Chronic obstructive pulmonary disease (COPD) is characterized by an obstructed or chronically limited airflow which progresses slowly and irreversibly. The main cause of COPD is the combination of chronic bronchitis and pulmonary emphysema, due mainly to smoking 1 .

Patients with COPD usually have a compromised nutritional status which is an independent predictor of morbidity and mortality 2 3 . Malnutrition affects approximately one-third of the adult patients with this disease 2 , mainly in elderly 4 . The fat-free mass decreases and body fat increases but body mass index (BMI) remains unchanged, suggesting that one body compartment is replaced by another 5 . Malnutrition in patients with COPD is associated with increased energy expenditure due to hypermetabolism, which in turn is caused by greater respiratory muscle effort, oxygen requirement and inflammation and lower food intake 6 .

It is essential to determine resting energy expenditure (REE) to prevent a negative caloric balance and consequently malnutrition, since REE is the main component of total energy expenditure (TEE) 7 and is vital for adequate food intake 8 . Additionally, it is also critical to know which energy substrate is the most oxidized so that appropriate dietary adjustments can be made.

Changes in energy metabolism stemming from patients with COPD can be detected by indirect calorimetry, which measures oxygen consumption (O₂) and elimination of carbon dioxide (CO₂), thus determining REE and respiratory quotient (RQ). RQ depends on the mixture of energy substrates (carbohydrates, fats and proteins) that is the mixture metabolized during rest or exercise. In patients with COPD, a RQ < 1.0 is desirable since the patient will be exhaling less carbon dioxide 9 . However, no study assessed carbohydrate and fat oxidation separately in this group of patients (with COPD), and this is essential for understanding the energy metabolism of these individuals. An appropriate nutritional strategy for treating malnutrition in patients with COPD has not yet been established because, despite extensive studies on their energy metabolism, not much data is available on their oxidative capacity 10 .

Hence, the aim of the present study was to compare the oxidation amount of energy substrates and REE of elderly patients with and without COPD.

In the present study, we found that individuals with COPD had higher REE and resting carbohydrate oxidation than the controls, regardless of body composition, since both groups had similar muscle mass.

Other studies have also found that patients with COPD have higher REE (approximately 15 to 26%) 6 19 . The greater energy expenditure of individuals with COPD is probably due to increased respiratory muscle effort and inflammatory mediators, in addition to the effects of medication (oral or systemic corticosteroids, theophylline, hormones, benzodiazepines and antipsychotics) 19 20 21 .

This study found that mean RQ and carbohydrate oxidation were higher in the COPD group, while fat oxidation was similar in both groups. Increased carbohydrate oxidation in the COPD group was probably caused by increased anaerobic metabolism due to reduced ability to capture oxygen 22 . When carbohydrates are oxidized in the absence of oxygen, only 2 ATP molecules per millimol of carbohydrates are generated, while the presence of oxygen increases ATP/millimol generation to 36 ATPs 22 . Hence, individuals with COPD need to oxidize greater amounts of carbohydrates than healthy individuals to generate similar amounts of ATP molecules, because COPD patients present a higher ATP cost 23 .

Moreover, individuals with COPD show depletion of type I muscle fibers (aerobic) and a greater proportion of type IIx fibers, with consequent reduction in the number of mitochondria and oxidative enzymes and lower expression of peroxisome proliferator-activated receptors (PPAR-α) and PGC-1α, molecular markers that are related to mitochondrial biogenesis and higher activation of oxidative metabolism 24 . Although individuals with COPD have lower aerobic metabolism, fats are only oxidized in the presence of oxygen 9 , however their fat oxidation was not affected, which is necessary more studies to explain this fact.

BMI has been used as a good indicator of the nutritional status of individuals with COPD 25 . However, it is not possible to determine body composition with this index 26 . So this study also determined the body composition, muscle mass index, degree of sarcopenia, percentage of body fat, fat-free mass index and waist circumference of the participants.

The results showed that the COPD and control groups had similar body composition, which may be explained by the advanced age of the members of both groups 27 . It is estimated that people lose 5% of their muscle mass per decade after age 40 years and this loss intensifies after age 65 years 27 . The degree of sarcopenia was similar in both groups since both groups presented loss of muscle mass. However, loss was greater in individuals with COPD and class II sarcopenia than in controls. A similar result was found by Sergi et al., 2006, 19 who found a greater prevalence of sarcopenia in individuals with COPD than in healthy controls. COPD can intensify the loss of muscle mass, affecting respiratory and peripheral muscle performance, and thereby reducing ventilation and physical activity 28 . According to the II Brazilian Consensus on COPD 1 , patients with moderate COPD may have FFM depletion involving skeletal muscles, which results in weight loss. In the present study, the FFM-I of both groups was similar. Sergi et al., 2006, 19 found that individuals with COPD had lower FFM than healthy controls. Reduced FFM in these patients could be associated with age and particularly regard peripheral skeletal muscles, which may manifest as weakness in individuals with COPD 19 .

The present and other Brazilian studies have found that COPD affects mainly elderly males with a past or current history of smoking 1 29 . Another aspect observed in individuals with COPD is the change in nutritional status, such as malnutrition 30 . However, a recent study 19 found a higher prevalence of normal weight individuals. It is important for individuals with COPD not to become underweight since the severity of pulmonary diseases is associated with low BMI, which can result in worse nutritional prognosis and shorter survival 2 . The COPD participants of the present study were attending a pulmonary rehabilitation program and mean duration of disease was 4.65 years, that is, they were in the initial phase of the disease. Hence, this may explain the high prevalence of normal weight or overweight individuals in the present study.

Although most patients were normal weight or overweight, the risk of malnutrition was found in 15% of the patients with COPD. This risk was not observed in the control group. Progressive weight loss in these patients may be due to a set of factors, such as release of inflammatory mediators, which can contribute to hypermetabolism and generate an inappropriate response to food intake, and reduced food intake 31 . Moreover, increased serum concentration of leptin has already been observed and now it is known that this hormone promotes greater energy expenditure and consequently, greater weight loss 31 . Recently, Ying et al. (2008) 32 found that underweight individuals with COPD have high serum levels of ghrelin. Ghrelin reduces fat oxidation, which may explain why the COPD participants of the present study did not present more fat oxidation than the controls. However, more studies are necessary to explain these findings.

Diet affects nutritional status and may change the progression rate of pulmonary disease 33 . Recent studies do not recommend high-fat diets, but an energy intake that allows individuals to reach or maintain an appropriate nutritional status 3 . A high-fat, low-carbohydrate diet can improve the prognosis of COPD patients with acute exacerbation 34 . Patients with marginal ventilatory reserve might benefit from a high-fat diet 35 . Although the present study did not assess the pulmonary ventilation of the participants, it has found that carbohydrates are the main substrates oxidized. The recommended amount of carbohydrates is 50 to 60% of the total energy expenditure of the patient. Excessive carbohydrate intake could cause lipogenesis with consequent excessive production of carbon dioxide and hepatic steatosis, which in turn increases RQ and production of carbon dioxide, resulting in respiratory failure 36 . Hence, the recommended carbohydrate intake of 50 to 60% of the total energy expenditure seems not to induce hyperventilation and also avoids malnutrition by replacing the burned carbohydrates.

In the group studied in this work it is possible to conclude that elderly patients with COPD have higher REE, RQ and carbohydrate oxidation than healthy controls.

COPD: Chronic obstructive pulmonary disease; REE: Resting Energy Expenditure; BMI: Body Mass Index; RQ: Respiratory Quotient; NCEP-ATPIII: Expert Panel on Detection; Evaluation and Treatment of High Blood Cholesterol in Adults; FFM: Fat-free mass; MM: Muscle mass; MM-I: Muscle mass index; WC: Waist Circumference.

The authors declare that they have no competing interests.

BRR, DMN, MLG and MMF collected the data and elaborated the manuscript. EPO, GDP, LSV wrote and corrected the manuscript. KCPM revised the final manuscript. All authors read and approved.