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Aging and disease    2019, Vol. 10 Issue (5) : 1109-1129     DOI: 10.14336/AD.2018.1226
Review Article |
Handgrip Strength and Pulmonary Disease in the Elderly: What is the Link?
Tatiana Rafaela Lemos Lima1, Vívian Pinto Almeida1, Arthur Sá Ferreira1, Fernando Silva Guimarães1, Agnaldo José Lopes1,2,*
1Rehabilitation Sciences Post-Graduate Program, Augusto Motta University Center (UNISUAM), Bonsucesso, 21041-010, Rio de Janeiro, Brazil
2Post-graduate Program in Medical Sciences, School of Medical Sciences, State University of Rio de Janeiro (UERJ), Vila Isabel, 20550-170, Rio de Janeiro, Brazil
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Abstract  

Societies in developed countries are aging at an unprecedented rate. Considering that aging is the most significant risk factor for many chronic lung diseases (CLDs), understanding this process may facilitate the development of new interventionist approaches. Skeletal muscle dysfunction is a serious problem in older adults with CLDs, reducing their quality of life and survival. In this study, we reviewed the possible links between handgrip strength (HGS)—a simple, noninvasive, low-cost measure of muscle function—and CLDs in the elderly. Different mechanisms appear to be involved in this association, including systemic inflammation, chronic hypoxemia, physical inactivity, malnutrition, and corticosteroid use. Respiratory and peripheral myopathy, associated with muscle atrophy and a shift in muscle fiber type, also seem to be major etiological contributors to CLDs. Moreover, sarcopenic obesity, which occurs in older adults with CLDs, impairs common inflammatory pathways that can potentiate each other and further accelerate the functional decline of HGS. Our findings support the concept that the systemic effects of CLDs may be determined by HGS, and HGS is a relevant measurement that should be considered in the clinical assessment of the elderly with CLDs. These reasons make HGS a useful practical tool for indirectly evaluating functional status in the elderly. At present, early muscle reconditioning and optimal nutrition appear to be the most effective approaches to reduce the impact of CLDs and low muscle strength on the quality of life of these individuals. Nonetheless, larger in-depth studies are needed to evaluate the link between HGS and CLDs.

Keywords handgrip strength      sarcopenia      pulmonary disease      elderly      rehabilitation     
Corresponding Authors: Lopes Agnaldo José   
About author:

Present address: Department of Neurology, National Neuroscience Institute, Tan Tock Seng Hospital, Singapore.

Just Accepted Date: 31 December 2018   Issue Date: 27 September 2019
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Lima Tatiana Rafaela Lemos
Almeida Vívian Pinto
Ferreira Arthur Sá
Guimarães Fernando Silva
Lopes Agnaldo José
Cite this article:   
Lima Tatiana Rafaela Lemos,Almeida Vívian Pinto,Ferreira Arthur Sá, et al. Handgrip Strength and Pulmonary Disease in the Elderly: What is the Link?[J]. Aging and disease, 2019, 10(5): 1109-1129.
URL:  
http://www.aginganddisease.org/EN/10.14336/AD.2018.1226     OR     http://www.aginganddisease.org/EN/Y2019/V10/I5/1109
Figure 1.  Schematic representation of the scope of the current review.
Figure 2.  Schematization of the main alterations in the respiratory system of the elderly that may contribute to the pathogenesis of chronic lung diseases.
Figure 3.  Alterations that cause impairment in the protective mechanisms of the elderly and predisposition to chronic lung diseases.
Figure 4.  Scheme showing the pathophysiology of age-related changes in muscle tissue.
DiseaseFindingReferences
COPDLoss of pulmonary elastic recoil together with ventilation-perfusion mismatch lead to poor peripheral musculature oxygenation[10, 23, 24, 47, 57]
There is an association of respiratory and peripheral muscle weakness with HGS impairment[10, 11, 13, 25, 28, 36]
Slow-to-fast twitch fiber type transformation results in increased respiratory work and reduced HGS[11, 39, 42, 45]
High sympathetic nervous activity causes increased muscle vasoconstrictor stimulation[55]
Endothelial dysfunction and cardiac damage with low oxygen pulse affect muscle function[59-61]
Coexistence of peripheral arterial occlusive disease contributes to a lower HGS[61]
Low-grade chronic inflammation (inflamm-aging) affects skeletal muscle function[7, 24, 44, 66]
Oxidative stress and high IL-6 and TNF-α levels reduce muscle function[1, 18, 39, 44]
Muscle atrophy, loss of type I fibers and lower oxidative enzyme activity impair muscle function[44]
Reduced muscle fiber capillarization negatively impacts muscle activity[4]
Low levels of anabolic hormones may influence the decline in muscle strength[34, 37, 48]
Sedentary lifestyle and physical inactivity are related to lower HGS[8, 10-12, 40, 41, 46]
Accelerated intracellular protein degradation causes myopathy[43]
Malnutrition acts as a contributor to the sarcopenic state and reduced HGS[77, 78]
Both systemic and inhaled chronic corticosteroid therapy reduce protein synthesis and increase muscle proteolysis[4, 42, 81, 82, 92]
Depression acts as a contributor to the decline in HGS[24, 34]
Acute exacerbations of the disease and need for intensive care further reduce HGS[8, 92]
There are interrelationships between frailty, worse HRQoL, mortality and low HGS[34, 40, 46, 53]
AsthmaLoss of pulmonary elastic recoil and increased small airway closure volume cause peripheral muscle hypoxia (especially in acute exacerbations)
[23]
Persistent, low-grade systemic inflammation causes accelerated muscle catabolism[19, 67]
Proinflammatory cytokines cause injury to skeletal muscles[19]
Reduction of insulin-like growth factor I contributes to muscle dysfunction[48]
There are interrelationships between difficult-to-control asthma, long-term asthma and decreased HGS[67]
Sex hormones may play a role in explaining intrinsic differences in HGS between genders[48]
Corticosteroid use negatively impacts HGS in difficult-to-control asthma[67, 83]
The combination of sarcopenia and obesity (sarcopenic obesity) exposes common inflammatory pathways that enhance each other[16, 54, 86, 87]
Increased ROS production and secretion of adipokines and cytokines such as IL-6, TNF-α and mcp-1 affect skeletal muscle quality[16, 87]
Increased insulin resistance and dysregulation in the hypothalamic-pituitary-adrenal axis increase the risk of depression[16, 37]
IPFOxidative stress and catabolic inflammatory processes increase sarcopenia[1, 62, 63, 70]
Mitochondrial dysfunction and accumulation of aged mitochondria damage skeletal muscle[1, 17, 70]
The cumulative amount of corticosteroids independently predicts reduced muscle strength[61, 62, 72, 81]
Muscle fiber disorganization and cellular metabolic changes impair metabolic demand in episodes of disease exacerbation[23, 24]
Physical deconditioning and long-term disease are associated with lower HGS[73]
Lung cancerMitochondrial dysfunction and ROS increase muscle fatigue[69]
Increased energy expenditure, changes in metabolism and cachexia compromise peripheral muscles[51, 79, 80]
Possible tumor-host interactions may cause muscle dysfunction[49, 51, 79, 80]
Gluconeogenic precursors are crucial for maintenance of muscle function and are related to survival[9]
The amount of skeletal muscle mass directly impacts survival[48-51]
“Acute sarcopenia” secondary to hospitalization aggravates peripheral muscle performance[74]
Lifestyle change imposed by cancer worsens HGS reduction[9, 51]
Table 1  Main findings that support a link between different chronic lung diseases and reduced handgrip strength in the elderly.
Figure 5.  Possible mechanisms of the linkage between handgrip and pulmonary disease in the elderly.
Figure 6.  Relationship between inflamm-aging, muscle function, and chronic lung disease in the elderly. While inflamm-aging can lead to damage to muscle and lung tissue, muscle can exert a protective effect on the genesis of chronic lung diseases. IL-1β = interleukin 1β; IL-6 = interleukin 6; TNF-α = tumor necrosis factor-α.
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