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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 (TNFÎ±) 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 post-translational 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-Î±, 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-Î± 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 63-66, 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.
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.
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 (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.
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.