E. Jeffrey Metter, Laura A. Talbot, Matthew Schrager and Robin A.

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J Appl Physiol 96:814-821, 2004. First published Oct 10, 2003; doi:10.1152/japplphysiol.00370.2003

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J Appl Physiol 96: 814–821, 2004.
First published October 10, 2003; 10.1152/japplphysiol.00370.2003.
HIGHLIGHTED TOPIC Physiology of Aging
Arm-cranking muscle power and arm isometric muscle strength
are independent predictors of all-cause mortality in men
E. Jeffrey Metter,1 Laura A. Talbot,2 Matthew Schrager,1 and Robin A. Conwit3
1
Clinical Research Branch, National Institute on Aging, Harbor Hospital, Baltimore 21225;
2
Uniformed Services University of the Health Sciences, Bethesda 20814-4799; and 3National
Institute of Neurological Diseases and Stroke, Bethesda, Maryland 20894
Submitted 11 April 2003; accepted in final form 2 October 2003
Metter, E. Jeffrey, Laura A. Talbot, Matthew Schrager, and
Robin A. Conwit. Arm-cranking muscle power and arm isometric
muscle strength are independent predictors of all-cause mortality in
men. J Appl Physiol 96: 814–821, 2004. First published October 10,
2003; 10.1152/japplphysiol.00370.2003.—Poor muscle strength is
associated with mortality, presumably due to low muscle mass.
Notably, muscle power declines more rapidly than muscle strength
with increasing age, which may be related to more complex central
nervous system movement control. We examined arm-cranking power
against four workloads and isometric strength measured in the upper
extremities of 993 men longitudinally tested over a 25-yr period.
Muscle mass was estimated by using 24-h creatinine excretion;
physical activity was assessed by self-reported questionnaire. Muscle
power and strength were modeled by time by using mixed-effects
models, which developed regression equations for each individual.
The first derivative of these equations estimated rate of change in
strength or power at each evaluation. Survival analyses, using the
counting method, examined the impact of strength, power, and their
rates of change on all-cause mortality while adjusting for age. Arm-
cranking power [relative risk (rr) ⫽ 0.984 per 100 kg䡠m䡠min⫺1, P ⬍
0.001] was a stronger predictor of mortality than was arm strength
(rr ⫽ 0.986 per 10 kg, P ⫽ not significant), whereas rate of power
change (rr ⫽ 0.989 per 100 kg䡠min⫺1 䡠yr⫺1) and rate of arm strength
change (rr ⫽ 0.888 per 10 kg/yr) were risks independent of the power
or strength levels. The impacts of power and strength were partially
independent of muscle mass and physical activity. The risk of mor-
tality was similar across the four power workloads (rr ⫽ 0.93–0.96
per 100 kg䡠m䡠min⫺1), whereas the lowest load generated less than
one-half the power as the higher loads. Arm-cranking power is a risk
factor for mortality, independent of muscle strength, physical activity,
and muscle mass. The impact is found with loads that do not generate
maximal power, suggesting an important role for motor coordination
and speed of movement.
muscle mass; aging; physical activity
AGING IS ASSOCIATED WITH DECLINES in muscle strength [whether
measured isometrically or isokinetically (2, 8, 12, 22, 27, 32)]
and muscle mass (12, 26, 27, 33) that, when considered
together, is referred to as sarcopenia (36). Several studies have
shown a lower mortality over longer intervals of time (up to 40
yr) in stronger individuals where strength has been assessed by
handgrip, knee extension, or using sit-ups (12, 25, 34, 41).
Mortality was more closely related to strength levels than to
Address for reprint requests and other correspondence: E. J. Metter, National
Institute on Aging, Intramural Research Program, NIA-ASTRA, Harbor Hos-
pital, 5th Floor, 3001 South Hanover St., Baltimore, MD 21225 (E-mail:
metterj@grc.nia.nih.gov).
814
body mass (41) and, at least in part, was independent of muscle
mass (34). Although strength can be measured using different
testing paradigms and in different upper or lower extremity
muscle groups, strong relationships are observed among vari-
ous strength measurements (33). Such relationships suggest
Downloaded from jap.physiology.org on May 17, 2010
that any strength measurement may reflect the pattern of
strength within an individual. Thus the relationship of muscle
strength to mortality may lay in the higher functional capability
associated with strength (24) and the inverse association with
functional limitations and disability (25, 40).
Muscle power has been shown to decline with increasing age
to an even greater extent than muscle strength (3, 4, 6, 28, 29,
31, 32, 46). The observation is consistent across various power
testing methodologies that include instantaneous knee exten-
sion power (3, 4), jumping power (7), stair-climbing power
(28), and cranking (cycling) power (28, 32, 46). Whereas
strength is the force generated by a muscle, power is the work
(force ⫻ distance) performed per unit of time, or force times
velocity of movement caused by the muscle.
Muscle strength is dependent on the length-tension relation-
ship that specifies that there is an optimal muscle length for
maximal force generation. For isometric contractions, maximal
strength is specific for the muscle (or muscle group) only at the
tested joint angle. For isokinetic contractions, the peak force
will be angle dependent and specific to the velocity of move-
ment. Note that power can be calculated for the isokinetic
contraction (47), but, because velocity is controlled, it does not
represent maximal power capability. However, peak torque at
high velocity is highly correlated with power (23, 43).
Maximal power emphasizes the force-velocity relationship,
which states that there exists a contraction velocity that max-
imizes power generation. To attain maximal power, optimal
force and velocity levels need to be achieved, and these are
measurement specific. The optimal force level to achieve
maximal power may not represent maximal strength. Similarly,
the optimal velocity may not represent the maximal velocity
that can be attained. For example, optimal cycling performance
on a Wingate test occurs in a fixed range of revolutions per
minute, not necessarily at the maximal revolutions per minute.
Muscle power is measured in several different ways that
reflect different contributions of metabolic and neural control
of muscle activity. Immediate, instantaneous, or explosive
The costs of publication of this article were defrayed in part by the payment
of page charges. The article must therefore be hereby marked “advertisement”
in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
http://www.jap.org
 MUSCLE POWER, STRENGTH, AND ALL-CAUSE MORTALITY IN MEN
power has been measured in the lower extremities by a vertical
jump test (7, 11) or single-leg extension (3, 4). These are very
rapid movements that are dependent on muscle anaerobic
energy utilization in the muscle and primarily depend on
creatine phosphate. Short-term power is work performed over
a brief period of time using a maximal effort. This approach
uses arm-cranking or cycling and is the basis for the Wingate
test, which is a 30-s cycling effort (5). It is both an anaerobic
test, dependent on the creatine phosphate and on glycolysis,
and a test of motor coordination. Longer power tests are
considered to be aerobic and tend not to reflect maximal, but
rather an optimal, power production. Whereas the three types
of power tests reflect different aspects of muscle function, they
are all dependent on the same factors described by Josephson
(20) for cyclic movements, including the muscle velocity and
force-velocity relationship, the muscle length-tension relation-
ship, and the pattern of muscle activation. Other factors con-
tributing to short-term power performance include muscle
coordination (39, 46), percentage of type II muscle fibers (14,
36), age-associated slowing of movement and reaction times
(55), motor unit recruitment patterns (50, 52), and declining
function of basal ganglia (42) and cerebellar systems (6).
Short-term power testing appears to be more dependent on
nervous system control of the neuromuscular system than is
required for muscle strength testing.
We suggest that power generated during isokinetic move-
ments is primarily related to maximal activation of the muscle,
requiring little direct motor control. This activation is very
similar to that obtained by electrical stimulation of a muscle or
its nerve. Single-leg extension generates power through some
motor control to maximize the force-velocity relationship.
Vertical squat jump is more complex, requiring the coordina-
tion of multiple muscle groups but, as with leg extension, is a
single, direct movement. The most complex motor control is
required for pedaling or cranking tasks characterized by the
Wingate test, requiring a sequential set of movements that
maximize force and velocity throughout a repetitive process.
Whereas muscle strength is related to functional disability in
the elderly (25, 40), explosive and short-term power may be
more directly related to age-associated loss of physical func-
tioning than maximal strength (3, 4). If muscle strength is
related to mortality through disability, then muscle power may
also be a predictor of mortality. A short-term cranking power
task is likely to predict mortality independent of muscle
strength. Such a task, which requires a well-coordinated repet-
itive movement, is potentially more dependent on motor con-
trol by the central nervous system than the movements required
for isometric strength. We are unaware of any studies that have
directly compared the impact of arm muscle strength and
arm-cranking power on mortality, although Fujita et al. (13)
found a relationship between vertical jump and all-cause mor-
tality.
Therefore, we hypothesize that short-term power and max-
imal muscle strength tested in the same muscle groups would
be independently associated with mortality. To test this hy-
pothesis, longitudinal data collected over ⬃25 yr from the
Baltimore Longitudinal Study of Aging (BLSA) are used to
determine the impact of isometric arm strength and arm-
cranking power on all-cause mortality over a 40-yr time period
in men.
J Appl Physiol • VOL
815
METHODS
Subjects. Subjects consisted of 993 male participants in the BLSA
(45) who had strength and power measurements. These measurements
were collected from 1960 to 1985. The BLSA protocol is approved by
a combined institutional review board of the Gerontology Research
Center and Johns Hopkins Bayview Medical Center. All subjects signed
institutional review board-approved informed consents. Women entered
the study starting in 1978. A total of 204 women had strength and power
measurements with 24 deaths, which was inadequately powered to
evaluate mortality risk. The subjects were self-volunteered and examined
every 1–2 yr. They were well educated and considered themselves well
off and healthy. No specific health selection criteria were used to screen
participants whose data are included in this analysis. All subjects had a
medical evaluation at each visit that included medical questionnaires,
physical examination, and a cardiovascular evaluation consisting of an
angina questionnaire, a resting electrocardiogram, and an exercise elec-
trocardiogram on alternate visits. Based on the cardiovascular evaluation,
subjects were categorized as having no known, possible, or definite
coronary heart disease (CHD). Total body muscle mass was estimated by
using 24-h creatinine excretion by standard clinical procedures (53).
Twenty-four-hour creatinine excretion has been a widely used method to
Downloaded from jap.physiology.org on May 17, 2010
estimate muscle mass (9, 15). Muscle is estimated to be 17–20 kg whole
wet mass/g urinary creatinine.
Arm-cranking power. Power was measured by using a bicycle that
was converted to act as a drive shaft to power a calibrated automobile
generator (32, 46). The pedal arms were replaced with handgrips that
contained ball bearings for smooth movement. The chain wheel drove
a 12-in. flywheel that replaced the rear bicycle wheel. A large drive
sprocket wheel was attached to the flywheel and by chain to a sprocket
wheel mounted on the armature shaft of the generator. The generator
was connected to a meter. The system was calibrated by running the
generator as a motor, determining the power required to drive the
system between 20 and 200 rpm. Power output of the generator was
expressed in kilograms times meters per minute (kg䡠m䡠min⫺1). As
noted by Shock and Norris (46), “The output of the generator was
connected to a 0.2 ohm constant standard resistor. A recording
voltmeter was used to measure the voltage difference across the load
resistor. Thus the output to the system during cranking was calculated
for each calibration speed as the sum of 1. windage, friction, and
electrical losses, 2. power output of the generator, and 3. the meter
loss.”
Subjects were recumbent on a reinforced bed that limited power
losses caused by bed movement. The power apparatus was mounted
overhead so that the hand cranks were in a comfortable cranking
position. Subjects were instructed to perform a maximum effort for
10–15 s at each of four load settings (1, 2, 3, and 4 A). The order in
which the loads were presented was systematically varied. The max-
imum scale reading was converted to power units by a calibration
curve. Between trials, subjects rested for at least 30 s. Total power was
calculated as the sum of the power generated against the four work-
loads and will be referred to as “power.”
Isometric muscle strength. Isometric strength was tested by using
an apparatus with subjects seated with the upper arms perpendicular to
the floor and the forearm parallel to the anterior-posterior axis and
perpendicular to the head-to-seat axis. Shoulders were supported by a
backboard and by shoulder straps. Hands lay on 1-in.-thick wooden
grips connected by wires to a supporting frame. Subjects pulled
against the grips in four ways: up, down, forward, and backward along
the axis of the forearm. Each direction was tested three times with the
maximal value accepted. A 10-s rest period occurred between trials.
Grip strength was measured with hand dynamometer, as described by
Kallman et al. (22). Total strength scores were calculated by summing
the eight arm measurements and both grip strengths and will be
referred to as “strength.” Test-retest reliabilities for power and total
strength were estimated by repeated measurements on 2 consecutive
days. The Pearson R correlation for total muscle strength was 0.87
96 • FEBRUARY 2004 • www.jap.org
816 MUSCLE POWER, STRENGTH, AND ALL-CAUSE MORTALITY IN MEN

Table 1. Baseline characteristics of the sample

All Censored Died P

N 916 449 467

Age, yr 48.6⫾15.9 37.2⫾9.9 59.6⫾12.7 ⬍0.0001
Height, cm 176.8⫾6.5 178.3⫾6.5 175.4⫾6.1 ⬍0.0001
Weight, kg 78.6⫾11.0 79.6⫾11.3 77.7⫾10.7 0.01
BMI, kg/m2 25.1⫾3.0 25.0⫾3.1 25.2⫾2.9 0.27
Strength, kg 406.7⫾71.4 429.0⫾63.1 385.3⫾72.5 ⬍0.0001
Power, kg䡠m䡠min⫺1 6,254⫾1,370 6,731⫾1,236 5,795⫾1,336 ⬍0.0001
Rate of change in strength, kg/yr ⫺2.33⫾1.76 ⫺0.87⫾3.85 ⫺3.72⫾3.92 ⬍0.0001
Rate of change in power, kg䡠m䡠min⫺1 71.3⫾50.8 75.9⫾54.8 66.9⫾46.1 0.0075
Total activity, METs/day 2,143⫾466 2,259⫾468 1,993⫾420 ⬍0.0001
High MET activity 137.8⫾199.6 186.8⫾227.5 74.4⫾131.9 ⬍0.0001
Moderate MET activity 309.7⫾259.2 334.3⫾262.1 277.7⫾252.3 0.0002
CHD—none, % 87 69 ⬍0.0001*
CHD—probable, % 10 21
CHD—definite, % 3 10
Creatinine excretion, mg/day 1,734⫾338 1,870⫾314 1,606⫾309 ⬍0.0001
Time to censor/death, yr 24.2⫾9.2 28.6⫾6.4 20.5⫾9.5 ⬍0.0001
Values are means ⫾ SD; N, no. of subjects. BMI, body mass index; MET, metabolic equivalent; CHD, coronary heart disease. *␹2 Test for difference in the
distribution of CHD.

Downloaded from jap.physiology.org on May 17, 2010

(N ⫽ 29, P ⫽ 0.000) and 0.83 (N ⫽ 30, P ⫽ 0.000) for power, with
no differences in mean values.
A small systematic drift in the power and strength data was
observed by year. At this time, there are no records as to when
equipment was replaced or to specifics regarding the measuring
equipment. In examining the distribution of both the power and
strength data by date, there was no time point observed where there
was a sudden change in the measurements. The systematic drift was
unrelated to gender or age and was adjusted by regressing power and
strength by date to obtain predicted values (32). The predicted values
were subtracted from the average predicted value from 1958–1962
and then added to the actual measurement for the visit. The resulting
corrected data no longer had a significant correlation with the date.
Leisure time physical activity. Leisure time physical activity
(LTPA) was self-reported based on the amount of time spent in 97
activities since the last visit (30). Time spent in daily-performed
activities was estimated based on a typical day, with less frequent
activities appropriately apportioned. Thus an activity performed for 3
h/wk would be considered to occupy 3/7 h, i.e., 25.3 min/day (48).
The intensity of the reported activities was converted to metabolic
equivalent (METs) based on published values in the literature, which
were established in healthy younger adults (1, 18). One MET approx-
imates resting energy expenditure, 3.5 ml䡠kg⫺1 䡠min⫺1. To offset
over- and underestimation of total time spent in daily activities, the
sum of all 97 activities was normalized to 1,440 min, i.e., 24 h. LTPA
for each reported activity was then converted into MET minutes by
multiplying the minutes reported for the activity by the MET value
assigned to that activity.
The activities were then grouped and totaled based on their MET
levels. Low-intensity LTPA included activities requiring an energy
expenditure of ⬍4 METs; moderate-intensity LTPA included those
activities requiring between 4 and 5.9 METs; and high-intensity
LTPA included those activities requiring ⱖ6 METs.
Assessment of mortality. Deaths were determined by intermittent
telephone follow-up of inactive participants, correspondence from
relatives, and annual searches of the National Death Index up to 2000.
Cause of death was determined by a consensus of three physicians
who reviewed death certificates, medical records, correspondences,
and other available material on a given subject.
Statistical analysis of the data. Differences in baseline character-
istics between survivors and decedents were assessed by Student’s
t-test, whereas ␹2 tests were applied to compare percentages. Descrip- Fig. 1. Age-associated differences in muscle strength (A) and muscle power
tive data are expressed as means ⫾ SD, unless otherwise stated. For (B) for all of the data. A loess regression line was included to demonstrate the
all analyses, a two-tailed P value of ⬍0.05 was used to indicate average levels at each age.

J Appl Physiol • VOL 96 • FEBRUARY 2004 • www.jap.org

 MUSCLE POWER, STRENGTH, AND ALL-CAUSE MORTALITY IN MEN
statistical significance. All analyses were performed by using S-PLUS
version 6 (Insightful, Seattle, WA).
Longitudinal analyses of strength and power over time were based
on mixed-effects models (38). The model considered initial age,
elapsed time from first study visit, and this term squared and cubed.
The time term and time squared were included as random effects. The
form of the equation was
Strength or Power ⫽ (b0 ⫹ b0i) ⫹ b1 ⫻ first-age ⫹ (b2 ⫹ b2i) ⫻
time ⫹ (b3 ⫹ b3i) ⫻ time2 ⫹ b4 ⫻ time3 ⫹ error
where b0i, b2i, and b3i are random effects that reflect individual
variation from the mean effect. Based on the models, individual
regression equations were developed. Rate of change for strength and
power were defined as the first derivative of the individual equations
with estimates made at each time of power or strength measurement.
J Appl Physiol • VOL 96 • FEBRUARY 2004 •
817
Proportional hazards analysis was used to determine the longitudi-
nal contribution of strength, power, and rates of change of strength
and power on mortality using the survival functions developed by
Therneau and Grambsch (51). Time-dependent covariates in the
longitudinal analyses used the Anderson-Gill formulation as a count-
ing 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. Thus the independent variables can increase or
decrease over time.
RESULTS
Of the 916 men, 467 died over the course of follow-up.
Causes of death were cardiovascular (41%), cancer (20%),
trauma (4%), other diagnoses (22%), and undetermined or
unknown (13%). Those who died were older at first evaluation
Downloaded from jap.physiology.org on May 17, 2010
Fig. 2. Age-associated changes in 4 (A–D) subjects for muscle
strength (a) and power (b). The 4 subjects were from those who
had ⬎20 yr of follow-up and demonstrated a different pattern
of change. The data were plotted by age, and the line represents
the quadratic fit of strength or power on age.
www.jap.org
818 MUSCLE POWER, STRENGTH, AND ALL-CAUSE MORTALITY IN MEN

and had a greater prevalence of possible or definite CHD at

initial evaluation (Table 1). Those men who died were shorter
and weighed less than those who were still alive, although
there were no differences in body mass index. During follow-
up, the men who died had a higher prevalence of possible and
definite CHD and cancer. Also, ⬃5% of the men who died
reported participating in weight lifting as an exercise at some
time in their lives (⬍1% reporting doing 20 min/day), com-
pared with 18% of the men who were censored (⬃4% reporting
20 min/day).
Age-associated changes in muscle arm-cranking power and
arm strength. Both muscle power and strength showed declines
with increasing age for all measurements. Figure 1 demon-
strates the difference with age in strength and power. Both
power and strength showed a significant quadratic decline with
age (P ⬍ 0.0001). To observe how these changes differentially
impact individual men, Fig. 2 shows the longitudinal changes
in four men who were followed for ⬎20 yr. The men were
chosen to demonstrate the range of changes that are observed
in middle-aged men. The changes in strength and power do not

Downloaded from jap.physiology.org on May 17, 2010

Fig. 3. Age-associated differences in rate of change in muscle strength (A) and
muscle power (B) for each evaluation.
necessarily follow similar patterns with increasing age. Figure
3 shows the rate of change in power and arm strength by age
for all measurements. Both power and strength showed a
significant cubic relationship between rates of change with age
(P ⬍ 0.0001). The variability in the rate of change in power
increased with increasing age.
Survival analysis. Proportional hazard analysis using the
counting method found that power was a stronger predictor of
mortality than was muscle strength (Table 2). When considered
simultaneously, power significantly predicted mortality,
whereas strength did not. To demonstrate the impact of power
on mortality, the power model in Table 2, adjusting for age,
was solved for 55-yr-old men who tracked age-adjusted power
levels at the 5th, 50th, and 95th percentiles (Fig. 4). Differ-
ences in survival appear by 10 yr of follow-up and persisted to
30 yr of follow-up.
After adjusting for body size, physical activity, and body
muscle mass, the effects persisted for power on mortality. With
the adjustments, an independent effect of strength appeared

Table 2. Proportional hazard models for the impact of strength and power on all-cause mortality
Models

Strength Strength Strength

Strength Power power Strength Power power Strength Power power

Strength/10 kg 0.986 1.003 0.978* 0.992 0.977* 0.987

(0.968–1.00) (0.983–1.023) (0.959–0.997) (0.971–1.014) (0.957–0.998) (0.964–1.01)
Power/100 0.984‡ 0.983‡ 0.984‡ 0.986† 0.987† 0.990*
kg䡠m䡠min⫺1 (0.997–0.991) (0.975–0.992) (0.976–0.992) (0.977–0.995) (0.978–0.996) (0.980–1.00)
Age, yr 1.081‡ 1.075‡ 1.076‡ 1.079‡ 1.076‡ 1.074‡ 1.075‡ 1.074‡ 1.072‡
(1.072–1.09) (1.066–1.085) (1.066–1.086) (1.068–1.090) (1.065–1.086) (1.063–1.086) (1.063–1.087) (1.062–1.086) (1.060–1.08)
BMI 1.010 1.003 1.006 1.025 1.018 1.021
(0.978–1.043) (0.973–1.034) (0.974–1.039) (0.987–1.065) (0.980–1.057) (0.983–1.02)
Height, cm 0.990 0.992 0.993 0.996 0.997 0.998
(0.975–1.005) (0.977–1.007) (0.978–1.007) (0.978–1.014) (0.980–1.016) (0.980–1.02)
High MET/10 0.992* 0.993* 0.993* 0.997 0.997 0.997
METs (0.985–0.999) (0.986–1.000) (.986–1.000) (0.990–1.004) (0.990–1.004) (0.990–1.00)
Moderate MET/ 0.997 0.997 0.997 0.998 0.998 0.998
10 METs (0.993–1.001) (0.993–1.001) (0.993–1.001) (0.994–1.002) (0.994–1.002) (0.994–1.00)
Creatinine/10 mg 0.996 0.997 0.997
(0.992–1.000) (0.993–1.001) (0.993–1.00)
Each column represents the findings of an individual model, which includes the variables in each row that contain relative risks and 95% confidence intervals
in parentheses. *P ⬍ 0.05; †P ⬍ 0.01; ‡P ⬍ 0.001.

J Appl Physiol • VOL 96 • FEBRUARY 2004 • www.jap.org

 MUSCLE POWER, STRENGTH, AND ALL-CAUSE MORTALITY IN MEN 819
come the resistance with potentially a slower movement speed.
The differences can be seen in the average power generated by
amperage load: 1-A load gave mean power of 768 ⫾ 245
kg䡠m䡠min⫺1; 2-A load, 1,497 ⫾ 344 kg䡠m䡠min⫺1; 3-A load,
1,763 ⫾ 411 kg䡠m䡠min⫺1; and 4-A load, 1,848 ⫾ 427
kg䡠m䡠min⫺1. Higher power generated for each of the four loads
was associated with a lower risk of mortality when adjusting
for age [relative risk per increase of 100 kg䡠m䡠min⫺1: 1-A load,
0.935 (0.897–0.974); 2-A load, 0.958 (0.933–0.984); 3-A load,
0.955 (0.931–0.980); and 4-A load, 0.961 (0.939–0.983)].
DISCUSSION

In this study, muscle power using an arm-cranking task was

Fig. 4. Probability of survival for a 55-yr-old man who tracks the 5, 50, or
95% of age-adjusted power over 30 yr.
(Table 2). The instantaneous rate of change in power and
a more powerful predictor of all-cause mortality than isometric
arm muscle strength in men followed for up to 40 yr. The rates
of change over time in strength and power were significant
independent risk factors for mortality, independent of strength,
body size, physical activity, and muscle mass. In part, the
effect of the cranking task appears to be independent of
maximal arm-cranking power generation, for the effect on

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strength was stronger than either strength or power as predic-
tors of mortality (Table 3). The impact of rate of change
persisted even with adjustments for body size, LTPA, and
muscle mass. As a final model, we included a history of
weight-lifting training (yes/no) as an adjustment, which did not
alter the findings nor did the inclusion of CHD.
Movement speed in arm cranking. The difference in the
impact between power and strength on mortality may depend
on differences in the movements between the two tasks. The
arm isometric strength measurements were obtained without
movement. The arm-cranking power measure was obtained by
using four different workloads that potentially could lead to
different effects on mortality. The lowest load provides the
least resistance to the arm-cranking movement, so power is
dependent primarily on the speed at which the wheel can be
cranked. Higher loads require greater use of strength to over-
mortality is observed against low levels of resistance to crank-
ing at which maximal power is not generated. Specifically, at
1 A of resistance, power output is one-half of the maximal
power observed at higher resistance levels. This suggests that
at least part of the impact of arm-cranking power is based on
movement speed.
The requirement of coordinated movements for the cranking
task implies that the coordination of motion by the nervous and
other systems contributes to the importance of power on
mortality. With increasing age, movement time, accuracy, and
reaction time have been shown to decline in BLSA subjects
(10). These age-associated changes do not directly assess the
issue of coordinated movement during the power task, which is
a different type of movement, but suggest that the aging
neuromuscular system leads to slower movement. That some
level of coordination is important can be inferred from

Table 3. Proportional hazard models including rate of change in strength and power on all-cause mortality
Models

Strength Power Strength power Strength Power Strength power Strength Power Strength power

Strength/10 kg 0.970* 0.986 0.969† 0.980 0.955‡ 0.975*

(0.952–0.989) (0.966–1.006) (0.949–0.990) (0.958–1.003) (0.935–0.976) (0.950–1.000)
Rate of change strength 0.888‡ 0.920‡ 0.896‡ 0.937* 0.854‡ 0.915†
(0.851–0.927) (0.880–0.962) (0.852–0.942) (0.888–0.988) (0.809–0.901) (0.859–0.975)
Power/100 kg䡠m䡠min⫺1 0.989† 0.988† 0.990* 0.992 0.994 0.995
(0.998–0.999) (0.979–0.997) (0.982–0.998) (0.982–1.001) (0.985–1.003) (0.985–1.006)
Rate of change power 0.998‡ 0.998‡ 0.988‡ 0.998‡ 0.998‡ 0.998‡
(0.998–0.999) (0.998–0.999) (0.998–0.999) (0.998–0.999) (0.998–0.999) (0.998–0.999)
Age, yr 1.064‡ 1.091‡ 1.076‡ 1.064‡ 1.092‡ 1.079‡ 1.052‡ 1.084‡ 1.067‡
(1.052–1.075) (1.081–1.101) (1.063–1.089) (1.051–1.077) (1.081–1.104) (1.065–1.094) (1.038–1.066) (1.071–1.096) (1.051–1.083)
BMI 1.009 1.008 1.012 1.026 1.017 1.021
(0.977–1.043) (0.977–1.041) (0.979–1.047) (0.986–1.067) (0.977–1.059) (0.980–1.065)
Height, cm 0.990 0.993 0.994 0.997 0.995 0.996
(0.974–1.043) (0.979–1.009) (0.979–1.010) (0.979–1.015) (0.976–1.013) (0.978–1.014)
High MET/10 METs 0.992* 0.991* 0.992* 0.997 0.994 0.995
(0.985–0.999) (0.84–0.998) (0.985–0.999) (0.990–1.004) (0.987–1.002) (0.988–1.003)
Moderate MET/10 0.996 0.997 0.997 0.997 0.997 0.997
METs (0.992–1.000) (0.993–1.001) (0.993–1.001) (0.993–1.001) (0.993–1.002) (0.993–1.001)
Creatinine/10 mg 0.996* 0.996 0.996
(0.992–1.000) (0.992–1.000) (0.992–1.000)
Each column represents the findings of an individual model, which includes the variables in each row that contain relative risks and 95% confidence intervals
in parentheses. *P ⬍ 0.05; †P ⬍ 0.01; ‡P ⬍ 0.001.

J Appl Physiol • VOL 96 • FEBRUARY 2004 • www.jap.org

820 MUSCLE POWER, STRENGTH, AND ALL-CAUSE MORTALITY IN MEN
Sargeant et al. (44), who noted that, during a leg-cranking task,
maximal power was a parabolic function of velocity peaking at
110 rpm.
Movement is controlled through neural systems, including
cortical motor, basal ganglia, and cerebellar systems, which are
modified by spinal reflex loops and sensory inputs (42, 55).
Aging in the extrapyramidal system, particularly the dopamin-
ergic systems, is likely key in the loss of motor speed and
power with age. Dopamine neurons, dopaminergic receptors,
and transmitters have been shown to decline with age (starting
in the third decade of life) in the substantia nigra, basal ganglia,
and cortical regions to which they project (17, 54). Joseph and
Roth (19) have shown an association between dopaminergic
declines and the decline in movement in aging animals. Ingram
(16) has argued that all species show a progressive decline in
habitual physical activity with increasing age that, in part, can
be attributed to a declining dopaminergic system. Furthermore,
he noted that replacing or activating the dopaminergic system
leads to greater exploratory activity, suggesting increased mo-
tivation for movement. To what degree this contributes to
slowing of force generation at present is not known, but is
likely important. Aging in the cerebellum also occurs. A loss of
cerebellar pyramidal neurons occurs with increasing age that is
associated with the central control of organized movement,
particularly motor learning (6). One could conceive that the
difference in age-associated strength and power loss reflects
the alteration in motor control, including the speed of move-
ment.
How these changes impact on mortality is less clear. One
explanation is that aging in the dopaminergic system leads to
the progressive decline of physical activity with increasing age,
thus causing an increased risk of death. However, the impact of
arm-cranking power on longevity was only muted by physical
activity and not eliminated. This could be due to the inade-
quacy of the physical activity questionnaire used to assess the
impact of activity on mortality. No specific questions were
asked that would allow for the quantification of type or char-
acterization of any weight-lifting activity. However, Talbot et
al. (48) found that high-MET activity identified from this
questionnaire was a risk for cardiac mortality. Alternatively,
power partially reflects the activity, but also other factors are
contributing to its impact.
The observations by Bassey et al. (3, 4) argue that differ-
ences in explosive leg power with age are far greater than those
in strength. We (31) previously reported a less dramatic age
difference than Bassey et al. between arm strength and arm-
cranking power. The likely explanation for the differences lies
in the tasks: the 10- to 15-s duration of our task was different
from the initial maximal power. Maximal acceleration is crit-
ical for immediate power, which is likely partially dependent
on muscle mass and fiber composition. For example, Newton et
al. (37) found an increase in muscle strength and squat jump
power associated with an increase in type II fibers following
mixed-methods resistance training. The sustained short-term
power in our study, while dependent in part on muscle mass
and fiber-type composition, has a greater dependence on a
well-coordinated turning movement. Differences in power tests
and potential differences in their degree of change with age
suggest that they may have independent effects on performance
with age, with differential impacts on the development of
disability, frailty, and mortality. An optimal evaluation in
J Appl Physiol • VOL
future work might consider including power measurements of
both arm and leg musculature and the inclusion of both a
measure of instantaneous power, e.g., leg extension or vertical
jump, and a cycling/cranking task, along with functional mea-
sures of daily activities and mobility.
Although strength and power are important contributors to
functional capability and a reduction in disability, less is
known about whether power training is better than strength
training in improving functional capability. Jozsi et al. (21)
showed that muscle power improved in response to progressive
resistive training in both older and younger subjects. Miszko et
al. (35) found that adding a power exercise to a strength-
training program improved performance on the Continuous
Scale Physical Functional Performance test over strength train-
ing alone. This improvement occurred without differences in
strength or power training responses. The improvements in
functional performance likely would lead to reduced disability
and frailty, but it is unclear whether it would impact on the
findings regarding mortality, as observed in this study. The
observations presented here were independent of reported
Downloaded from jap.physiology.org on May 17, 2010
strength training and of leisure time activity. In addition, the
relationship of arm-cranking power to mortality was present
against low resistance, which is primarily dependent on speed
of movement.
Which factors, immediate acceleration of movement, rapid
movements, or movement coordination, are directly associated
with the increased mortality observed with arm-cranking
power loss cannot be determined in this study. What is appar-
ent is that, in addition to the impact of strength (and rate of
change in strength), the speed and potentially the coordination
of movement as reflected by arm-cranking power influence
longevity.
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