This Article Abstract Full Text (PDF) Services Download to citation manager Citing Articles Citing Articles via HighWire PubMed PubMed Citation

Skeletal Muscle Strength as a Predictor of All-Cause Mortality in Healthy Men

^a National Institute on Aging, Gerontology Research Center, Baltimore, Maryland
^b Schools of Nursing, The Johns Hopkins University, Baltimore, Maryland
^c Schools of Medicine, The Johns Hopkins University, Baltimore, Maryland
^d Department of Kinesiology, University of Maryland, College Park

E. Jeffrey Metter, Gerontology Research Center, 5600 Nathan Shock Drive, Baltimore, MD 21224 E-mail: metterj{at}grc.nia.nih.gov.

Decision Editor: James R. Smith, PhD

	Abstract

Top Abstract Methods Results Discussion References

 
Low muscle strength is associated with mortality, presumably as a result of low muscle mass (sarcopenia) and physical inactivity. Grip strength was longitudinally collected in 1071 men over a 25-year period. Muscle mass was estimated by using 24-hour creatinine excretion and physical activity values, obtained by questionnaire. Survival analysis examined the impact of grip strength and rate of change in strength on all-cause mortality over 40 years. Lower and declining strength are associated with increased mortality, independent of physical activity and muscle mass. In men <60 years, rate of loss of strength was more important than the actual levels. In men 60 years, strength was more protective than the rate of loss, which persisted when muscle mass was considered. Strength and rate of change in strength contribute to the impact of sarcopenia on mortality. Although muscle mass and physical activity are important, they do not completely account for the impact of strength and changes in strength.

AGING is associated with a decline in skeletal muscle mass and muscle strength, termed sarcopenia ⁽¹⁾, which may lead to poorer physical function in several activities of daily living. Poor physical performance has been shown to predict disability, nursing home admission, and mortality in community-dwelling older adults ⁽²⁾. The sequence of events illustrates a downward spiral of strength reduction, fewer activities performed, further declines in strength, diminished functional abilities, disabilities, loss of independent living, and subsequent death.

There is no single theory that adequately explains the age-associated decrements in muscle mass and strength. The aging process accounts for 30–40% of the declines in strength ⁽³⁾, with the remaining decrease explained by a reduction in habitual activity ⁽⁴⁾⁽⁵⁾, nutritional deficiencies, or chronic disease. Physical inactivity is a modifiable risk factor that, when decreased, has been associated with greater muscle strength ⁽⁶⁾ and reduced mortality rates ⁽⁷⁾⁽⁸⁾. However, the relationship between strength and mortality is less clear than the relationship between physical activity and mortality.

The effects of muscle strength may lie in the higher functional capability associated with greater strength ⁽⁹⁾; the association with greater lean body mass relative to overall size; or the association with higher levels of physical activity and cardiovascular fitness. Several studies have shown that stronger individuals have a lower mortality ^(10)(11)(12), and that mortality is more closely related to strength levels than to body mass ⁽¹²⁾. At present, we are unaware of evidence that the effect of strength on mortality is independent of the level of physical activity or muscle mass, though Rantanen and colleagues ⁽⁴⁾ have shown that changing strength levels in 75- to 80-year-old subjects are related to their levels of activity. We are also unaware of studies that have examined the impact of nonterminal changes in muscle strength over time on mortality. This study addresses whether muscle strength in men (as assessed by grip strength) or rate of change in grip strength over time has an independent impact on all-cause mortality when body mass, muscle mass, and physical activity are considered over a 40-year period of follow-up.

	Methods

Top Abstract Methods Results Discussion References

 
Study Population
The subjects are male participants in the Baltimore Longitudinal Study of Aging (BLSA), a prospective study of the aging process that started in 1958 ⁽¹³⁾. Women entered the study starting in 1978, and too few women have had grip strength measurements and deaths for us to evaluate the effect of strength on mortality. BLSA participants are community-residing volunteers who tend to be well educated, with above-average income and access to medical care. These subjects visit the Gerontology Research Center at regular intervals for 2 days of medical, physiological, and psychological testing. Each participant has a health evaluation by a health provider (physician, nurse practitioner, or physician assistant).

Isometric Grip Strength
Grip strength was measured as described by Kallman and colleagues ⁽¹⁴⁾ from 1960 to 1985. A Smedley hand dynamometer, calibrated to known weights, was adjusted for hand comfort and fit. Subjects were told to place their arms in a relaxed, stationary position. Three maximal grips were taken, and the highest was recorded for each hand. The coefficient of variation between measurements in each hand was 6%. Test–retest reliability showed a correlation of .94 in 40 subjects tested on 2 subsequent days with no difference in mean strength levels.

Assessment of Physical Activity
Leisure-time physical activity (LTPA) was self-reported and based on the amount of time spent performing 97 activities since the last biennial visit. The reported time spent in daily activities was based on a routine day. The intensity of each reported activity was expressed in metabolic units (METs, or metabolic equivalents of oxygen consumption) based on the coding catalog described by Ainsworth and colleagues ⁽¹⁵⁾ and Jetté and colleagues ⁽¹⁶⁾. One MET corresponds to an oxygen uptake of 3.5 ml per kilogram per minute, which approximates resting oxygen utilization. The number of minutes spent performing each activity was multiplied by the assigned MET value (MET-minutes). As a way to adjust for overestimation or underestimation of time reported performing activities, the data from all 97 activities and reported sleep were normalized to 1440 minutes, that is, 24 hours ⁽¹⁷⁾. Activities were further categorized according to estimated intensity: low-intensity LTPAs were those activities requiring an energy expenditure of less than 4 METs, such as playing cards or walking slowly; moderate-intensity LTPAs were those requiring between 4 and 5.9 METs, such as walking quickly or bicycling recreationally; and high-intensity LTPAs were those requiring an energy expenditure of 6 METs or greater, such as swimming laps or running. Total LTPA was computed by totaling the MET-minutes for all three intensity levels of LTPA. The questionnaire was not necessarily completed at each visit, but at 3300 of 4749 visits. When the questionnaire was completed in subsequent visits within 10 years of the missing visit, the response from the subsequent visit was used. We did not use data from earlier visits because of known age-associated declines.

Assessment of Muscle Mass
Total body muscle mass was estimated by using 24-hour creatinine excretion values, obtained by standard clinical procedures ⁽¹⁸⁾, which is a widely used method to estimate muscle mass ^(19)(20). Muscle is estimated to be 17–20 kg whole wet mass/g of urinary creatinine. The variability in excretion has been reported ⁽²¹⁾ with a mean residual that was 8.5% of the mean, which is within the test–retest variability range reported in the literature ^(20)(22). Body mass index (BMI) was calculated as weight (kilograms) divided by the square of height (meters).

Assessment of Endpoints
Deaths were ascertained by intermittent telephone follow-up of inactive participants, correspondence from relatives, and annual searches of the National Death Index. Ascertainment of deaths was high, with an ability to track 98% of subjects. For deceased BLSA subjects, the cause of death was determined by the consensus of three physicians reviewing all available information, including death certificates, letters from physicians and families, medical records, and autopsy reports.

Data Analysis
Differences in baseline characteristics between survivors and decedents were assessed, for the whole sample and when stratified at age 60, by one-way analysis of variance to determine the equality of means while chi-square tests were applied to compare percentages. Descriptive data are expressed as mean ± SD unless otherwise stated. For all analyses, a two-tailed value of p < .05 was used to indicate statistical significance.

As a way to assess how initial levels of strength were associated with time to death, proportional hazard models and Kaplan–Meier survival curves were estimated from data collected at the first assessment. A log rank test ⁽²³⁾ was applied to test for equality of survival among various strata in the Kaplan–Meier analysis. Two strata were constructed on the basis of age greater than or equal to 60 years, or less than 60 years, and initial strength was categorized into four groups on the basis of quartiles of grip strength derived from the entire cohort of men. S-PLUS 2000 (Insightful, Seattle, WA) was used to perform all analyses.

Proportional hazard analysis was used to determine the longitudinal contribution of strength and rate of change in grip strength on mortality, using the survival functions developed by Therneau ⁽²⁴⁾. Time-dependent covariates in the longitudinal analyses used the Anderson–Gill formulation as a counting process. For each subject, time was divided into intervals between evaluations, and the covariates were based on the evaluation at the start of the interval. Rate of change in muscle strength at a given evaluation was calculated as the difference in strength from the previous visit divided by the time between visits. Thus, both grip strength and rate of strength change could increase or decrease over time. Longitudinal models included, for each visit, rate of changes in grip strength, grip strength itself, age, height, and BMI, with physical activity and creatinine excretion added sequentially. Analysis included all subjects with stratification at age 60, and separate analyses for men who were <60 years of age and for those who were 60 years. Age cut points were chosen (a) to ensure a sufficient number of events in the two age groups, (b) to account for a Martingale residual analysis which found excess mortality in older subjects starting near age 60 years, and (c) to depict the age-associated loss in grip strength observed in men over age 60 ⁽¹⁴⁾.

	Results

Top Abstract Methods Results Discussion References

 
Subjects consisted of 1071 men who were followed for a total of 24,357 years, with 533 deaths. Deaths were grouped into categories as presented in Table 1 . Cardiovascular diseases and cancer accounted for over 60% of the deaths. The average age at death was 79.5 ± 11.5 years; the average age in September 1999 for survivors was 66.3 ± 13.8 years. The mean time from the last evaluation to death was 10.3 ± 7.0 years (range 0.1–32 years), and that from initial evaluation to death was 17.5 ± 9.4 years (range 0.1–38 years). Subject characterization at baseline for the entire sample and by age group is shown in Table 2 . For men <60 years, survivors were younger, had longer follow-up, lower BMI, greater height, and greater muscle mass; they did more physical activity but did not differ in grip strength. For those men 60 years at baseline, the main differences between those still alive and those who were dead were in the length of follow-up, level of physical activity, and grip strength. Strength decreased with increasing age, as has been previously reported ⁽¹⁴⁾. In addition, the mean strength decline between visits was 0.8 ± 6.5 kg per year (p < .0001), with decedents showing a significantly greater decline in strength between visits, at 1.5 ± 6.2 kg per year, than the 0.22 ± 6.6 kg per year decline for those who survived (p = .004, adjusted for age differences). The differences in rates of decline persisted when only visits that were more than 5.0 years before death were considered (p = .004).

View larger version (22K): [in this window] [in a new window]   Figure 1. Kaplan–Meier plot of survival in men by quartile strength at their initial assessment age stratified at 60 years. The four groups are based on quartiles (lowest quartile group is 83 kg sum of grip in both hands, second quartile group is 83.1–96 kg, third quartile group is 96.1–108 kg, and fourth quartile group is >108 kg). The quartile groups differed (p = .0002) in men 60 years and older, but were not significantly different in younger men (p = .14). The four groups were divided at the quartiles (83, 96, and 108 kg)

View larger version (18K): [in this window] [in a new window]   Figure 2. Longitudinal plots by age of total right- and left-hand grip strength for the 11 men who had 12 or more assessments. Each plot represents the data from an individual man over many years. Each subject is presented as a separate line with symbols denoting measurement times. The same symbol and line element are used for more than one subject.

View larger version (33K): [in this window] [in a new window]   Figure 3. Rate of change in total right- and left-hand grip strength between adjacent evaluations by age for all men. As an example, a point would represent the slope of the line between each pair of visits for a subject shown in Fig. 2. The rate of change declines with increasing age by .045 kg/y (p < .0001).

View this table: [in this window] [in a new window]   Table 4. Men 60 Years: Change in Muscle Strength Relationship to Mortality by Proportional Hazard Analysis

	Discussion

Top Abstract Methods Results Discussion References

 
Lower muscle strength and muscle mass and greater declines in strength over time are associated with increased risk of mortality, independent of physical activity and body mass. In older men, the protective effect of muscle strength was greater than the effect of rate of change in muscle, whereas in younger men, the rate of change in strength was far more important than the actual levels. The effect of strength on mortality can be accounted for in part by the level of muscle mass. However, strength continued to have an independent contribution to all-cause mortality in men 60 years, while loss of strength over time continued to be important in younger men.

In younger men, strength levels tend to be high and are not likely to contribute to functional disabilities and mortality. In previous work, we have shown that younger men tend to have a large degree of functional reserve that allows for an excess in strength, well above thresholds required for functional requirements ⁽⁹⁾. Thus, the level of strength tends to be less important. Changes in strength over time appear to have a different impact, because men who gain strength over time have a lower risk than men who lose strength. The protective effect appears to be independent of muscle mass and may have to do with levels of fitness, while being independent of physical activity. Physical activity and cardiovascular fitness are only modestly correlated ⁽¹⁷⁾, so both may have an independent impact on strength, disability, and mortality.

In older men, functional performance becomes more directly dependent on strength, as these men show age-associated changes in strength and muscle mass, that is, sarcopenia. Sarcopenia is associated with increasing frailty in the elderly population ⁽²⁵⁾, with functional disability, and with increased risk for age-associated diseases. In men 60 years, we found that lower strength is a risk for mortality that persists after the amount of lean body mass, which primarily represents muscle, is accounted for. In general, the more muscle mass, the stronger the individual. However, this association is modulated by age, as the quality (the force generated per unit of muscle) declines with age ⁽²⁶⁾. The persistence of strength as an independent risk after muscle mass is accounted for suggests that the quality of the muscle as well as the muscle size is likely important in determining risk. Sarcopenia likely contributes to mortality through both a reduction in muscle size and the amount of force the muscle can generate. This combination is associated with functional disability, frailty, and decreased coping ability ^(25)(27).

Muscle strength represents a potential surrogate for other aspects of the changing body physiology that occur with increasing age. Strength is associated with loss of muscle mass and motor units, altered hormonal, insulin, and growth factor secretion, and other changes. Declining hormonal and growth factor secretion is associated with decreasing muscle protein metabolism ⁽²⁸⁾, altering muscle function and mass. However, muscle protein metabolism does not necessarily change with age ⁽²⁹⁾. Replacement of at least some of these hormones is associated with increasing levels of muscle mass and strength ^(30)(31). Whether such therapeutic approaches have an impact on mortality is currently an open question.

The importance of strength on mortality has not been completely studied. Rantanen and colleagues ⁽¹²⁾ found, in middle-aged men, that grip strength is an independent risk factor when stratifying based on body weight with a RR of 1.24 (1.11–1.39) in the lowest tertile and 1.14 (1.03–1.26) in the middle tertile, with the strongest tertile as the reference with adjustments for age, occupation, smoking, physical activity, and body size. Fujita and colleagues ⁽¹⁰⁾ found, in a Japanese health promotion program, that strength independently predicts mortality with a RR of 1.92 (1.16–3.16) in low versus high strength levels for men, but not in women. The RRs found in both studies are similar to our findings for grip strength. Neither of these studies examined the effect of strength over time or rate of changes in strength. In fact, the rate of changes in strength appears to have a greater effect than the actual level, at least in men <60 years of age.

The effect of rate of change in strength raises the question of whether the observations are based on terminal changes that occur during the latter years of life. Against this argument is that the time from the last grip strength measurement to death was on average over 10 years, and two measurements were required to be included in the longitudinal analyses involving rate of change in grip strength. In addition, participation in the study required a visit to the Gerontology Research Center, and 2–3 days of research studies. Subjects tended to be in excellent to good self-reported health. Furthermore, the consideration of only those subjects who survived at least 5 years following an evaluation did not affect the findings. A terminal effect seems unlikely to explain the observations in this study.

Increasing mortality with decreasing strength and muscle mass may be related to changing levels of physical fitness with age. Work by Fleg and Lakatta ⁽³²⁾ has shown that BLSA subjects demonstrate the typical age-related loss of cardiovascular fitness measured by _V•O₂ max as observed in other studies. Talbot and colleagues ⁽¹⁷⁾ have shown a direct, but relatively weak, association between physical activity and cardiovascular fitness in the BLSA. The declining level of high-intensity activity with age was found to be an independent predictor of mortality in this study after strength changes were accounted for. These observations suggest that the contributions of strength and fitness to mortality are somewhat different, but both are directly related to what happens to muscle mass.

A major limitation of this study is that we had little data for women. We have followed women for the past 20 years, but we had only 6–7 years of hand grip measurements on approximately 200 women, with very few deaths. Initial exploration of the data found little influence of muscle strength in women, but the analysis did not have sufficient power to justify elaboration. Another consideration is the degree to which grip strength is a reasonable choice for body strength. Grip strength was chosen because it has been reported in other studies that have examined the relationships between muscle strength and disability ⁽³³⁾ and mortality ⁽¹²⁾.

Muscle strength and rate of change in muscle strength have an impact on all-cause mortality. Risk of mortality was directly related to strength in older men (60 years), whereas rate of change in strength was more important in men <60 years of age. Having a low level of muscle mass, which has been referred to as sarcopenia, is an important contributor to mortality but did not totally account for the effect of strength.

	Acknowledgments

 
The BLSA is part of the Intramural Research Program of the National Institute on Aging, which supported this work.

We thank the participants and staff of the BLSA who have made this study possible.

Received May 7, 2002

Accepted August 2, 2002

	References

Top Abstract Methods Results Discussion References

 

1. Dutta C, Hadley EC, 1995. The significance of sarcopenia in old age. J Gerontol Biol Sci Med Sci 50A: (Special Issue) 1-4.
2. Guralnik JM, Simonsick EM, Ferrucci L, et al. 1994. A short physical performance battery assessing lower extremity function: association with self-reported disability and prediction of mortality and nursing home admission. J Gerontol Med Sci 49:M85-M94.
3. Stamford BA, 1988. Exercise and the elderly. Exerc Sport Sci Rev 16:341-379. [Medline]
4. Rantanen T, Era P, Heikkinen E, 1997. Physical activity and the changes in maximal isometric strength in men and women from the age of 75 to 80 years. J Am Geriatr Soc 45:1439-1445. [Medline]
5. Physical Activity and Health: A Report of the Surgeon General. Atlanta, GA: Centers for Disease Control and Prevention, National Center for Chronic Prevention and Health Promotion; 1996. US Department of Health and Human Services publication S/N 97-023-00196-5.
6. Metter EJ, Conwit R, Tobin J, Fozard JL, 1997. Age-associated loss of power and strength in the upper extremities in women and men. J Gerontol Biol Sci 52A:B267-B276. [Abstract]
7. Paffenbarger RSJ, Hyde RT, Wing AL, Lee I-M, Jung DL, Kampert JB, 1993. The association of changes in physical-activity level and other lifestyle characteristics with mortality among men. N Engl J Med 328:538-545. [Abstract/Free Full Text]
8. Lee IM, Hsieh CC, Paffenbarger RS, Jr et al. 1995. Exercise intensity and longevity in men. JAMA 273:1179-1184. [Abstract/Free Full Text]
9. Kwon IS, Oldaker S, Schrager M, Talbot LA, Fozard JL, Metter EJ, 2001. The relationship between muscle strength and the time taken to complete a standardized walk-turn-walk test. J Gerontol Biol Sci 56A:B398-B404. [Abstract/Free Full Text]
10. Fujita Y, Nakamura Y, Hiraoka J, et al. 1995. Physical-strength tests and mortality among visitors to health-promotion centers in Japan. J Clin Epidemiol 48:1349-1359. [Medline]
11. Laukkanen P, Heikkinen E, Kauppinen M, 1995. Muscle strength and mobility as predictors of survival in 75–84-year-old people. Age Ageing 24:468-473. [Abstract/Free Full Text]
12. Rantanen T, Harris T, Leveille SG, et al. 2000. Muscle strength and body mass index as long-term predictors of mortality in initially healthy men. J Gerontol Med Sci 55A:M168-M173. [Abstract/Free Full Text]
13. Shock NW, Gruelich RC, Andres RA, et al. Normal Human Aging. The Baltimore Longitudinal Study of Aging. Washington, DC: US Government Printing Office; 1984.
14. Kallman DA, Plato CC, Tobin JD, 1990. The role of muscle loss in the age-related decline of grip strength: cross-sectional and longitudinal perspectives. J Gerontol Med Sci 45:M82-M88.
15. Ainsworth BE, Haskell WL, Leon AS, et al. 1993. Compendium of physical activities: classification of energy costs of human physical activities. Med Sci Sports Exerc 25:71-80. [Medline]
16. Jetté M, Sidney K, Blümchen G, 1991. Metabolic equivalents (METS) in exercise testing, exercise prescription, and evaluation of functional capacity. Clin Cardiol 13:555-565.
17. Talbot LA, Metter EJ, Fleg JL, 2000. Leisure-time physical activity patterns and their relationship to cardiorespiratory fitness in healthy men and women 18–95 years old. Med Sci Sports Exerc 32:417-425. [Medline]
18. Tzankoff SP, Norris AH, 1977. Effect of muscle mass decrease on age-related BMR changes. J Appl Physiol 43:1001-1006. [Free Full Text]
19. Forbes GB, Bruining GJ, 1976. Urinary creatinine excretion and lean body mass. Am J Clin Nutr 29:1359-1366. [Abstract/Free Full Text]
20. Heymsfield SB, Arteaga C, McManus C, Smith J, Moffitt S, 1983. Measurement of muscle mass in humans: validity of the 24-hour urinary creatinine method. Am J Clin Nutr 37:478-494. [Abstract/Free Full Text]
21. Metter EJ, Lynch N, Conwit R, Lindle R, Tobin J, Hurley B, 1999. Muscle quality and age: cross-sectional and longitudinal comparisons. J Gerontol Biol Sci 54A:B207-B218. [Abstract]
22. Greenblatt DJ, Ransil BJ, Harmatz JS, Smith TW, Duhme DW, Koch-Weser J, 1976. Variability of 24-hour urinary creatinine excretion by normal subjects. J Clin Pharmacol 16:321-328. [Abstract]
23. Kalbfleisch JD, Prentice RL. The Statistical Analysis of Failure Time Data. New York: Wiley; 1980.
24. Therneau TM, Grambsch PM. Modeling Survival Data: Extending the Cox Model. New York: Springer; 2000.
25. Walston J, Fried LP, 1999. Frailty and the older man. Med Clin North Am 83:1173-1194. [Medline]
26. Lynch NA, Metter EJ, Lindle RS, et al. 1999. Muscle quality. I. Age-associated differences between arm and leg muscle groups. J Appl Physiol 86:188-194. [Abstract/Free Full Text]
27. Roubenoff R, 2001. Origins and clinical relevance of sarcopenia. Can J Appl Physiol 26:78-89. [Medline]
28. Proctor DN, Balagopal P, Nair KS, 1998. Age-related sarcopenia in humans is associated with reduced synthetic rates of specific muscle proteins. J Nutr 128: (suppl 2) 351S-355S.
29. Volpi E, Sheffield-Moore M, Rasmussen BB, Wolfe RR, 2001. Basal muscle amino acid kinetics and protein synthesis in healthy young and older men. JAMA 286:1206-1212. [Abstract/Free Full Text]
30. Basaria S, Dobs AS, 2001. Hypogonadism and androgen replacement therapy in elderly men. Am J Med 110:563-572. [Medline]
31. Rudman D, Feller AG, Nagraj HS, et al. 1990. Effects of human growth hormone in men over 60 years old. N Engl J Med 323:1-6. [Abstract/Free Full Text]
32. Fleg JL, Lakatta EG, 1988. Role of muscle loss in the age-associated reduction in VO2 max. J Appl Physiol 65:1147-1151. [Abstract/Free Full Text]
33. Rantanen T, Guralnik JM, Foley D, et al. 1999. Midlife hand grip strength as a predictor of old age disability. JAMA 281:558-560. [Abstract/Free Full Text]

This article has been cited by other articles:

				S. Walsh, D. Liu, E. J. Metter, L. Ferrucci, and S. M. Roth ACTN3 genotype is associated with muscle phenotypes in women across the adult age span J Appl Physiol, November 1, 2008; 105(5): 1486 - 1491. [Abstract] [Full Text] [PDF]

				E. E. Dupont-Versteegden, R. Nagarajan, M. L. Beggs, E. D. Bearden, P. M. Simpson, and C. A. Peterson Identification of cold-shock protein RBM3 as a possible regulator of skeletal muscle size through expression profiling Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2008; 295(4): R1263 - R1273. [Abstract] [Full Text] [PDF]

				D. Liu, E. J. Metter, L. Ferrucci, and S. M. Roth TNF promoter polymorphisms associated with muscle phenotypes in humans J Appl Physiol, September 1, 2008; 105(3): 859 - 867. [Abstract] [Full Text] [PDF]

				J. R Ruiz, X. Sui, F. Lobelo, J. R Morrow Jr, A. W Jackson, M. Sjostrom, and S. N Blair Association between muscular strength and mortality in men: prospective cohort study BMJ, August 13, 2008; 337(jul01_2): a439 - a439. [Abstract] [Full Text] [PDF]

				B. D. Hand, M. C. Kostek, R. E. Ferrell, M. J. Delmonico, L. W. Douglass, S. M. Roth, J. M. Hagberg, and B. F. Hurley Influence of promoter region variants of insulin-like growth factor pathway genes on the strength-training response of muscle phenotypes in older adults J Appl Physiol, November 1, 2007; 103(5): 1678 - 1687. [Abstract] [Full Text] [PDF]

				J. T. Selsby, S. Rother, S. Tsuda, O. Pracash, J. Quindry, and S. L. Dodd Intermittent hyperthermia enhances skeletal muscle regrowth and attenuates oxidative damage following reloading J Appl Physiol, April 1, 2007; 102(4): 1702 - 1707. [Abstract] [Full Text] [PDF]

				C. R Gale, C. N Martyn, C. Cooper, and A. A. Sayer Grip strength, body composition, and mortality Int. J. Epidemiol., February 1, 2007; 36(1): 228 - 235. [Abstract] [Full Text] [PDF]

				S. G. Wannamethee, A. G. Shaper, L. Lennon, and P. H. Whincup Height Loss in Older Men: Associations With Total Mortality and Incidence of Cardiovascular Disease Arch Intern Med, December 11, 2006; 166(22): 2546 - 2552. [Abstract] [Full Text] [PDF]

				B. H. Goodpaster, S. W. Park, T. B. Harris, S. B. Kritchevsky, M. Nevitt, A. V. Schwartz, E. M. Simonsick, F. A. Tylavsky, M. Visser, A. B. Newman, et al. The loss of skeletal muscle strength, mass, and quality in older adults: the health, aging and body composition study. J. Gerontol. A Biol. Sci. Med. Sci., October 1, 2006; 61(10): 1059 - 1064. [Abstract] [Full Text] [PDF]

				D. Kuh, R. Hardy, S. Butterworth, L. Okell, M. Wadsworth, C. Cooper, and A. Aihie Sayer Developmental origins of midlife grip strength: findings from a birth cohort study. J. Gerontol. A Biol. Sci. Med. Sci., July 1, 2006; 61(7): 702 - 706. [Abstract] [Full Text] [PDF]

				A. B. Newman, V. Kupelian, M. Visser, E. M. Simonsick, B. H. Goodpaster, S. B. Kritchevsky, F. A. Tylavsky, S. M. Rubin, T. B. Harris, and on Behalf of the Health, Aging and Body Compositio Strength, But Not Muscle Mass, Is Associated With Mortality in the Health, Aging and Body Composition Study Cohort J. Gerontol. A Biol. Sci. Med. Sci., January 1, 2006; 61(1): 72 - 77. [Abstract] [Full Text] [PDF]

				E. J. Metter, M. Schrager, L. Ferrucci, and L. A. Talbot Evaluation of Movement Speed and Reaction Time as Predictors of All-Cause Mortality in Men J. Gerontol. A Biol. Sci. Med. Sci., June 1, 2005; 60(7): 840 - 846. [Abstract] [Full Text] [PDF]

				J. C. Gallegly, N. A. Turesky, B. A. Strotman, C. M. Gurley, C. A. Peterson, and E. E. Dupont-Versteegden Satellite cell regulation of muscle mass is altered at old age J Appl Physiol, September 1, 2004; 97(3): 1082 - 1090. [Abstract] [Full Text] [PDF]

				R. M. Tucker, C. May, R. Bennett, J. Hymer, and B. McHaney A Gym-Based Wellness Challenge for People With Type 2 Diabetes: Effect on Weight Loss, Body Composition, and Glycemic Control Diabetes Spectr, July 1, 2004; 17(3): 176 - 180. [Abstract] [Full Text] [PDF]

				E. J. Metter, L. A. Talbot, M. Schrager, and R. A. Conwit Arm-cranking muscle power and arm isometric muscle strength are independent predictors of all-cause mortality in men J Appl Physiol, February 1, 2004; 96(2): 814 - 821. [Abstract] [Full Text] [PDF]

				J. S. Pattison, L. C. Folk, R. W. Madsen, and F. W. Booth Selected Contribution: Identification of differentially expressed genes between young and old rat soleus muscle during recovery from immobilization-induced atrophy J Appl Physiol, November 1, 2003; 95(5): 2171 - 2179. [Abstract] [Full Text] [PDF]

				R. Roubenoff Sarcopenia: Effects on Body Composition and Function J. Gerontol. A Biol. Sci. Med. Sci., November 1, 2003; 58(11): M1012 - 1017. [Abstract] [Full Text] [PDF]

				J. E. Morley Editorial: Sarcopenia Revisited J. Gerontol. A Biol. Sci. Med. Sci., October 1, 2003; 58(10): M909 - 910. [Full Text] [PDF]

				J. S. Pattison, L. C. Folk, R. W. Madsen, T. E. Childs, and F. W. Booth Transcriptional profiling identifies extensive downregulation of extracellular matrix gene expression in sarcopenic rat soleus muscle Physiol Genomics, September 29, 2003; 15(1): 34 - 43. [Abstract] [Full Text] [PDF]

				J. E. Morley The Need for a Men's Health Initiative J. Gerontol. A Biol. Sci. Med. Sci., July 1, 2003; 58(7): M614 - 617. [Full Text] [PDF]

				M.-M. G. Wilson "PREEMPTIVE STRIKE?": SARCOPENIA AND NUTRITIONAL INTERVENTION J. Gerontol. A Biol. Sci. Med. Sci., July 1, 2003; 58(7): M672 - 673. [Full Text] [PDF]

This Article Abstract Full Text (PDF) Services Download to citation manager Citing Articles Citing Articles via HighWire PubMed PubMed Citation