Dual morphometrical changes of the deltoid muscle in patients with COPD

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Abstract

The present study was specifically aimed at evaluating if the structure of the deltoid muscles is modified in patients with chronic obstructive pulmonary disease (COPD). Twenty-eight male volunteers (61±13 yr) were assigned, according to pulmonary function, to either the COPD (n=14, FEV1=22–74%pred) or control group (n=14, FEV1=83–121%pred). Biopsies from non-dominant deltoid muscle were obtained and processed for morphometric analysis of the fibre types. Both type I and type II muscle fibres were distributed in the typical mosaic pattern. The mean value of the fibre size was within the normal range. However, three differentiated modes were observed in the deltoid from COPD patients: a central mode of normal sized fibres, a mode of atrophic fibres and a mode of hypertrophic fibres. This observation was evident even within single fascicles and especially prevalent in the most severe COPD patients. We conclude that factors with opposite effect (promotion of either atrophy or hypertrophy) exert relevant roles in the histomorphometrical characteristics of the deltoid muscles in COPD patients.

Introduction

Dyspnea, impaired exercise capacity, and a decreased quality of life are common in patients with chronic obstructive pulmonary disease (COPD) (American Thoracic Society/European Respiratory Society, 1999). It has recently been demonstrated that a decrease in exercise capacity is associated with an increased use of health care services and a higher mortality in COPD patients (Strauss et al., 1986, Decramer et al., 1997, IPPB Trial Group, 1983). This exercise limitation is the result of several factors rather than exclusively dependent on impaired pulmonary function (Dillard et al., 1989). One of these additional factors has been related to dysfunction of the peripheral muscles (Decramer et al., 1996, Decramer et al., 1998). Therefore, interest in identifying both the structural changes underlying skeletal muscle dysfunction in COPD has increased over the last few years.

The origins of muscle dysfunction found in patients with COPD remain to be elucidated. From a clinical point of view, this interest is strongly justified as evident from studies relating skeletal muscle dysfunction to particular characteristics of the patients (e.g. tolerance to exercise) as well as a greater use of health care resources and a higher mortality rate (American Thoracic Society/European Respiratory Society, 1999). It is possible that a better characterisation of muscle dysfunction would permit definition of the potential cause(s) and optimize treatment.

Most of the preceding studies evaluating functional or structural characteristics of the muscles in patients with COPD have assessed the lower limbs, especially the quadriceps (vastus lateralis) (American Thoracic Society/European Respiratory Society, 1999). This approach is probably logical as a strong correlation exists between quadriceps strength and exercise tolerance in COPD patients (Hamilton et al., 1995). This muscle has been found to be weaker in COPD patients displaying both a decreased size and a lower oxidative enzyme activity in the muscle fibres (Whittom et al., 1998). From a methodological point of view, extrapolation of data obtained from analysis of lower limb muscles to other skeletal muscles possesses several limitations. In fact, it is difficult to define to what extent changes are homogeneously associated to the COPD itself and not to coexisting diseases or solely to progressive deconditioning. The authors have, therefore, considered it relevant to study both the function and structure of peripheral muscles pertaining to other territories (e.g. arms, shoulders, or even the trunk) because they may be affected to a lesser degree by sedentariness (Orozco-Levi and Gea, 2000). In a recent study assessing the metabolic pathways of the deltoid (a muscle of the upper limbs), the oxidative capacity of muscle homogenates was found to be preserved or even increased in severe COPD patients (Gea et al., 2001). It is not clear why these findings are different to those previously observed in muscles from the lower limbs, a crucial point when evaluating the causes thought to be involved in modulating the changes of the peripheral muscles in relation to the disease. The present study was specifically aimed to further characterise the cellular structure of the deltoid muscle in COPD patients with several degrees of airflow obstruction, in comparison to individuals with normal pulmonary function.

Section snippets

Study design, settings and population

This was a cross-sectional observational study, conducted in accordance with good clinical practice and World Medical Association guidelines for research in humans. Twenty-eight male individuals (61±13 yr) were recruited and assigned according to pulmonary function to either the COPD (n=14, FEV1=22–74%pred) or control group (n=14, FEV1=83–121%pred). All were sedentary individuals and their daily physical activities were similar. The control group included individuals attending ophthalmologists

Results

All selected individuals agreed to participate in the study. Adverse effects or complications derived from the evaluations were not detected. Nutritional status assessed using both anthropometrical and serum parameters was found to be within normal ranges (Table 1). The main dynamic and static lung volume data is presented in Table 2. The COPD patients disclosed pulmonary air trapping (i.e. residual lung volume >120%pred), lowered transfer factor for carbon monoxide (Tlco) and lowered arterial P

Discussion

The present study is the first demonstrating that the deltoid muscle shows dual histomorphometrical changes in patients with COPD. Although the mean value of the muscle fibre size was found to be within the normal range in the deltoid from the COPD patients, further analyses revealed intrafascicular variation in muscle fibres as a result of the coexistence of a group of fibres with normal size with groups of both atrophic and hypertrophic fibres.

Conclusions

The present study demonstrates that the deltoid muscle discloses dual structural changes in patients with COPD. The mean value of the fibre size is preserved. However, this is due to the coexistence of a mode of fibres with normal diameter and both atrophic and hypertrophic fibres. This phenomenon has not previously been described in other skeletal muscles of COPD patients and allows us to hypothesise on the existence of opposing factors acting simultaneously on the deltoid muscles of COPD.

Acknowledgements

This study was supported, in part, by grants BIOMED (ERESMUS in COPD) and ARMAR. The authors gratefully acknowledge Dr M.C. Aguar and Dr J. Sauleda for participating in some of the studies; Dr J. Vila for statistical advice; Mrs N. Soler and A. Roig for technical assistance; A. Currid and H. Lock for editing the manuscript.

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