It is known that non-cachectic patients with chronic obstructive pulmonary disease (COPD) respond well to pulmonary rehabilitation, but whether cachectic COPD patients are capable of adaptive responses is both important and unknown.10 cachectic and 19 non-cachectic COPD patients undertook high-intensity cycling training, at the same relative intensity, for 45 min?day -1 , 3 days?week -1 for 10 weeks. Before and after rehabilitation vastus lateralis muscle biopsies were analysed morphologically and for the expression of muscle remodelling factors (insulin-like growth factor (IGF)-I, myogenic differentiation factor D (MyoD), tumour necrosis factor (TNF)-a, nuclear factor (NF)-kB and myostatin) and key components of ubiquitin-mediated proteolytic systems (muscle ring finger protein (MURF)-1 and Atrogin-1).Rehabilitation improved peak work-rate and the 6-min walk distance similarly in non-cachectic (18¡3% and 42¡13 m, respectively) and cachectic (16¡2% and 53¡16 m, respectively) patients, but quality of life only improved in non-cachectic COPD. Mean muscle fibre cross-sectional area increased in both groups, but significantly less in cachectic (7¡2%) than in non-cachectic (11¡2%) patients. Both groups equally decreased the proportion of type IIb fibres and increased muscle capillary/fibre ratio. IGF-I mRNA expression increased in both groups, but IGF-I protein levels increased more in non-cachectic COPD. MyoD was upregulated, whereas myostatin was downregulated at the mRNA and protein level only in non-cachectic patients. Whilst rehabilitation had no effect on TNF-a expression, it decreased the activation of the transcription factor NF-kB in both groups by the same amount. Atrogin-1 and MURF-1 expression were increased in cachectic COPD, but it was decreased in non-cachectic patients.Cachectic COPD patients partially retain the capacity for peripheral muscle remodelling in response to rehabilitation and are able to increase exercise capacity as much as those without cachexia, even if they exhibit both quantitative and qualitative differences in the type of muscle fibre remodelling in response to exercise training.
We investigated whether, during maximal exercise, intercostal muscle blood flow is as high as during resting hyperpnoea at the same work of breathing. We hypothesized that during exercise, intercostal muscle blood flow would be limited by competition from the locomotor muscles. Intercostal (probe over the 7th intercostal space) and vastus lateralis muscle perfusion were measured simultaneously in ten trained cyclists by near-infrared spectroscopy using indocyanine green dye. Measurements were made at several exercise intensities up to maximal (WR max ) and subsequently during resting isocapnic hyperpnoea at minute ventilation levels up to those at WR max . During resting hyperpnoea, intercostal muscle blood flow increased linearly with the work of breathing (R 2 = 0.94) to 73.0 ± 8.8 ml min −1 (100 g) −1 at the ventilation seen at WR max (work of breathing ∼550-600 J min −1 ), but during exercise it peaked at 80% WR max (53.4 ± 10.3 ml min −1 (100 g) −1 ), significantly falling to 24.7 ± 5.3 ml min −1 (100 g)at WR max . At maximal ventilation intercostal muscle vascular conductance was significantly lower during exercise (0.22 ± 0.05 ml min −1 (100 g) −1 mmHg −1 ) compared to isocapnic hyperpnoea (0.77 ± 0.13 ml min −1 (100 g) −1 mmHg −1 ). During exercise, both cardiac output and vastus lateralis muscle blood flow also plateaued at about 80% WR max (the latter at 95.4 ± 11.8 ml min −1 (100 g) −1 ). In conclusion, during exercise above 80% WR max in trained subjects, intercostal muscle blood flow and vascular conductance are less than during resting hyperpnoea at the same minute ventilation. This suggests that the circulatory system is unable to meet the demands of both locomotor and intercostal muscles during heavy exercise, requiring greater O 2 extraction and likely contributing to respiratory muscle fatigue.
During intense exercise in COPD, restriction of intercostal muscle perfusion but preservation of quadriceps muscle blood flow along with attainment of a plateau in cardiac output represents the inability of the circulatory system to satisfy the energy demands of locomotor and respiratory muscles.
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