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Volume 1 - Issue 1
Mini Review
Chronic diseases increase their prevalence as the population
pyramid inverses [1], and respiratory diseases are among the most
frequent conditions in elderly individuals [2]. For instance, chronic
obstructive pulmonary disease (COPD) is a multi factorial entity
with a wide range of clinical manifestations, and a leading cause
of morbidity and mortality worldwide [3]. The pathophysiology
of COPD is as wide as its clinical presentation. However, chronic
inflammation is an essential component. Also, increased
inflammation is associated with a higher rate of exacerbations and
a faster decline in lung function [3], while systemic inflammation
contributes to the extra-pulmonary manifestations of COPD.
On the other hand, sarcopenia, the age-associated decrease
in muscle mass and function [4], has a prevalence of around 50%
in patients above 80 years of age [5], and is particularly common
in elderly individuals with COPD. It has also been associated to
chronic inflammation [3,6]. The combination of pro-inflammatory
cytokines has shown to reduce protein synthesis and increase
proteolysis [7]. However, this is not the only factor associated to
both conditions. Muscle wasting is closely related to lower survival
and higher rates of exacerbation in patients with COPD [3,8]. Thus,
it seems relevant to consider the association between sarcopenia
and COPD.
Following are some of the various patho-physiologic
mechanisms associating sarcopenia and COPD. To begin with,
even short-term disuse of muscle can lead to a diminished muscle
mass [7]. The functional capacity decrease associated to chronic
respiratory diseases by itself is enough to cause muscle mass loss,
particularly during exacerbations. Byun [3] found that patients
with sarcopenia had more severe symptoms of dyspnea and higher
modified medical research council dyspnea scale (mMRC) scores
than those without muscle wasting [3]. Nevertheless, it seems some
factors may further exacerbate muscle loss. For instance, during
exacerbations, energy intake seems to lower, further decreasing
amino acid availability for muscular protein synthesis [9].
Also, hypoxemia, as found in chronic respiratory diseases has
been associated to proteolysis and decreased protein synthesis
[7]. Hypoxia decreases the efficiency of mitochondrial electron
transport chain generating reactive oxygen species. Interleukins 1
and 6 and C-reactive protein are also found in higher quantities in
hypoxic patients, and these are factors that have been associated to
sarcopenia [10].
Additionally, tumor necrosis factor alpha is a cytokine usually
found in cachexia and other catabolic processes which may account
for unexplained weight loss in a variety of diseases, including COPD
[11]. This becomes relevant given that low body weight has been
associated to mortality in this group of patients [7]. Also, plasma
concentrations of glutamine and glutamate seem to be normal in
ambulatory COPD patients with normal weight, while they decrease
in low-weight patients with emphysema [7].
In older adults, sarcopenia has proven to be a useful tool for
risk stratification, since its presence is associated to a variety of
deleterious outcomes. Furthermore, even if muscle mass decrease
is more frequent during COPD exacerbations, a prevalence of 15%
of sarcopenia has been reported in patients with stable COPD
[5]. Also, sarcopenia can be approached through anthropometry
and dynamometry, tools that might be available in an outpatient
consultation context. Even if these tools were not available, a
complete interrogation may lead to discoveries such as decreased
grip strength (e.g the patient keeps dropping objects involuntarily),
low gait speed (e.g decreased mobility or slowness for walking),
low muscle mass (e.g loss of weight), all of which are diagnostic
criteria for pre-sarcopenia and sarcopenia [4].
In addition to early diagnosis of sarcopenia, pulmonary
rehabilitation seems to not only improve symptoms in patients with
chronic respiratory disease [12], but has also proved to “reverse”
sarcopenia by decreasing the quantity of diagnostic criteria met
in order to diagnose this entity in terms of the European Working
Group on Sarcopenia in Older People diagnostic algorithm. Aerobic
training is useful for expanding inspiratory volume, leading to
Daniela Patino Hernandez*
Geriatric Medicine Unit, Ageing Institute. Pontificia Universidad Javeriana. Bogotá, Colombia
*Corresponding author: Daniela Patino-Hernandez, Geriatric Medicine Unit, Institute of Aging, Pontifical Xavierian University, Carrera 7 No. 40-62 -
Hospital Universitario San Ignacio, piso 8. Facultad de Medicina. City: Bogotá D.C. Country: Colombia. Tel/fax: (00571) 3208320 ext. 2751.
Email:
Submission: September 28, 2017; Published: November 09, 2017
Chronic Obstructive Pulmonary Disease (COPD) and
Sarcopenia: A Bidirectional Pathway
Mini Review Gerontol & Geriatric stud
Copyright © All rights are reserved by Daniela Patino-Hernandez.
CRIMSONpublishers
http://www.crimsonpublishers.com
ISSN 2578-0093
How to cite this article: Daniela P H. Chronic Obstructive Pulmonary Disease (COPD) and Sarcopenia: A Bidirectional Pathway. Gerontol & Geriatric Stud. 1(1).
GGS.000505. 2017. DOI: 10.31031/GGS.2017.01.000505
Gerontology & Geriatrics Studies
2/2
Gerontol & Geriatric Stud
Volume 1 - Issue 1
reduced dyspnea on exertion, while increasing exercise tolerance
and improving muscle function [12].
In summary, it is paramount to understand the relevance of
assessing sarcopenia in patients with chronic respiratory diseases
in order to allow timely diagnosis and management of both
conditions, increasing quality of life for our patients.
References
1.	 Mathers CD, Loncar D (2006) Projections of Global Mortality and Burden
of Disease from 2002 to 2030. PLOS Med 3(11): e442.
2.	 Prince MJ, Wu F, Guo Y, Robledo LMG, O Donnell M, et al. (2015) The
burden of disease in older people and implications for health policy and
practice. Lancet 385(9967): 549-562.
3.	 Byun MK, Cho EN, Chang J, Ahn CM, Kim HJ (2017) Sarcopenia correlates
with systemic inflammation in COPD. Int J Chron Obstruct Pulmon Dis
12: 669-675.
4.	 Cruz Jentoft AJ, Baeyens JP, Bauer JM, Boirie Y, Cederholm T, et al. (2010)
Sarcopenia: European consensus on definition and diagnosis: Report of
the European Working Group on Sarcopenia in Older People. Age Ageing
39(4): 412-423.
5.	 Bone AE, Hepgul N, Kon S, Maddocks M (2017) Sarcopenia and frailty in
chronic respiratory disease. Chron Respir Dis 14(1): 85-99.
6.	 Beyer I, Mets T, Bautmans I (2012) Chronic low-grade inflammation and
age-related sarcopenia. Curr Opin Clin Nutr Metab Care 15(1):12-22.
7.	 Jagoe RT, Engelen MP (2003) Muscle wasting and changes in muscle
protein metabolism in chronic obstructive pulmonary disease. Eur
Respir J Suppl 46: 52s - 63s.
8.	 Celis Preciado CA, Borda M, Patino Hernandez D, Cano C, Perez Cepeda
M (2017) Sarcopenia as a Predictor of Mortality in Obstructive Lung
Disease: A Secondary Analysis of the CRELES Study. Am J Respir Crit
Care Med 195: A1013.
9.	 Sanders KJC, Kneppers AEM, van de Bool C, Langen RCJ, Schols AMWJ
(2016) Cachexia in chronic obstructive pulmonary disease: new insights
and therapeutic perspective. J Cachexia Sarcopenia Muscle 7(1): 5-22.
10.	Wandrag L, Siervo M, Riley HL, Khosravi M, Fernandez BO, et al. (2017)
Does hypoxia play a role in the development of sarcopenia in humans?
Mechanistic insights from the Caudwell Xtreme Everest Expedition.
Redox Biol 13: 60-68.
11.	Di Francia M, Barbier D, Mege JL, Orehek J (1994) Tumor necrosis factor-
alpha levels and weight loss in chronic obstructive pulmonary disease.
Am J Respir Crit Care Med 150(5 Pt 1): 1453-1455.
12.	Attwell L, Vassallo M (2017) Response to Pulmonary Rehabilitation in
Older People with Physical Frailty, Sarcopenia and Chronic Lung Disease.
Geriatrics 2(1): 9.

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Crimson Publishers-Chronic Obstructive Pulmonary Disease (COPD) and Sarcopenia: A Bidirectional Pathway

  • 1. 1/2 Volume 1 - Issue 1 Mini Review Chronic diseases increase their prevalence as the population pyramid inverses [1], and respiratory diseases are among the most frequent conditions in elderly individuals [2]. For instance, chronic obstructive pulmonary disease (COPD) is a multi factorial entity with a wide range of clinical manifestations, and a leading cause of morbidity and mortality worldwide [3]. The pathophysiology of COPD is as wide as its clinical presentation. However, chronic inflammation is an essential component. Also, increased inflammation is associated with a higher rate of exacerbations and a faster decline in lung function [3], while systemic inflammation contributes to the extra-pulmonary manifestations of COPD. On the other hand, sarcopenia, the age-associated decrease in muscle mass and function [4], has a prevalence of around 50% in patients above 80 years of age [5], and is particularly common in elderly individuals with COPD. It has also been associated to chronic inflammation [3,6]. The combination of pro-inflammatory cytokines has shown to reduce protein synthesis and increase proteolysis [7]. However, this is not the only factor associated to both conditions. Muscle wasting is closely related to lower survival and higher rates of exacerbation in patients with COPD [3,8]. Thus, it seems relevant to consider the association between sarcopenia and COPD. Following are some of the various patho-physiologic mechanisms associating sarcopenia and COPD. To begin with, even short-term disuse of muscle can lead to a diminished muscle mass [7]. The functional capacity decrease associated to chronic respiratory diseases by itself is enough to cause muscle mass loss, particularly during exacerbations. Byun [3] found that patients with sarcopenia had more severe symptoms of dyspnea and higher modified medical research council dyspnea scale (mMRC) scores than those without muscle wasting [3]. Nevertheless, it seems some factors may further exacerbate muscle loss. For instance, during exacerbations, energy intake seems to lower, further decreasing amino acid availability for muscular protein synthesis [9]. Also, hypoxemia, as found in chronic respiratory diseases has been associated to proteolysis and decreased protein synthesis [7]. Hypoxia decreases the efficiency of mitochondrial electron transport chain generating reactive oxygen species. Interleukins 1 and 6 and C-reactive protein are also found in higher quantities in hypoxic patients, and these are factors that have been associated to sarcopenia [10]. Additionally, tumor necrosis factor alpha is a cytokine usually found in cachexia and other catabolic processes which may account for unexplained weight loss in a variety of diseases, including COPD [11]. This becomes relevant given that low body weight has been associated to mortality in this group of patients [7]. Also, plasma concentrations of glutamine and glutamate seem to be normal in ambulatory COPD patients with normal weight, while they decrease in low-weight patients with emphysema [7]. In older adults, sarcopenia has proven to be a useful tool for risk stratification, since its presence is associated to a variety of deleterious outcomes. Furthermore, even if muscle mass decrease is more frequent during COPD exacerbations, a prevalence of 15% of sarcopenia has been reported in patients with stable COPD [5]. Also, sarcopenia can be approached through anthropometry and dynamometry, tools that might be available in an outpatient consultation context. Even if these tools were not available, a complete interrogation may lead to discoveries such as decreased grip strength (e.g the patient keeps dropping objects involuntarily), low gait speed (e.g decreased mobility or slowness for walking), low muscle mass (e.g loss of weight), all of which are diagnostic criteria for pre-sarcopenia and sarcopenia [4]. In addition to early diagnosis of sarcopenia, pulmonary rehabilitation seems to not only improve symptoms in patients with chronic respiratory disease [12], but has also proved to “reverse” sarcopenia by decreasing the quantity of diagnostic criteria met in order to diagnose this entity in terms of the European Working Group on Sarcopenia in Older People diagnostic algorithm. Aerobic training is useful for expanding inspiratory volume, leading to Daniela Patino Hernandez* Geriatric Medicine Unit, Ageing Institute. Pontificia Universidad Javeriana. Bogotá, Colombia *Corresponding author: Daniela Patino-Hernandez, Geriatric Medicine Unit, Institute of Aging, Pontifical Xavierian University, Carrera 7 No. 40-62 - Hospital Universitario San Ignacio, piso 8. Facultad de Medicina. City: Bogotá D.C. Country: Colombia. Tel/fax: (00571) 3208320 ext. 2751. Email: Submission: September 28, 2017; Published: November 09, 2017 Chronic Obstructive Pulmonary Disease (COPD) and Sarcopenia: A Bidirectional Pathway Mini Review Gerontol & Geriatric stud Copyright © All rights are reserved by Daniela Patino-Hernandez. CRIMSONpublishers http://www.crimsonpublishers.com ISSN 2578-0093
  • 2. How to cite this article: Daniela P H. Chronic Obstructive Pulmonary Disease (COPD) and Sarcopenia: A Bidirectional Pathway. Gerontol & Geriatric Stud. 1(1). GGS.000505. 2017. DOI: 10.31031/GGS.2017.01.000505 Gerontology & Geriatrics Studies 2/2 Gerontol & Geriatric Stud Volume 1 - Issue 1 reduced dyspnea on exertion, while increasing exercise tolerance and improving muscle function [12]. In summary, it is paramount to understand the relevance of assessing sarcopenia in patients with chronic respiratory diseases in order to allow timely diagnosis and management of both conditions, increasing quality of life for our patients. References 1. Mathers CD, Loncar D (2006) Projections of Global Mortality and Burden of Disease from 2002 to 2030. PLOS Med 3(11): e442. 2. Prince MJ, Wu F, Guo Y, Robledo LMG, O Donnell M, et al. (2015) The burden of disease in older people and implications for health policy and practice. Lancet 385(9967): 549-562. 3. Byun MK, Cho EN, Chang J, Ahn CM, Kim HJ (2017) Sarcopenia correlates with systemic inflammation in COPD. Int J Chron Obstruct Pulmon Dis 12: 669-675. 4. Cruz Jentoft AJ, Baeyens JP, Bauer JM, Boirie Y, Cederholm T, et al. (2010) Sarcopenia: European consensus on definition and diagnosis: Report of the European Working Group on Sarcopenia in Older People. Age Ageing 39(4): 412-423. 5. Bone AE, Hepgul N, Kon S, Maddocks M (2017) Sarcopenia and frailty in chronic respiratory disease. Chron Respir Dis 14(1): 85-99. 6. Beyer I, Mets T, Bautmans I (2012) Chronic low-grade inflammation and age-related sarcopenia. Curr Opin Clin Nutr Metab Care 15(1):12-22. 7. Jagoe RT, Engelen MP (2003) Muscle wasting and changes in muscle protein metabolism in chronic obstructive pulmonary disease. Eur Respir J Suppl 46: 52s - 63s. 8. Celis Preciado CA, Borda M, Patino Hernandez D, Cano C, Perez Cepeda M (2017) Sarcopenia as a Predictor of Mortality in Obstructive Lung Disease: A Secondary Analysis of the CRELES Study. Am J Respir Crit Care Med 195: A1013. 9. Sanders KJC, Kneppers AEM, van de Bool C, Langen RCJ, Schols AMWJ (2016) Cachexia in chronic obstructive pulmonary disease: new insights and therapeutic perspective. J Cachexia Sarcopenia Muscle 7(1): 5-22. 10. Wandrag L, Siervo M, Riley HL, Khosravi M, Fernandez BO, et al. (2017) Does hypoxia play a role in the development of sarcopenia in humans? Mechanistic insights from the Caudwell Xtreme Everest Expedition. Redox Biol 13: 60-68. 11. Di Francia M, Barbier D, Mege JL, Orehek J (1994) Tumor necrosis factor- alpha levels and weight loss in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 150(5 Pt 1): 1453-1455. 12. Attwell L, Vassallo M (2017) Response to Pulmonary Rehabilitation in Older People with Physical Frailty, Sarcopenia and Chronic Lung Disease. Geriatrics 2(1): 9.