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Thorax 58:739-740 doi:10.1136/thorax.58.9.739
  • Editorial

Eat well to get well

  1. E F M Wouters
  1. Department of Respiratory Medicine, University Hospital Maastricht, PO Box 5800, 6202 AZ Maastricht, The Netherlands; ewo{at}slon.azm.nl

    Nutrition and energy supply are important components of rehabilitation programmes for patients with COPD.

    Improvement in functional performance is considered an important management goal in patients with chronic obstructive pulmonary disease (COPD). Pulmonary rehabilitation is now considered as an evidence based intervention to achieve an improvement in functional capacity as well as other management goals such as improved health status and reduction in breathlessness.1 Although exercise training is considered the core component of every pulmonary rehabilitation programme, the optimal method of exercise training as well as the optimal training intensity remains a matter of debate. Standard recommendations for exercise training in healthy subjects are generally transferred to disabled patients with COPD, and the complexity of the disease related changes which make an important contribution to the functional disability experienced is usually ignored.

    The metabolic demand of exercise, reflected in the energy expended on activities, is generally overlooked when patients are stressed to increase their activity level. Consideration of energy balance in COPD is important because weight loss and, specifically loss in fat mass, is the result of a negative energy balance. During the last decade most attention has been focused on resting energy expenditure in patients with COPD; in many of these patients hypermetabolism can be demonstrated which is partly related to the level of systemic inflammation.2,3 However, in normal subjects the energy expenditure for activities is the most variable component of total energy expenditure. While studies in other chronic wasting diseases characterised by hypermetabolism and systemic inflammation—for example, cancer, chronic heart failure, AIDS—have shown an adaptive decrease in activity induced energy expenditure so that total daily energy expenditure is normal, increased activity induced and total daily energy expenditure has been measured in free living ambulatory COPD patients.4 Great variations in total energy expenditure, physical activity, and energy intake have been reported in underweight patients with COPD living at home.5

    One obvious way of improving energy balance is to decrease energy expenditure. However, restricting energy output is not desirable as maintaining an active lifestyle is one of the management objectives in patients with COPD. This implies that patients with COPD who suffer from weight loss—and even some patients with a stable weight—should be encouraged to increase their apparently normal energy intake. The results presented by Steiner et al in this issue of Thorax outline the importance of energy balance in COPD patients advised to increase exercise.6 Patients participating in a rehabilitation programme who received a 570 kcal carbohydrate rich supplement gained weight, principally due to changes in fat mass, while those in the placebo group lost weight; these differences were even greater in patients with a body mass index (BMI) of >19 kg/m2, which suggests that, even under conditions of metabolic stress such as exercise, disturbances in energy balance can be introduced in this group of patients. The weight loss in the placebo group indicates the importance of asking patients for involuntary weight loss as an indicator of energy imbalance, either to increased energy expenditure or relatively decreased energy intake, and stresses the need to monitor body weight or body composition, especially during rehabilitation programmes. Recent epidemiological data underscore the clinical relevance of this observation.7

    Assuming that the long term aim of rehabilitation is the maintenance of physical fitness through a more active lifestyle, the implications of the findings of Steiner et al could be that this change in lifestyle can be complicated by a persistent negative energy balance contributing to progressive weight loss. A recent study by Goris et al8 supports this hypothesis. They studied the energy balance of depleted ambulatory COPD patients in relation to their habitual level of physical activity and consumption of oral nutritional supplements and found that the mean change in body mass over a period of 3 months was negatively related to the mean level of physical activity, indicating that knowledge of the individual physical activity is necessary for estimating the energy needs of the COPD patient. However, it has to be realised that supplementation of high carbohydrate diets, as in the study of Steiner et al, is the complete opposite for most people for whom trying to eat less and avoiding calorie-dense foods is the norm. The dietary advice for weight stable COPD patients is generally to eat a healthy diet, which is usually interpreted as a diet according to general dietary recommendations—that is, low in fat, high in fibre, containing complex carbohydrates and including large quantities of fruit and vegetables. Behaviour changes away from a habitual pattern and in a direction opposite to the social norm are difficult to establish. It is therefore very important that caregivers and heath professionals provide a consistent message on diet and nutrition and that they increase social support, pay attention to the patient’s nutritional status, and provide adequate dietary advice if weight loss is observed.9

    Generally considered as an energy storage, interesting data have recently been reported regarding the regulatory role of fat mass in body weight homeostasis by production of leptin. This hormone not only has an intriguing role in body weight homeostasis, but also plays a protective role in severe stress states and is involved in respiratory regulation.10,11 Circulating leptin concentrations are proportional to the amount of fat mass; in stable depleted patients with COPD, dietary intake—as well as weight gain after nutritional therapy—are inversely related to plasma leptin levels.12,13 It would be interesting to integrate leptin metabolism into future nutritional intervention studies.

    In a subgroup of patients with BMI >19 kg/m2, Steiner et al found a significantly greater increase in incremental shuttle walk distance after carbohydrate supplementation than in those receiving placebo treatment. Indeed, carbohydrates are an important source of energy for endurance. However, in addition to fuel supply, the adaptations of the metabolic machinery in the skeletal muscle tissue of COPD patients have to be taken into account. Patients with COPD have reduced oxidative capacity which is closely related to the reduction in type I fibres.14 Exercise training clearly contributes to an improvement in the aerobic enzyme capacity of patients with COPD.15 It would be intriguing to relate this reported functional improvement after carbohydrate supplementation to the metabolic enzyme content of the lower limb muscles. Although a BMI of 19 kg/m2 could be considered an acceptable lower limit of normal, the optimal BMI in patients with COPD is still open to question. Survival data showed a worse prognosis in COPD patients with a BMI of <21 kg/m2; a BMI of >19 kg/m2 could not therefore be considered as an acceptable lower limit in these patients.16,17

    The discrepancy between the definition of malnutrition based on BMI and an unintentional weight loss was recently demonstrated in a screening of nutritional status in a large study of hospitalised patients: 19% of the patients with weight loss >10% during the past 6 months still had a BMI of >25 kg/m2. The authors conclude that unintentional weight loss is a better indicator of disease related malnutrition since unintentional weight loss reflects insufficient energy and nutrient availability or increased needs.18

    Body compositional studies in COPD have clearly shown that weight loss is generally accompanied by a loss in fat free mass but that muscle wasting may also occur in stable subjects of normal weight. It is specifically the loss in fat free mass or other measures of muscle mass that are related to impaired skeletal muscle strength and exercise capacity.19,20 This wasting of muscle mass is due to an impaired balance between protein synthesis and protein breakdown. Besides nutritional abnormalities and physical inactivity, altered neuroendocrine response and the presence of a systemic inflammatory response may contribute to a negative protein balance in chronic diseases. This disproportionate muscle wasting linked to systemic inflammation is commonly referred to as the cachexia syndrome; processes that govern the maintenance of skeletal muscle and muscle plasticity such as skeletal muscle degeneration, apoptosis, and regeneration must also be considered in order to modify the muscle compartment in patients suffering from chronic inflammatory conditions. From a therapeutic perspective, it is important to analyse the relative contribution of each of these factors to altered protein synthesis and protein breakdown, respectively. Uncontrolled protein breakdown cannot be overcome simply by increasing protein synthesis. Furthermore, consistently reduced plasma levels of branched chain amino acids (BCAAs) have been reported in underweight COPD patients and in those with low muscle mass.21,22 These BCAAs are important precursors of glutamate which is one of the most important non-essential amino acids in muscle. A consistently reduced muscle glutamate level in patients with severe COPD was found to be further decreased during submaximal exercise.23 These metabolic changes illustrate the complexity of nutritional intervention strategies to gain muscle mass in depleted COPD patients. A recent study by Creutzberg et al24 demonstrates the possibility of achieving these treatment goals. Nutritional supplementation therapy, implemented on energy expenditure assessment as part of a pulmonary rehabilitation programme, was found to be effective in increasing body weight and muscle mass and these effects resulted in an improvement in muscle performance in these patients.24 The same authors had previously reported that non-response to nutritional therapy in patients with COPD is associated with ageing, relative anorexia, and an increased systemic inflammatory response.25

    The data reported by Steiner et al in this issue of Thorax show that nutrition and energy supply, although intuitively acknowledged, are important components of a multidisciplinary rehabilitation programme. Future studies of nutritional and metabolic regulation in the management of COPD must include an understanding of the complexity of the metabolic and structural adaptations as part of the multicomponent pathology of this condition.

    Nutrition and energy supply are important components of rehabilitation programmes for patients with COPD.

    REFERENCES