(Circulation. 2005;112:624-626.)
© 2005 American Heart Association, Inc.
Editorial |
From the University of Vermont College of Medicine, Burlington.
Correspondence to Philip A. Ades, MD, McClure 1, Cardiology, University of Vermont College of Medicine, Fletcher-Allen Health Care, Burlington, VT 05401. E-mail Philip.Ades{at}vtmednet.org
Key Words: Editorials exercise aging physiology
| Introduction |
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See p 674
| The Baltimore Longitudinal Study of Aging |
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The resulting dataset represents the most comprehensive examination of longitudinal changes in aerobic fitness throughout the aging spectrum in healthy individuals. By clustering repeated exercise test data within 6 age decades, a rate of decline within successive decades is calculated. Thus, the selection biases inherent in cross-sectional studiesin particular, the fact that older participants, by dint of their survival, are generally healthier than younger participants overallare avoided. Fleg and coworkers7 show that the previously defined linear decline of aerobic capacity of 5% to 10% per decade is indeed incorrect, particularly in the later decades of life. Most importantly, these data suggest that the age-related decrease in aerobic capacity is nonlinear, increasing progressively each decade. For example, whereas the decline in peak
O2 was 3% to 6% in the third and fourth decades, it was far greater, >20% per decade, after age 70. The accelerated decline persisted even when the data were adjusted by fat-free mass, which also declines with age. Although it is possible that the effect of fat-free mass on peak
O2 was not entirely corrected for by calculating a simple ratio of peak
O2 (mL/min) divided by fat-free mass,8 it is unlikely that loss of muscle mass alone accounts for the accelerated decline in fitness given the pattern of age-related changes in fat-free mass. Reduced peak
O2 was found in all physical activity quartiles. It should not be overlooked, however, that more physically active individuals had higher peak
O2 measures than less active individuals at all ages. From a physiological perspective, these results suggest that the loss of aerobic fitness with age is not attributable to the erosion of muscle mass or to physical inactivity. Instead, changes that alter the delivery of oxygen to exercising muscles or the ability of muscles to utilize oxygen are more likely determinants of declining aerobic fitness. If this is the case, age-related changes in muscle perfusion or oxidative capacity may lie at the root of diminished aerobic exercise capacity in the elderly. In support of an effect of age on muscle oxidative capacity, recent findings show that aging is associated with impaired skeletal muscle mitochondrial function secondary to mitochondrial DNA oxidative damage and loss.9
| Fitness Declines Precipitously in Late Middle Age: Bad News? |
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With regard to the implications of these data on mortality, I am reminded of the treatise of baseball statistician Bill James relating the peak of a players hitting ability to the length of his career in the Major Leagues.10 The higher the peak of the parabolic curve of hitting ability versus age, the broader the parabola as it crosses the x-axis (in years), the longer the stay in the Major Leagues. Although the data of Fleg et al7 support the concept that whatever the aerobic fitness level, whatever the physical activity level, there is a sharper decline over time after age 60 or 70 than before, they do not deny data from several sources that relate peak aerobic capacity and physical activity in middle-aged adults to increased longevity1113 and delayed disability.14,15 Again, a higher peak yields a broader parabola with increased longevity. Furthermore, if you accept the concept that some physical dysfunction will generally precede death (absent a sudden death), it is in fact preferable for the graph of the decline to have a shelf with maintained aerobic capacity, until an accelerating late drop, as opposed to a more protracted, linear deterioration.
A separate though relatively minor concern with these fitness data from the Baltimore Longitudinal Study of Aging is that of the healthy cohort effect.16 This suggests that individuals who volunteer for health-related research studies are often more fit and health oriented than the population as a whole. In the study of Vita et al,14 several lifestyle factors, including exercise patterns, body mass index, and smoking, were closely related to end-of-life disability patterns. Not only was the onset of disability delayed by up to 5 years in the lowest-risk group (those who were thin, did not smoke, and exercised), but it was also noted that these same factors led to a compacting of end-of-life disability. If indeed the data of Fleg et al7 are skewed by such healthier volunteers, along with the elimination of individuals who did not attain 85% of their maximal predicted heart rate and individuals who developed heart disease, we may be observing such an effect. Rebutting this, at least in part, would be their finding that even their least fit individuals also saw a decline in fitness in their 70s.
| Fitness Versus Disability |
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O2 dropped below
750 mL/min. Thus, although erosion of peak
O2 with age undoubtedly accompanies the development of disability, its overall contribution to the reduced capacity to perform normal daily activities is unclear. | Conclusions |
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| Acknowledgments |
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| Footnotes |
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| References |
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22. Ades PA, Ballor DL, Ashikaga T, Utton JL, Nair KS. Weight training improves walking endurance in healthy elderly persons. Ann Intern Med. 1996; 15; 124: 568572.
23. Brochu M, Savage P, Lee M, Dee J, Cress ME, Poehlman ET, Tischler M, Ades PA. Effects of resistance training on physical function in older disabled women with coronary heart disease. J Appl Physiol. 2002; 92: 672678.
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