilled the following criteria: No personal history of cardiovascular, pulmonary or other debilitating disease; no cardio- or vaso-active prescription drugs; no excessive alcohol, tobacco or illicit drug use. All subjects underwent resting cardiovascular screening consisting of physical examination, blood pressure measurement, 12 lead electrocardiogram (EGG) and echo/Doppler cardiogram. Cholesterol profile was determined but not used in screening.

III. Study protocol

Treadmill stress test. The goal of treadmill activity was to elicit the longest exercise duration with maximal heart rate and blood pressure response. To suit both the untrained and trained subjects, the Balke treadmill protocol based on a steady 3.3 mph speed and an increase in incline from 2% to a maximum of 22% every two minutes was selected(S). If anaerobic threshold was not reached, treadmill speed was increased until inability to continue. Continuous breath-by-breath gas analysis using a one-way valve mouthpiece and apparatus (Medgraphics, St. Paul, MN) was employed to obtain oxygen consumption (V02), anaerobic threshold (AT), and respiratory exchange ratio. A 12 lead EGG and heart rate were recorded continuously, and upper arm blood pressure was measured by cuff and stethoscope at baseline, at every change in treadmill incline and every 2 minutes during recovery.

M-mode and 2-D Echo/Doppler recording (Hewlett-Packard Sonos 2500, Andover, MA). Imaging was recorded on video tape from reclining subjects prior to the treadmill test, immediately after maximal effort, and throughout recovery. LV dimensions, LV wall and septal thickness as well as LV inflow Doppler velocities were quantitated. LV function parameters were calculated using established methodology(9).

Cholesterol profile: Venous blood for 12-hour fasting cholesterol profile was drawn just prior to exercise.

IV. Results

Demographic and exercise characteristics are summarized in Table I. Athletes had a markedly lower weight and body mass index, undoubtedly an advantage in aerobic athletic achievement. The resting heart rate and diastolic pressure were lower in the athletes. The differences in total exercise duration and in time before anaerobic threshold was reached in the two groups were remarkable. The maximal oxygen consumption was exceptionally high in the athletes, considering their age.

Results of echo/Doppler analysis are summarized in Table II. Few parameters were found statistically different between the groups. LV dimensions were larger in the athletes and resulted in a greater calculated LV mass index. No differences could be demonstrated in Doppler diastolic filling indices (diastolic function or myocardial compliance).

Analysis of lipid measurements is shown in Table III. All parameters measured, including HDL, were similar in the two study groups.

V. Discussion

Numerous publications have dealt with the benefits of regular aerobic exercise on cardiovascular systems and weight control in adults. In the current era, a physically active lifestyle is being promoted heavily in the media and by the medical profession. Thus, it is difficult to identify truly sedentary healthy senior men to serve as study controls. Many elderly subjects spend leisure time walking, hiking, jogging, bicycling or swimming as part of health maintenance activity. By the design of this study, however, such activities do not qualify as competitive athletics.

The primary objective of a committed elderly endurance athlete is competing, rather than health maintenance. To be competitive, older men follow a demanding training regimen, control their weight, do not smoke and drink little, if any, alcohol.

The two diverse cohorts were selected for this study on the assumption that if mild to moderate exercise benefits myocardial function, then high levels of physical activity may result in even greater differences in LV compliance between athletes and nonathletes.

This study does reveal major differences in measured parameters between athletes and nonathletes. However, LV diastolic function was not among them, The superior physical fitness in athletes was reflected in high capacity for tissue oxygen utilization (VO2max) and low body mass index (BMI). The diastolic blood pressure fell during exercise in the athletes and rose in controls, implying that peripheral arterial dilatory capacity in athletes is enhanced (10,11).

Unexpected was the absence of higher HDL cholesterol in the group of athletes. Prior investigators have demonstrated that HDL cholesterol rises in proportion to the level of aerobic exercise(12,13). The relatively high HDL cholesterol in physically inactive controls implies an exercise independent genetic endowment.

These results suggest that there may be no level of exercise intensity that directly affects age related normative decline of LV myocardial compliance. Considering the recent reports(10,11) that endurance exercise improves peripheral arterial vasoreactivity, we hypothesize that this improvement applies to coronary arteries as well. We further hypothesize that it is the enhanced dilatory capacity in the coronary arterial bed that allows high myocardial oxygen utilization and overall cardiac performance during exercise. In this statistically limited echo/Doppler exercise stress test study, older athletes were found to have age-related LV myocardial stiffening similar to their physically inactive counterparts. Cardio-vascular and cardio-pulmonary fitness reflected in high VO2max does not appear to alter age related normative reduction of LV myocardial compliance.

VI. Summary

In this study, we compared left ventricular function indices of competitive elderly endurance athletes with age matched nonathletic subjects using a stress echo/Doppler tread mill exercise protocol. No differences could be demonstrated between the two groups regarding LV systolic or diastolic function. These data imply that physiologic mechanisms that enable senior men to exercise at a high level may have to he found elsewhere, perhaps in better myocardial tissue oxygen utilization.

VII. Implications regarding endurance exercise in senior population

Any conclusions derived from our results must be considered in light of the small number of subjects studied (low statistical power). It is doubtful that larger cohorts of seniors with required characteristics could be recruited in the forseeable future. With these limitations in mind, the benefits of vigorous exercise at older age remain unchallenged by this study.

The precise mechanisms by which exercise enhances cardiovascular function require further clarification. An aging, but otherwise healthy, myocardium is likely to maintain adequate LV function into old age as long as the myocardial blood supply remains adequate.

Since the normal aging myocardium is capable of supporting vigorous sporting activities, physicians should encourage endurance training in motivated healthy seniors. The argument that many physically inactive seniors reach advanced old age without experiencing cardiovascular symptoms can be countered with the fact that freedom from premature cardiac catastrophe can not be anticipated based solely on good family history and an acceptable cholesterol profile. The exact mechanisms by which habitual exercise benefits the LV function, however, will need to be explored further.

Table I

Population and Exercise Characteristics

Variable                          Athletes   Controls  p value

n                                  13        12 **
Age (yrs)                          69 (5)    69 (3)     0.80
Height (cm)                       173 (5)    173 (9)    0.96
Weight (kg)                       66 (6.2)   79 (16)    0.011 *
BMI                               22 (1.7)   26 (3.4)   0.001 *
Heart rate-rest (bpm)             57 (8)     69 (17)    0.03 *
Heart rate-max (bpm)              169 (11)   160 (16)   0.09
SBP-R (mm-Hg)                     141 (15)   148 (21)   0.38
SBP-M (mm Hg)                     192 (21)   182 (17)   0.24
DBP-R (mm Hg)                     77 (6)     82 (9)     0.14
DBP-M (mm Hg)                     77 (13)    89 (10)    0.016 *
Exercise duration (min)           24 (3)     12 (6)    <0.001 *
Exercise duration after AT (min)   10 (4.2)  4 (3.1)   <0.001 *
Peak Vo2 (ml/kg/min)              44 (6.3)   27 (4.2)  <0.001 *
Vo2 AT (ml/kg/min)                35 (5.4)   24 (3.6)  <0.001 *

(X [+ or -] SD)

* p<0.05 vs control

** One control subject removed because of exercise included myocardial
ischemia
AT     Anaerobic Threshold
BPM    beats per minute
BMJ    Body Mass Index
cm     centimeters
DBP-R  Diastolic Blood Pressure--resting
DBP-M  Diastolic Blood Pressure--maximal
Kg     kilograms
min    minutes
mmHG   millimeters of mercury
ml     milliliters
SBP-R  Systolic Blood Pressure n resting
SBP-M  Systolic Blood Pressure n maximal
VO2    Oxygen Consumption
VO2AT  Oxygen Consumption at Anaerobic
       Threshold
yrs    Years

(Reference 10, published with permission from the authors, the Am J Ger
Cardiol and Le Jacq Communications).
Table II

Echo/Doppler Filling Variables

Variable                    Athletes      Controls      p value

LVID-s (cm)                 3.2 (0.5)     2.8 (0.5)     0.033 *
LVTD-d (cm)                 5.3 (0.6)     4.7 (0.5)     0.008 *
IVST-d (cm)                 0.9 (0.2)     0.9 (0.1)     0.50
PWT-d (cm)                  1.0 (0.1)     1.0 (0.2)     0.52
LVMI                        61 (13)       51 (8)        0.001 *
IVST-d (cm)                 0.9 (0.2)     0.9 (0.1)     0.50
PWT-d (cm)                  1.0 (0.1)     1.0 (0.2)     0.52
LVMI                        61 (13)       51 (8)        0.001 *
Frac Short %                0.4 [+ or -]  0.4 [+ or -]  0.73
                            0.04          0.06
E - Peak baseline (cm/sec)  79 (16)       76 (22)       0.70
E - Peak stress (cm/sec)    93 (20)       97 (34)       0.70
A - Peak baseline (cm/sec)  79 (16)       73 (19)       0.80
A - Peak stress (cm/sec)    112 (18)      107 (18)      0.60
B/A - Baseline              1.1 (0.20)    1.1 (0.28)    0.70
B/A - Stress                09. (0.30)    0.9 (0.14)    0.80
AFF - Baseline              0.3 (0.10)    0.4 (0.07)    0.07
IVRT - Baseline             101 (23)      100 (24)      0.90
IVRT - Recovery             89 (24)       86 (22)       0.70
(X [+ or -] SD)

(cm -- Centimeters) (sec-second)
A           A wave maximal velocity
AFF         A trial filling fraction
E           E wave maximal velocity
E/A         Maximal E/Maximal A wave velocity
Frac Short  Fractional Shortening
IVRT        Isovolumic relaxation time
IVST-d      Interventricular Septal Wall Thickness n Diastole
LVID-s      Left Ventricular Internal Dimensions n Systole
LVID-d      Left Ventricular Internal Dimensions n Diastole
PWT-d       Posterior Wall Thickness n Diastole
LV MI       Left Ventricular Mass Index

(Reference 10, published with permission from the authors, the Am Ger J
Cardiol and Le Jacq Communications).
Table III.

Fasting Lipid Measurements

Variable                   Athletes  Controls  p value

Total cholesterol (mg/dL)  213 (26)  213 (40)  0.98
Triglycerides (mg/dL)      98 (42)   93(42)    0.75
HDL (mg/dL)                52 (11)   48 (8.2)  0.31
LDL (mg/dL)                142 (26)  148 (37)  0.66
ApoA-1 (mg/dL)             157 (29)  145 (13)  0.24
ApoB (mg/dL)               113 (22)  118 (27)  0.67

(X [+ or -] SD) (all measurements in mgm/dl milligrams per deciliter)
HDL    -  High Density
          Lipoproteins
LDL    -  Low Density
          Lipoproteins
ApoA-1 -  Apoprotein A-1
ApoB      Apoprotein B

(Reference 10, published with permission from the authors, the Am J Ger
Cardiol and Le Jacq Communications).

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