Maturitas 71 (2012) 109–114

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Maturitas
journal homepage: www.elsevier.com/locate/maturitas

Review

Sarcopenia in the elderly: Diagnosis, physiopathology and treatment

Vincenzo Malafarina a,∗ , Francisco Úriz-Otano a , Raquel Iniesta b , Lucía Gil-Guerrero c
a
Department of Geriatrics, Hospital San Juan de Dios, Calle Beloso Alto 3, 31006 Pamplona, Spain
b
Servicio de Soportes Estadísticos, Fundació per a la Recerca Sant Joan de Deu, Carrer Santa Rosa 39-57, Level 3, 08950 Esplugues de Llobregat, Barcelona, Spain
c
Department of Internal Medicine, Hospital San Juan de Dios, Calle Beloso Alto 3, 31006 Pamplona, Spain

a r t i c l e i n f o a b s t r a c t

Article history: Sarcopenia, defined as a syndrome rather than as a pathology, is the loss of muscle mass and function
Received 3 November 2011 associated with age. Sarcopenia is an enigma for medicine, and despite the numerous publications avail-
Received in revised form 9 November 2011 able in the literature and the number of papers currently being published, there is no agreement about
Accepted 10 November 2011
its definition, and even less about its root causes. One salient aspect that proves the lack of consensus is
the fact that different working groups are still debating about the right name for this syndrome (which
is associated with the loss of muscle mass and strength in the elderly).
Keywords:
In hospitalized patients, sarcopenia has been shown to raise the risk of complications such as infections,
Sarcopenia
Bioelectrical impedance analysis
pressure ulcers, loss of autonomy, institutionalization and poor quality of life, as well as to increase
Muscle mass mortality.
Neuromuscular aging The factors that contribute to the development of sarcopenia in the elderly are: the state of chronic
Inflammaging inflammation, atrophy of motoneurons, reduced protein intake (secondary among others to the condition
defined as geriatric anorexia), and immobility. There is ongoing debate about the causes of sarcopenia,
but the aspect that generates most interest today is the quest to achieve repeatable and clinically useful
diagnostic criteria for its diagnosis, prevention and treatment.
The aim of this narrative review is to summarise the abundant information available in the literature
and to draw useful conclusions.
© 2011 Elsevier Ireland Ltd. All rights reserved.

Contents

1. Definition of sarcopenia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110

2. Instrumental diagnosis of sarcopenia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110
3. Physiopathology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111
3.1. Neuromuscular aging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111
3.2. Inflammation, sarcopenia, and advanced age . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111
3.3. Immobility and bed confinement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111
3.4. Sarcopenic obesity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111
3.5. Sarcopenia versus cachexia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112
4. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112
4.1. Non-drug treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112
4.2. Drug treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112
4.3. Testosterone . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112
4.5. Dehydroepiandrosterone . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112
4.6. Vitamin D . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112
5. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112
Contributors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113

∗ Corresponding author. Tel.: +34 948 231800; fax: +34 948230607.

E-mail addresses: vmalafarina@gmail.com (V. Malafarina),
patxi.urizotano@gmail.com (F. Úriz-Otano), riniesta@pssjd.org (R. Iniesta),
luciagil5@yahoo.es (L. Gil-Guerrero).

0378-5122/$ – see front matter © 2011 Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.maturitas.2011.11.012
110 V. Malafarina et al. / Maturitas 71 (2012) 109–114

Competing interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113

Provenance and peer review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113

1. Definition of sarcopenia calculating fat infiltration in muscle, which is a very interesting

parameter. MRI has many advantages but is very expensive, is not
Sarcopenia is a subject of great interest for geriatricians, and the easily accessible, and is not routinely indicated to study muscle
possibility of considering it as a geriatric syndrome has been in the mass, but has been used mainly for research purposes. It is a very
air since 2010 [1]. The first author to speak of sarcopenia was Rosen- complex test that requires highly specialized staff, specific soft-
berg, who wondered in 1989 why the loss of muscle mass seen in ware, and a relatively large amount of time.
elderly subjects had not been given adequate attention [2]. It was he Dual-energy X-ray absorptiometry (DEXA) is a well-defined
who first used the term of sarcopenia. The term sarcopenia derives technique for analyzing body composition. DEXA is currently the
from the Greek terms “sarx” (meat) and “penia” (loss) [3]. However, procedure of choice for routine assessment of bone mineral den-
in the strong relationship between muscle mass and function, the sity. It exposes the patient to a low radiation dose, is less costly
latter is the more significant predictor of hospital admission, falls, than MRI but expensive enough so as not to be considered a rou-
fractures, gait disorders, and mortality [4]. Sarcopenia increases the tine test, requires patients to travel to a center, as in the case of MRI,
risk of functional loss and disability two-fold in men and three-fold and requires specialized staff and a relatively long performance
in women [5]. time.
A progressive loss of muscle mass occurs from approximately 40 Bioelectrical impedance analysis (BIA) is currently recognized as
years of age. This loss has been estimated at about 8% per decade a routine test to study body composition. BIA focuses on the study
until the age of 70 years, after which the loss increases to 15% per of body composition at level II or molecular level and represents a
decade [6]. This loss causes a 40% decrease in muscle circumference reliable analysis for the study of lean mass and muscle mass. Many
from 30 to 60 years of age. A 10–15% loss of leg strength per decade studies have shown the validity of measurements made by BIA as
is seen until 70 years of age, after which a faster loss, ranging from compared to DEXA.
25% to 40% by decade, occurs [7,8]. Muscle mass loss is greater in BIA has many advantages, is portable and allows the test to
men as compared to women [9,10]. be performed at the bedside of the patient, is relatively simple,
The presence of functional impairment in the elderly is asso- requires no specialized staff, is relatively inexpensive, and does not
ciated with increased morbidity and mortality. It is estimated that expose patients to radiation. The most important disadvantages are
approximately 14% of people aged 65–75 years require help in basic that the result can be distorted by the patient’s hydration status
activities of daily living, a proportion that increases to 45% in people and the presence of edema. The time required for an examination
over 85 years of age [11]. Healthcare costs attributable to sarcope- is relatively short.
nia in the United States (US) in 2000 were estimated at 18.5 billion Table 1 lists the advantages and disadvantages of the most
dollars [12]. important diagnostic technique for the diagnosis of sarcopenia.
Decreased appetite and food intake, called geriatric anorexia, In 1998, Baumgartner published an important study on the
occurs with age and in elderly people with chronic diseases, an ade- prevalence of sarcopenia in New Mexico. Sarcopenia was defined as
quate increase in dietary intake, required for coping with increased skeletal muscle mass in the limbs, as measured by DEXA, divided by
catabolism, has not been detected [13,14]. What is seen in elderly height in meters, 2 standard deviations below the mean in healthy
people is a decreased sensation of hunger and an increased sati- young people under 30 years of age participating in the Rosetta
ety after a normal meal as compared to young people. Among study [16].
other factors, one of the main causes of this process appears to Janssen subsequently used a muscle mass index consisting of
be the production and action of “satiety cytokines” [15]. IL-6 plays muscle mass, as measured by BIA in kilograms, divided by body
a significant role in sarcopenia through two mechanisms: a direct mass, multiplied by one hundred, and adjusted for size (cm) and
mechanism, increased muscle catabolism, and an indirect mecha- non-skeletal muscle tissue (fat, organs and bone) [17], and found
nism that decreases appetite and increases the risk of malnutrition. sarcopenia rates of 7% and 10% respectively in men and women
over 80 years of age.
2. Instrumental diagnosis of sarcopenia Baumgartner [18] and Melton [19] published cut-off val-
ues for diagnosis of sarcopenia with DEXA, while Janssen [20]
Magnetic resonance imaging (MRI) allows us to calculate seg- reported similar values with BIA. Their values are detailed in
mental and total muscle mass, and to assess muscle quality by Table 2.

Table 1
Advantages and disadvantages of instrumental tests for the diagnosis of sarcopenia.

MRI CT DEXA BIA

Costs Very high Very high High Relatively inexpensive

Sensitivity Very high Very high High Medium
Specificity Very high Very high High Medium
Personnel Highly specialized Highly specialized Specialized Non-specialized
Portable No No No Yes
Radiation No Considerable Little No
Time 15–20 min 15–20 min 15 min 5 min
Indication in diagnosis of No, for research purposes No, for research purposes No, for research purposes. Yes, fat mass, fat-free
sarcopenia Indicated to assess BMD mass
Validated Yes Yes Yes Yes
 V. Malafarina et al. / Maturitas 71 (2012) 109–114
Table 2
Values of fat-free mass used for diagnosing sarcopenia.
Baumgartner [18] Melton [19] Janssen [20]
Women (kg/m2 ) 5.45 6 <5.76
Men (kg/m2 ) 7.26 8.7 <8.51
3. Physiopathology
3.1. Neuromuscular aging
Neuron loss is a progressive, irreversible process that increases
with age.
Among the causes that contribute to strength loss observed in
sarcopenia we must mention changes on nervous system due to
age, which provoke the loss of motor units. A motor unit is made
up of a single alpha motoneuron and all the muscle fibers connected
with it. If alpha motoneuron is lost, denervated muscle fibers join
to connect to surviving alpha motoneurons. This determines that
a single alpha motoneuron must connect with more muscle fibers,
constituting bigger motor units [21]. This leads to loss of efficacy
and could be the cause of the typical tremor and fatigue in the
elderly and results in the loss of motor precision and the poor coor-
dination seen with age [22]. Slowing of the contraction peak also
occurs, leading to a reduction in the strength produced and the
strength–speed ratio. These effects are secondary to changes in two
proteins essential for contraction control: (1) the ryanodine recep-
tor and (2) Ca-ATPase. A longer relaxation time may increase the
time required for a new contraction.
Skeletal muscle consists of two types of fibers: type II fast fibers,
which have a high glycolytic potential, low oxidative capacity, and
a faster response as compared to type I slow fibers. The latter are
known as fatigue-resistant fibers because of their characteristics,
greater density of mitochondria and capillaries, and higher myo-
globin content; except for postural muscles, consisting of type I
fibers only, most muscles consist of both types of fibers. During
slow, low intensity activity, most strength generated comes from
type I fibers, while in high intensity exercise strength comes from
type I and II fibers. With age, atrophy almost only affects type II
fibers [23].
3.2. Inflammation, sarcopenia, and advanced age
Increased circulating levels of tumor necrosis factor-alpha
(TNF-alfa), interleukin-6 (IL-6), interleukin-1 (IL-1), and C-reactive
protein (CRP) are seen in the elderly [24]. These age-related changes
in immune function are associated with a progressive increase
in glucocorticoid and catecholamine levels and decreased GH
and sexual hormone levels. These characteristics are similar to
those of chronic stress. Inflammatory cytokines are directly asso-
ciated with muscle mass loss and muscle strength reduction in
the elderly. Pro-inflammatory cytokines, particularly TNF-alfa, are
potent stimulants of proteolysis through the UPS activation path-
way (ubiquitin–proteosome system). For each increase in standard
deviation in the TNF-alfa value, a 1.2–1.3 kg reduction is seen in
hand grip strength. For each increase in standard deviation of IL-6,
a 1.1–2.4 kg reduction is found in hand grip strength [25].
Inflammation may be a key factor in the genesis of sarcopenia. A
low level of chronic inflammation is highly prevalent in the elderly,
as shown by the increased levels of cytokines and acute phase
proteins, and by prolonged inflammatory infectious diseases [10].
This underlying age-related chronic inflammation phenomenon
has been called “inflamm-aging” [26].
In patients with sarcopenia, higher cortisol levels are found
than in healthy elderly people [27]. IL-1, IL-6, and TNF-␣ have
been shown to decrease food intake and to reduce body weight by
111
various means, including delayed gastric emptying and suppression
of small bowel motility. Aging itself may be considered as a form
of stress. It is associated with increased circulating levels of corti-
sol and catecholamines and with decreased hormone levels (sexual
and growth hormones), changes which stimulate in turn the release
of IL-6 and TNF-␣. IL-1 and IL-6 levels are elevated in elderly peo-
ple with cachexia. Dehydroepiandrosterone (DHEA), a sex hormone
precursor, is an inhibitor of IL-6 production. The reduction of DHEA
with age leads to a failed inhibition of IL-6 production.
In healthy elderly subjects, the presence of high inflammatory
cytokine levels may contribute to the development of sarcopenia.
In 2008, Solerte published an interesting study of the effects
of nutritional supplementation with amino acids on fat-free mass,
insulin resistance, and inflammatory indices [28]. Authors found
a body mass index (BMI) increase secondary to increased fat-
free mass. They also noted significantly higher TNF-␣ levels
(160 ± 33 pg/mL versus 86 ± 18 pg/mL) and lower IGF-1 levels
(17 ± 2 ng/L versus 19 ± 3 ng/L) in sarcopenic patients as compared
to healthy controls. After two months of supplementation, they
noted a decrease in TNF-␣ levels and an increase in IGF-1 levels.
These changes persisted at 8 and 16 months.
3.3. Immobility and bed confinement
Bed confinement and immobility are unfortunately common
consequences of hospital admission for disease or trauma. Studies
have shown that there is a reduction in protein synthesis, and a sig-
nificant loss of muscle mass without significant changes in the fat
mass, in healthy elderly patients confined to bed for 10 days, while
in young people such effects are only observed after 28 days of bed
rest [29,30]. This shows that the elderly person is especially prone
to losing muscle mass when confined to bed. In patients undergoing
trauma surgery, increased cortisol levels have severe effects upon
the protein metabolism of the skeletal muscle, causing increased
proteolysis and affecting insulin levels. The effects of amino acid
supplementation during the post-traumatic inactivity period could
improve the effects induced by high cortisol levels.
3.4. Sarcopenic obesity
Patients with sarcopenic obesity, high fat mass, and low muscle
mass are more susceptible to mobility and disability problems than
those who only have obesity or sarcopenia [31]. Muscle mass loss
in the elderly is associated with an increased fat mass. Between
30 and 60 years of age, 0.23 kg of muscle are lost and 0.45 kg of
fat are gained every year. This change in muscle composition may
be masked by a stable body weight, and results in the phenotype
called sarcopenic obesity [32].
The quality of muscle in obese people is very poor due to
intramuscular fat infiltration, which contributes to muscle fatigue,
fragility, and disability. In elderly people, an increased fat content
may be seen between muscle groups (intermuscular adipose tissue)
and between muscle fascicles (intramuscular adipose tissue).
The catabolic role of IL-6 in sarcopenia may be exacerbated
in overweight or obese people, because IL-6 levels are related
to increased abdominal fat. Increased fat mass is also associ-
ated with low testosterone and GH levels and increased cortisol.
All of these factors facilitate muscle catabolism, accumulation of
abdominal fat, and development of insulin resistance. Adipose
tissue cannot be regarded as a benign energy store alone. Abdom-
inal adipocytes contribute to production of pro-inflammatory
adipokines, cytokines, and other factors that contribute to main-
taining a chronic inflammation status [33].
112 V. Malafarina et al. / Maturitas 71 (2012) 109–114

3.5. Sarcopenia versus cachexia 4.3. Testosterone

Cachexia, from the Greek words “kakos”, bad, and “hexis”, con-
dition, was defined not many years ago as a complex metabolic
syndrome associated with an underlying disease and characterized
by loss of muscle mass, with or without fat mass loss [34]. Cachexia
is often associated with inflammation, insulin resistance, anorexia,
and increased protein catabolism [35]. In cachexia, inflammation is
the key factor, and weight loss is the main symptom. This is why
many cachectic people also have sarcopenia, but many sarcopenic
people cannot be considered cachectic. Cachexia occurs in people
of any age and may be viewed as an accelerated primary model of
sarcopenia [36].
It remains to be shown whether functional consequences of
acute muscle mass loss (cachexia and bed confinement) may be
compared to the effects of slow and chronic loss of muscle mass,
characteristic of sarcopenia [37].
From a therapeutic viewpoint, it is important to distinguish sar-
copenia from cachexia and starvation, because they all cause loss
of skeletal muscle mass and strength [38], but starvation read-
ily responds to renutrition, while cachexia is highly refractory to
nutritional interventions [39].
4. Treatment
4.1. Non-drug treatment
The practice of physical resistance exercise has been shown to
improve muscle mass and strength, but is not always feasible in
elderly subjects, and it is not yet known how long its effects last
after it is discontinued [40]. It has also been shown that it is not
sufficient to reverse the loss of muscle mass in elderly people.
4.2. Drug treatment
Pharmacological treatment of sarcopenia is a major area for
research. Many drugs are being tested for their effects on muscle
mass and strength, such as Ghrelin, GH secretagogue and myostatin
inhibitor, but at present few results have been achieved, some of
which are controversial. We shall therefore only report on the treat-
ments that have been most thoroughly investigated. Diet is the
other major field of study for treating sarcopenia, but falls beyond
the scope of this review. Table 3 shows the characteristics of the
most studied drug for the treatment of sarcopenia.
Testosterone is a steroid hormone that stimulates develop-
ment of secondary sexual characteristics in men, including muscle
growth [41]. The results of the different studies are not consistent.
Administration of testosterone to young people is associated with
an increase in muscle mass, but not in strength. In the elderly,
high testosterone doses increase contraction force [42], but this
treatment has been associated with severe complications, con-
traindicating its use.Growth hormone
Growth hormone (GH) supplementation has created a multi-
million market in anti-aging medicine programs. Administration of
GH improves body composition by increasing muscle mass, reduc-
ing fat mass, and decreasing bone demineralization rate, but there
is strong evidence that it does not improve contraction or functional
capacity and does not induce positive metabolic changes [43]. It is
also associated to severe side effects [44].
4.5. Dehydroepiandrosterone
DHEA is a precursor that is converted into sexual hormone in
specific target organs. Administration of DHEA to elderly people
increases bone density, but causes no changes in muscle size, con-
traction, or function. Its side effects are unknown, but the lack of
proven benefit restricts its indications. A recent review confirms
that the DHEA treatment data are inconclusive and its use is not
recommended for treating sarcopenia [45].
4.6. Vitamin D
25(OH)-vitamin D (vitD) levels decrease with age. Many stud-
ies have reported extremely low vitD levels in elderly people.
vitD levels above 30 ng/mL are considered normal; levels less than
12 ng/mL are diagnostic of vitD deficiency, and levels between 12
and 30 ng/mL suggest vitD insufficiency.
Low vitD levels are associated with decreased muscle strength
and statin-induced myopathy [46]. Supplementation with vitD is
associated with functional improvement, increased strength, and
decreased falls and mortality [47]. Di Monaco showed that vitD
levels were associated with recovery after rehabilitation in women
with hip fracture, but were not significantly associated with an
increased fat-free mass [48].
5. Conclusion
Despite the considerable volume of publications, there is no
conclusive definition of sarcopenia and it is not recognized as a
pathology. There is no clear association between the loss of muscle

Table 3
Summary of the major characteristics of treatment.

Studies in RCT in Improved muscle Results concerning Secondary effects Indications Indicated
the elderly sarcopenia strength mass in
in humans sarcopenia

Testosterone Yes No No Reduces fatty mass, Aggressive behavior, Androgen deficiency No

increases muscle thrombosis, OSAS, edema,
mass gynecomastia, prostate
cancer
GH Yes No No Reduces fatty mass, Joint pain, carpal tunnel Growth disorders and No
increases muscle syndrome, edema, growth hormone
mass carbohydrate intolerance, deficiency
diabetes, tumor
DHEA Yes No Dubious, temporary Dubious increase in None known Testosterone deficiency No
increase in handgrip muscle mass
vitD Yes Yes No No vitD toxicity Osteoporosis and VitD No
deficiency

OSAS, obstructive sleep apnoea syndrome; RCT, randomized controlled trial.

 V. Malafarina et al. / Maturitas 71 (2012) 109–114
mass and strength, or the factors that contribute to their develop-
ment. It would be logical to assume that there is a direct relationship
between muscle mass and strength: the greater the mass the
greater the strength, and vice versa. An active life style and diet
seem to be associated protective factors against sarcopenia, and
nutritional supplementation is the treatment of choice, mainly in
hospitalized patients.
Most of the published studies on which the diagnosis of sar-
copenia is based were carried out in the USA. We believe that the
differences in lifestyle and diet between the European population
and that of other continents mean that prudence should be exerted
before adopting such criteria. This points to the need for population
studies to identify parameters that would match the characteristics
of each population.
Chronic inflammation in the elderly represents one of the most
widely studied aspects of the physiopathology of sarcopenia, but
we were unable to locate any studies that assess the influence of
anti-inflammatory treatment on sarcopenia. It would be interesting
to conduct a study to assess whether the presence and development
of sarcopenia in hospitalized patients are associated with higher
levels of inflammatory indices, and whether a reduction in these
during the hospital stay is associated with a reduction in sarcopenia
and greater functional recovery.
Screening for and proper diagnosis of sarcopenia at an early
stage should form the object of preventive geriatrics, the main aim
of which is to help the elderly to stay independent and healthy,
so that they do not have to be hospitalized as a result of underly-
ing pathologies that may be present. If we are to manage sarcopenia
properly, we need to understand its physiopathology better in order
to provide specific, effective treatment. This is the task of acute
geriatric care, which is designed to help elderly people who are
hospitalized to return to their previous baseline state as soon as
possible. Patients whose recovery is delayed, or who need inter-
mediate care, will benefit from the type of care given to chronic
patients. Among the elderly, disease can develop very quickly, but
recovery and healing are very long, complex processes.
Future double-blind randomized clinical trials with placebo are
vitally important to assess the true role of treatment in sarcopenia,
and would be particularly useful in the area of nutrition.
Current data concerning the effectiveness of nutritional mea-
sures for reversing sarcopenia are dubious, since most published
studies present the possible bias of large numbers of patients who
do not follow their treatment regimens conscientiously or abandon
the diet completely.
It has not been proven that elderly people who take nutritional
supplements have an increase in muscle mass; however, sarcope-
nia has been shown to be present in all malnourished patients.
We consider that it would be vitally important to conduct a study
of the effect of dietary supplements in elderly patients who have
undergone a functional loss with respect to their baseline state and
developed sarcopenia, to ascertain whether such treatment helps
them to restore the functional state they had before the onset of
acute disease.
Contributors
All of authors contributed to the preparation of this manuscript
equally.
Competing interests
None of the authors is currently receiving funds or grants for
research of any kind. The conclusions reached reflect the thinking
of the authors. The present study did not receive funding.
113
Provenance and peer review
Not commissioned, externally peer reviewed.
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