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
]. 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
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.,
] 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
]. 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.