Muscle fibre type shifting in the vastus lateralis of patients with COPD is associated with disease severity: a systematic review and meta-analysis

Abstract

Background: Skeletal muscle dysfunction is a common feature in chronic obstructive pulmonary disease (COPD) which is associated with intrinsic muscular abnormalities. One of the most consistently reported alterations is a shift from fibre type I to II in the vastus lateralis of these patients. Surprisingly, the relationship between this shift and the severity and phenotype of COPD remains unclear. A study was conducted to determine whether vastus lateralis muscle fibre type proportions are associated with COPD disease severity and to provide reference values for the proportions of fibre types in the vastus lateralis in COPD. Methods: A systematic review and a meta-analysis were conducted in which muscle fibre type data and markers of disease severity were collected from the literature. Results: The forced expiratory volume in 1 s (FEV 1 ), the ratio of FEV 1 to forced vital capacity (FVC) and body mass index were positively associated with the proportion of type I fibres in COPD. A proportion of 51% for vastus lateralis fibre type I and 13% for fibre type IIX were calculated from the combined data as normal values for patients with typical GOLD stage 3-4 COPD aged 60-70 years. Based on these reference values, a proportion of fibre type I ,27% and of fibre type IIX .29% were defined as pathologically abnormal. Conclusions: This review sheds new light on the relationship between skeletal muscle abnormalities and important hallmarks of the disease in severe COPD, and identifies absence of data in GOLD stages 1-2. This review also provides reference values on fibre type composition for diagnostic purposes in COPD.

Quadriceps wasting and physical inactivity in patients with COPD

“…It should be noted, however, that inactivity may act as a significant confounder when observing quadriceps dysfunction as an effect of smoking. Further studies are needed to explore whether the fibre type switch from oxidative type I fibres to anaerobic type II fibres reported in advanced COPD [38] occurs earlier in the disease process as a consequence of physical inactivity interacting with systemic effects.…”

Skeletal Muscle Dysfunction in Patients with Chronic Obstructive Pulmonary Disease

“…A subsequent study by Maltais and colleagues (1999) confi rmed a shift toward type II fi bers and a reduction in the proportion of type I fi bers in the vastus lateralis muscles of patients with severe COPD. Recent meta-analysis has revealed that the proportion of type I fi bers in the vastus lateralis muscle correlates with FEV 1 , FEV 1 /forced vital capacity (FVC) and the body mass index (BMI) in patients with moderate to severe COPD (Gosker et al 2007b). Although the exact functional consequences of this fi ber type redistribution remain under investigation, the fact that type II fi bers are fatigue-prone suggests that an increased proportion of type II fi bers might be an important factor in increased leg muscle fatigability and reduced endurance.…”

COPD: Is there evidence to support a role for resistance training in improving measurable health-related quality of life in pulmonary rehabilitation?

“…26 and reductions in peroxisome proliferator-activated receptors (involved in mitochondrial biogenesis). 43 Gosker et al 21 recently confirmed that the severity of COPD is associated with reductions in the proportion of type I fibres. The aforementioned factors together with the finding that lactic acidosis occurs earlier during exercise in COPD patients compared with healthy subjects, 33 may partly explain why COPD patients fatigue quicker and experience exercise intolerance.…”

“…21,34,47 A shift in distribution from slow to fast twitch fibres gives rise to altered activities of key oxidative and glycolytic enzymes 62 that may decrease oxidative capacity and increase the risk of developing insulin resistance. 48 Whether resistance training exacerbates this phenotype switch, decreasing functional and oxidative capacity further, or maintains the status quo, has not been determined in COPD patients.…”