Download Study of the Prevalence of sarcopenia

Study of the Prevalence of sarcopenia
Lau et al (2005) conducted a survey involving 262 male and 265 female
elderly Chinese at least 70 years old. This study determined occurrence of
sarcopenia among these samples and determined muscle mass through
dual-energy X-ray absorptiometry. Sarcopenia is more prevalent among
Chinese men at 12.3% compared to only 7.6% among the women.
Tichet et al. (2008) performed an assessment of muscle mass using
bioelectrical impedance analysis among 782 healthy French adults 40 years
and above. Prevalence was approximated among 888 middle aged and 218
seniors. Among women below two standard deviations were 6.2 kg/m2 and
26.6% for muscle mass and smooth muscle index, respectively; for men,
these values were 8.6 kg/m2 and 34.4%. Only a few middle aged individuals
had sarcopenia while in senior citizens, rate of sarcopenia prevalence is 2.8%
and 3.6% for women and men, correspondingly.
Kim et al. (2009) determined the prevalence of sarcopenia among a sample
of 526 Korean participants and then subjected to dual X-ray absorptiometry.
The study showed that sarcopenia prevalence was higher in the elderly
respondents. By employing two standard deviations of ASM/height2 below
the reference values obtained in healthy, young adults, sarcopenia
prevalence was 6.3% in men (60 years) men and 4.1% in women. Using the
residual method, prevalence rates of 15.4% and 22.3% were noted in older
men and women, respectively. For using two standard deviations of SMI,
sarcopenia occurred at a rate 5.1% (older men) and 14.2% (older women).
Berger and Doherty (2010) found in large population studies that occurrence
of sarcopenia in adults 60-70 years old was at least 20% and nears 50% in
adults over 75 years old. In defining sarcopenia, whole body or appendicular
muscle mass determination has been popularly adopted.
The New Mexico Elder Health Survey defined sarcopenia as a health
condition wherein the appendicular muscle mass index is standard deviations
below the average for a young population used as the reference. In a random
subsample composed of 199 from 883, Baumgartner et al. (1998) noted
between 15-25% who are 70 years old suffer from sarcopenia while those
older than 80, the chance to develop sarcopenia is greater at 40% for women
and 50% for men.
Janssen et al. (2002) noted that a statistically significant association exists
between sarcopenia which was measured by means of Bioelectrical
Impedance and various functional impairments using data from the NHANES
III. Sarcopenia prevalence among adults 60 years old above is 7% for males
and among women, it is 10%.
Another assessment conducted by Janssen et al. (2006) from data collected
by the Cardiovascular Health Study (CHS). Out of 5036 elderly individuals 65
years old and above, 17.1% and 10.7% had sarcopenia among men and
women, respectively.
Newman et al. (2003) used two definitions of sarcopenia, the ASM/height2
and the residuals. They also examined that association between them and
function of the lower extremity from the Health Aging and Body Composition
(ABC) Study. Employing ASM/height2, sarcopenia prevalence was 8.9% in
the overweight and 0% in obese men and 7.1% in overweight and 0% in
obese women. In the residuals method, among men, 15.4% who are
overweight and 11.5% who are obese had sarcopenia. Among sarcopenic
women, 21.7% were overweight and and 14.4% were obese.
Delmonico et al. (2007) employed these two definitions of sarcopenia,
determined prevalence rate and incident limitation of the lower extremity five
years after the Health ABC study. Out of 2979 samples, using the residuals
approach, highest sarcopenia was recorded among Caucasian women
(30.5%), followed by 27.1% among Caucasian men. Among the blacks, 8.2%
were males and 8.1% were females. In the ASM/h2 definition, the same trend
was noted with Caucasian women having the highest prevalence at 31.4%
while 6.8% were women of African American descent.
Melton et al. (2000) conducted a cross-sectional analysis using the data from
the Rochester Epidemiology Project. In the said study, there were 345
samples. In measuring muscle mass, DXA was used. Eighteen percent of
men 60 years old and above are sarcopenic and only 7.3% among women.
Estrada et al. (2007) found that sarcopenia among 189 elderly, healthy
women had a prevalence rate of 25.9% as measured using DXA. They also
observed that low muscle mass is associated with leg strength and low grip.
Iannuzzi-Sucich, Prestwood, and Kenny (2002) evaluated baselines
characteristics of 137 aged adults. In the study, assessment of sarcopenia
was done through DXA. Using ASM/h2 definition, sarcopenia was more
prevalent among men (26.85%) compared to the women (22.6%).
Using the EPIDOS cohort, Rolland et al. (2003) determined sarcopenia
prevalence from an elderly French population composed of 1458 samples.
Using SMI the rate of sarcopenia incidence is 9.5%.
Gillette-Guyonnet et al. (2003) used the cohort in the study of Rolland et al.
(2003). DEXA estimated whole body composition among 1321 elderly
women. Sarcopenia prevalence increased with maturity. Almost 9% (8.9%) of
76-80 year olds were sarcopenic while 10.9% among 86-95 year olds.
Lauretani et al. (2003) analyzed InCHIANTI cohort data composed of 1030
Italians dwelling in a community through a CT-scan for the purpose of
evaluating sarcopenia. Prevalence was correlated with age. The prevalence
range is 20%-70% in men while 5% to 15% among the women.
Cesari et al. (2006) made use of the InCHIANTI cohort in assessing the
association between muscle area and and frailty syndrome using the criteria
of Fried. The cross-sectional analysis among 923 samples showed that the
unadjusted correlation between muscle area and low walking speed, low
physical activity, and exhaustion. Subsequent adjustments showed that the
only variable that remained statistically significant was low physical activity.
Visser, Deeg and Lips (2003) assessed sarcopenia through DXA in the
Longitudinal Aging Study Amsterdam which involved 520 respondents. In the
study, the definition of sarcopenia was >3% of muscle mass decline during
follow-ups. Decline in the ASM was noted among 37.5% of subjects and
15.7% met the sarcopenia criterion. Also, there were no significant
differences in the baseline characteristics between these two groups.
Kyle et al. (2001) found that in 191 elderly participants 65 years old and
above, sarcopenia was noted in 11% for both males and females using the
DXA. The level of physical activity was not significantly lower in individuals
with sarcopenia.
Causes of sarcopenia
The high adaptability of muscles enables it to respond to a variety of stress
especially inactivity and physical activity. Muscular atrophy occurs with
diminished contractile activity leading to decreased output of force. If the
senior citizens live sedentary lives, decline in physical activity may partially
explain sarcopenia. The slow muscle fibers or Type I dominant in postural
muscles appear suffer the highest susceptibility towards inactivity (Husom,
Ferrington & Thompson, 2005). Disuse of muscles, however, is not the only
cause of sarcopenia.
As the nervous system aged, the number of motor units starts to decrease
which is correlated to reduced strength (Galea, 1996; Doherty et al. 1993).
Comprising the motor unit is a alpha-motor neuron and the entire muscle
innervations. If alpha-motor neurons are lost progressively, the body
compensates through the production of neural cell adhesion molecules
(NCAM) at the neuromuscular junction so that regenerating axons are
attracted to abandoned muscle cells. There is an increase in NCAM in
muscles taken from aged individuals, which suggest that remodeling occurs
after age-related denervation due to the decline in alpha-motor neurons
(Anderson et al. 1993). Consequently, the remodeling gives rise to larger
motor units thus each neuron innervates As a result of this remodeling, motor
unit size increases. Nervous system reorgnaization has been pointed out to
cause less precision in the control of motor functions and coordination which
is commonly observed by physical therapists working with elderly infividuals
(Desrosiers et al. 1999).
As individuals age, testosterone and growth hormone levels decrease and
these changes significantly affect muscle maintenance and growth. The
lowering of testosterone among males in the functional drop of Leydig cells
(Vermeulen & Kaufman, 1999). Testosterone, an anabolic hormone impacts
protein synthesis and evidence suggest sarcopenic men have less testosterone compared to those not having the condition (Szulc et al. 2004). GH
which impacts protein synthesis in muscles positively likewise declines as
individuals mature resulting in changes in the number of secretory bursts and
rate of secretion (Iranmanesh, Lizarralde & Veldhuis, 1991).
Inflammation markers and their function in sarcopenia have not only attracted
researchers but also clinicians (Kurabayashi et al. 1999). Inflammatory
processes frequent among aged adults are osteoarthritis and rheumatoid
arthritis; both increase cytokine production (Vergunst et al. 2005). Cytokines
are causative agents of muscle wasting, particularly interleukin-6 (IL-6) which
among elderly populations are elevated (Wei et al. 1992). When IL-6 levels
are high, it leads to slower speed in walking speed and lower strength of grip
( Ferruci et al. 2002; Schrager et al. 2007). Dehydroepiandrosterone (DHEA)
which is a precursor molecule in sex hormone synthesis inhibits the
production of IL-6. When DHEA decreases with old age, there is attenuation
in the inhibitory effect of DHEA on IL-6 production (Daynes et al. 1993).
The catabolic role of IL-6 in this condition may be aggravated among the
obese or overweight since elevations in IL-6 levels are associated with
abdominal fat deposition (Schrager et al. 2007). Moreover, decline in
testosterone and GH levels were also correlated with high fat mass
(Roubenoff et al. 1998; van den Beld et al. 2000). Consequently, body fat
may be instrumental in sarcopenia as it influences cytokines and hormones
that influence muscle mass. Individuals whose body is higher than the normal
limit may have sarcopenia; this gives rise to the condition known as
“sarcopenic obesity” (Schrager et al. 2007).
Interestingly, increased production of IL-6 was found to have a role in
anorexia or appetite loss (Agnello et al. 2002). Anorexia concerns older adults
as insufficient intake of nutrients results in muscle loss. IL-6 have an
intermediate effect on sarcopenia directly via muscular catabolism and
indirectly since appetite reduction increases malnutrition risk. Research has
indicated that the current recommended daily allowance for protein
(0.8g/kg/day) is not sufficient in meeting protein needs among elderly
individuals, especially in the maintenance of muscle mass through exercise
(Evans, 2004). Baumgertner et al. (1996) said that albumin, a significant
protein markier indicating nutritional status becomes reduced with maturity
and this is associated with diminishing muscle mass . When physical
therapists suspect a sarcopenic patient, he or she may be referred to a
specialist who is able to test patients for sarcopenia and recommend other
warranted referrals.
A noteworthy observation that the muscle’s regeneration ability after an
injury or overload decreases with old age. The ability of the muscle to
regenrate and growth require the action of satellite cells (Roth, Ferrel &
Hurley 2000). These are cells localized in the basal membrane of a muscle
cell and are eseential in the development of novel muscle tissues. Frequency
of satellite cells in a skeletal muscle lowers with increasing age, providing a
possible mechanism for loss of mass and strength of muscles (Roth, Ferrel &
Hurley 2000). All these physiological events warrant the need for resistance
training among the elderly after a prescription of a progressive overload.
Evidence also linked hormonal changes which are age-related to decline in
muscular mass and strength. These hormones include corticosteroids,
catecholamines, thyroid hormones, prolactin, growth hormone, androgens,
estrogens, and insulin. However, these issues remained controversial with
respect to their roles and impact on the skeletal muscles in adulthood and in
old age.
There may be a gradual increase in intramyocelluar and body fat mass
accompanying sarcopenia. Both have been identified to be correlated with
with increased insulin resistance risk (Melton et al. 2000). The role of insulin
in the pathogenesis and etiology of sarcopenia is important though its impact
on the synthesis of muscles sparked scientific controversy (Volpi et al. 2001;
Boirie et al. 2000; Goulet et al. 2007). Through the action of insulin, synthesis
of mitochondrial proteins in the skeletal muscles is stimulated (Boirie et al.
2001). However, insulin’s anabolic effect on synthesis of muscles is impaired
as age advances. In comparison with the young adults, insulin levels increase
following amino acid and glucose ingestion resulting in lower rate of protein
synthesis (Volpi et al. 2000), and reduced mitochondrial function among the
elderly (Guillet & Boirie, 2005). In response to insulin, there is an impairment
in the usual increase in the rate of protein synthesis in aged muscles since
the signaling mechanisms in initiating translation is altered (Guillet et al.
2004). The increase in weight in middle age results in the decline of insulin’s
anabolic effect which potentially predisposes an individual to sarcopenia
(Roubenoff, 2003), but the high intake of amino acids stimulates the effect of
insulin (Rasmussen & Phillips, 2003).
The impact of estrogen on this condition yielded conflicting results.
Intervention and epidemiological studies suggested that estrogens prevent
muscle mass loss (Rolland et al. 2007; Dionne, Kinaman, & Poehlman,
2000), as its decrease with old age increase proinflammatory cytokines
involved in the development of sarcopenia process like tumor necrosis factor
alpha (TNFα) and interleukin 6 (Il-6) (Girasole et al. 1999; Kramer, Kramer, &
Guan, 2004). However, all the five current clinical trials were not successful in
adding muscle mass after subjecting to hormone replacement therapy
(Jacobsen et al. 2009).
How estrogen affects function and strength of muscles is also controversial
according to Taafe et al. (2005). Taafe et al. (2005) mentioned in the Health,
Aging and Body Composition Study, hormone replacement therapy using
estrogen increased quadriceps cross sectional area but not strength of knee
extensor. However, recent studies on the clinical HRT trials found that
strength of the muscles increased (Jacobsen et al. 2007). The concentration
of sex hormone binding protein is increased by estrogens and cause the
reduction in serum free testosterone levels (Gower & Nyman, 2000),
therefore HRT should decrease muscle mass rather than increase it (Volpi,
Nazemi & Fujita, 2004).
Mechanisms of sarcopenia
The biological mechanisms accounting for the development of sarcopenia are
multifaceted and not comprehensively identified. To a certain degree even
veteran athletes could possibly be affected by sarcopenia; thus age-related,
behavior- and environment-independent mechanisms should be tested. The
main cause is damage attributed to reactive oxygen species (ROS) generated
inside the mitochondria of muscles where ATP is produced in copious
concentrations through the electron transport chain. No evidence has been
presented to directly link ROS production and aging-dependent increase in
oxidative stress (Ji, 2001). However, convincing evidence suggest both tissue
and serum concentrations of superoxido-dismutase (SOD) is positively
associated with age. This is considered to be sensitive to oxidative stress
increments, though current studies were unable to support this claim and an
alternative hypotheses were proposed (Ji, 2001). In normal physiology, small
ROS amounts is a positive state since its purpose is the stimulation of
antioxidant production, activation of metabolic turnover and continuous
stimulation of substitution and renovation of damaged muscle fibers. If ROS is
produced in excessive amounts, juvenile organisms are able to generate
sufficient antioxidants while in mature organisms, there is progressive loss of
this compensatory capability. Therefore in more mature adults, antioxidant
activity is higher but this degree remains insufficient in protecting muscles
from the action of ROS (RQ6). Interestingly, SOD increments incurred in
antioxidant activity did not result in a corresponding increase in mRNA coding
for SOD. This implies that gene expression does not cause increases in
antioxidant activity, and some still contend there are unidentified posttranslational mechanisms at play.
Another mechanism for sarcopenia is the catabolic action of chronic
inflammation. In vitro and in vivo studies implied the catabolic effect of TNF-α,
IL-1, and IL-6 on muscle fibers (Pedersen et al. 1998; Tsujinaka et al. 1996;
Visser et al, 2002). Cicoira et al. (2002) noted that levels of IL-6 and TNF-α in
circulation is cross sectionally related with muscle strength and in a lesser
degree, muscle mass. Ferrucci et al. (2002) demonstrated that IL-6 strongly
predicted accelerated decrease in physical activity among frail older women
was attributed to the rail older women was accounted for by the harmful effect
of IL-6 on the strength of muscles. These evidence together imply the
importance of inflammation in sarcopenia. In fact, IL-6 and IL-1 production
leads to turnover of muscle cells in response to micro-damage after exercise.
It is demonstrated that upsurges of pro-inflammatory cytokines accelerate the
decline of primate muscle mass (Ershler, 1993). This specially important
research result have opened novel treatment perspectives. Incidentally,
current research suggests that increase in physical acitivty is associated with
lowered levels of inflammatory markers circulating in the body (Geffken et al.
et al. 2001). This is a contrast to the fact that following acute exercise, there
is a marked elevation of pro-inflammatory cytokines serum levels (Siegel et
al. 2001). However, noted is the progressive decline of cytokine levels among
individuals regularly exercising over time (Mattusch et al. 2000), and at rest,
these cytokines diminish (Greiwe et al. 2001; Mattusch et al. 2000). This
could possibly explain how exercise prevents development of sarcopenia.
Several recent lines of research have approached the problem of sarcopenia
as a function of body composition changes during the aging process. It is an
established fact that a decrease in leanness of body mass and an increase in
fat mass happens in aging. The definitive process governing tissue
substitution is yet to be elucidated; however there are two hypotheses to
date. First, an empty space filled with adipose cells is left after muscle
atrophy. The second hypothesis is that as adipose tissue expands, muscular
atrophy is facilitated. Roubenoff (1998) proposed that when adipocyte
number increases, circulating leptin levels also elevates leading to sarcopenia
through growth hormone inhibition. This hypothesis opens new preventive
options for sarcopenia.
Prevention of sarcopenia
Resistance training (RT) is considered a powerful preventive measure for
sarcopenia (Roth, Ferrel & Hurley 2000). RT is reportedly to have a positive
influence on protein synthesis, hormone concentrations, and the
neuromuscular system. Roubenoff (2001) and Roth et al. (2000) emphasized
that when an RT program is designed properly, it may result in the increase in
the firing rates of motor neurons, enhanced recruitment of muscle fibers, and
more efficient motor units. Muscles contract at a much faster rate and greater
amount of force is produced when more muscle fibers are recruited in
combination with increased firing rate in motor neurons.
Though the rate of protein synthesis is decreased among elderly individuals,
research found that progressive RT increases protein synthesis rates at least
two weeks. Hasten et al. (2000) reported that after two weeks of supervised
RT program the rate of protein synthesis in the muscles increased by 182%
from the baseline in seven respondents between 78 and 84 years of age.
Yarasheski, Zachwieja, and Bier (1993) likewise noted that in adults ages 6366, muscle protein synthesis significantly increased following two weeks of
RT. Moreover, a three-month duration of supervised progressive resistance
training enhanced protein synthesis rate by 50% in 17 sickly 76 to 92-year
olds. These findings imply that aged individuals are able to preserve their
ability of increasing muscle protein synthesis following acute and sustained
RT. Furthermore, with short-term and acute RT, frequency of satellite cells is
increased resulting in faster rate of regeneration of muscles (Roth, Ferrel &
Hurley 2000).
Treatment of sarcopenia
This review will highlight the benefits of pharmacological interventions
professionals in the health care system should be aware about and how it
could influence development or progression of sarcopenia. Addressed in this
review are two hormone treatments namely testosterone and growth
hormone, DHEA and myostatin.
Testosterone
Since sex hormone levels diminish in old age, administration of testosterone
among elderly males has been investigated to serve as a pharmacological
therapy that preserves muscle mass and prevent loss of muscle strength
(Wang et al. 2000). Testosterone functions in muscle growth among males
along with other secondary sexual characteristics. When testosterone is
administered, level of testosterone in circulation increases and in young men
result in larger muscle mass. However, no improvement in muscular strength
was noted (Snyder et al. 1999). According to Wang et al (2000), when
supraphysiological testosterone dosages are administered in elderly males,
mass of lean muscle as well as strength of extremities are increased.
Mudali and Dobs (2000) mentioned that though strength is significantly
increased in elderly males as testosterone levels are high, the risks are more
numerous than the advantages. These risks include prostate cancer,
gyenomastia, peripheral edema, sleep apnea, thrombotic complications, and
aggressive behavior.
Growth Hormone
As the growth hormone levels drop as a result of aging, growth hormone’s
role has a great impact in normal physiology serum (Iranmanesh, Lizarralde,
& Veldhuis, 1999). Vance (2003) described GH supplementation for retarding
the aging process as an industry worth multimillions of dollars. He also
implied that a third of the GH prescriptions in the US are for the purpose of
enhancing athletic performance and prevent aging, both had no FDA
approvals.
Though the administration of GH has appeared to show improvement in body
composition in the elderly like increase in muscle mass, decrease in fat mass
and bone demineralization, strong evidence suggested no gains in strength,
functional capacity or other positive physiological changes (Blackman et al.
2002; Papadakis et al. 1996). The detrimental effects of GH supplementation
are reported and these include diabetes, glucose intolerance, arthralgia,
edema, and carpal tunnel syndrome (Blackman et al. 2002).
Dehydroepiandrosterone
Dehydroepiandrosterone (DHEA) is a health product being marketed as a
supplement and could be purchased over-the-counter in health stores. Unlike
estrogen and testosterone, DHEA undergoes chemical modifications into sex
hormones in target cells (Labrie et al. 2005). The association between levels
of DHEA and testosterone/estrogen in the body has been the subject of
numerous research.
Because DHEA acts as a precursor molecule in sex hormone biosynthesis, its
supplementation in both sexes help increase strength and mass of muscles in
the absence of testosterone/estrogen therapy-related risks. When DHEA is
supplemented in both elderly men and women, libido, testosterone and
estadiol, and bone density increase; however there are no apparent changes
in function, strength or size of muscles (Labrie et al. 2005; Baulieu et al.
2000). Dayal et al (2005) suggested that the effect of utilization of DHEA in
elderly adults requires a longer period of experimentation and a higher
efficacy in DHEA medication result in androgen levels greater than in healthy
and young adults (Dayal et al. 2005).
While the disadvantages of DHEA supplementation are few, majority of
studies failed in proving that increase in muscle strength or size could
address sarcopenia concerns. Though there are other benefits associated
with DHEA supplementation like higher bone density and concentration of sex
hormones, there still are not proof that it could prevent sarcopenia.
Myostatin Regulation
A key molecule that regulates growth of muscles is myostatin; when inhibited,
there is occurrence of muscle hypertrophy (McPherron et al. 1997). The effect
of myostatin on muscle hypertrophy is a new topic in science and while
encouraging results were obtained based on animal experiments, only one
human study on myosin regulation is published (Wagner et al. 2008). The
potential mechanism of myostatin regulation in ameliorating the detrimental
effects of strength loss and muscle mass not only observed in sarcopenia and
other related pathologies are appealing. Three methods were proposed that
inhibit myostatin thereby preventing muscle hypertrophy namely myostatin
gene deletion, follistatin administration, and anti-myostatin antibodies
administration.
In mice studies, myostatin gene deletion resulted in the increase of muscle
mass due to hyperplasia and hypertrophy by 2.5 folds compared to the
control mice (McPherron et al. 1997). Another research involved
administration of follistatin, which when bound to myostatin, the latter’s action
of controlling size of muscles is diminished (Lee & McPherron, 2001). In mice
where follistatin is over expressed, a three-fold increase in muscle mass is
observed as opposed to the controls (Lee & McPherron, 2001). Whittemore et
al. (2003) used anti-myostatin antibodies to inhibit the action of myostatin.
Muscle mass was increased by 20% and for at least a four-week observation,
muscle strength was also increased.
When myostatin levels in human muscles are high, decrease in its mass is
related with aging. Of the two researches on mRNA coding for myostatin in
muscle cells from an aged individual, one study proved higher concentrations
in aged muscle cells while the other did not show significant differences with
the young control (Raue et al. 2006; Welle et al. 2002). One study
manipulated myostatin using recombinant human antibody on muscular
dystrophy patients. The results proved that it could be a treatment option in
stimulating growth of muscles among these patients. Pharmaceutical
companies have studied other inhibitors of myostatin in the hope of treating
sarcopenia and cachexia, one of other disorders of muscle wasting (Wagner
et al. 2008).
Role of exercise
A number of studies as early as the late 1980s have proven that weight or
resistance training could effectively reduce the risk for sarcopenia. Frontera et
al. (1988) said that muscle strength and cross sectional area in aged men
increased after 12 weeks of training. Highly significant changes were noted in
older women after undergoing resistance exercise (Charette et al. 1991).
Among sickly residents in nursing homes, results on the effects of progressive
resistance training on functional performance like stair climbing ability and
gait speed, strength, and muscle cross sectional area were promising
(Fiatarone et al. 1990, 1994). As a result, age does not seem to be a barrier
to muscle mass and functional enhancement after resistance exercise since
the improvement was comparable to that in young adults. In addition, the
programs are generally safe despite some of these have comorbidities and
aid in preventing falls (Gillespie et al. 2003), loss of independence, and
disability (Pennix et al. 2001; Fiatarone, 2002). A muscle cross sectional area
gain between 5-10% at the same time strength increase by 20–100% or more
are to be expected when the exercise regimen is properly implemented
(Galvao, Newton, & Taaffe, 2005). Aerobic activity on the other hand did not
result in any improvement in the mass and strength of muscles (Klitgaard et
al. 1990; Sipila & Suominen, 2005; Izquierdo et al. 2004). Resistance
exercise has also been associated with improved patient outcomes in
osteoarthritis (Ettinger et al. 1997), osteoporosis (Nelson 1994), coronary
heart disease (Ades et al. 2003), diabetes (Ibanez et al. 2005), and
depression (Singh et al. 2005).
The benefits of exercise do not only revolve around improvement of muscle
fiber contractility but also affect neurons that control muscular functions. It is
an accepted fact that response of muscles to strength training happens in two
phases; the first involves gaining of strength by muscles without evident
muscle hypertrophy typically due to neural adaptations like increased
maximal motor unit discharge rate, decreased antagonist co-contraction,
changes in motor unit recruitment, more effective motor unit synchronization,
and increased neural output from the central nervous system (Gabriel,
Kamen & Frost, 2006).
Another advantage of higher physical activity among elderly adults is it
prevents increase in IL-6 levels which occur with inflammatory process
associated with aging. Higher levels of physical activity were shown to
significantly decrease IL-6 concentrations among the elderly (Colbert et al.
2004). High IL-6 levels were observed to be correlated to decreased
muscular function, movement and strength (Ferrucci et al. 2002; Schrager et
al. 2007).
When nutrition is inadequate in the older population, the problem related to
sarcopenia is compounded. The question is the extent of influence of
exercise on appetite. Blundell and King (1999) noted 19% of research found
that intake of energy was increased following exercise, 16% showed appetite
reduction while in 65% of studies, intake of food remained unaffected after
intense physical activity. Empirical evidence though inconclusive tended to
imply that increasing physical activity significantly influenced energy intake.
The prescribing the resistance exercise regimen, these components could be
manipulated: duration, frequency, intensity, rest intervals, repetition velocity,
sets, and repetitions. The aim is to gradually overload muscles in order for
positive adaptations to occur such as improvement in the size and function of
the muscles (endurance, power, and strength). Exercise programs should not
be static but rather dynamic and target specific muscle groups in the body
through concentric and eccentric movements. Muscles in the lower
extremities like the plantar flexors, dorsiflexors, knee flexors, as well as knee
and hip extensors should be prioritized because these muscles are critical in
preventing falls, balancing, and moving. Exercise machines that make use of
weight hydraulics or stacks isolate specific muscles and are safe because the
weight cannot be dropped and required adjustments and movements can be
learned quickly and easily. The exercise program may allow the use of
barbells and dumbbells, but for bench press there is a need of a spotter.
Alternative weights around the ankles and wrists like those made out of sand
or pebbles are inexpensive and could be used effective in resistance training.
Elastic bands permit a variety of resistance levels and replicate activities in
resistance exercise equipment. An exercise partner can apply resistance
while extending and flexing elbows and knees. Muscle strength gains are
substantial during the initial phases of the exercise program until such time
that it plateaus after five to six months. These effects are reflective of both
muscular and neural adaptation with dominance of muscle fiber hypertrophy
when training was extended (Sale, 1988). Minor muscle soreness usually
occurs during the initial sessions but should resolve quickly.