Impaired training-induced adaptation of blood pressure in COPD patients: implication of the muscle capillary bed

Background and aims: Targeting the early mechanisms in exercise-induced arterial hypertension (which precedes resting arterial hypertension in its natural history) may improve cardiovascular morbidity and mortality in COPD patients. Capillary rarefaction, an early event in COPD before vascular remodeling, is a potential mechanism of exercise-induced and resting arterial hypertension. Impaired training-induced capillarization was observed earlier in COPD patients; thus, this study compares the changes in blood pressure (BP) during exercise in COPD patients and matches control subjects (CSs) after a similar exercise training program, in relationship with muscle capillarization. Methods: Resting and maximal exercise diastolic pressure (DP) and systolic pressure (SP) were recorded during a standardized cardiopulmonary exercise test, and a quadriceps muscle biopsy was performed before and after training. Results: A total of 35 CSs and 49 COPD patients (forced expiratory volume in 1 second =54%+/- 22% predicted) completed a 6-week rehabilitation program and improved their symptom-limited maximal oxygen uptake (VO2SL: 25.8 +/- 6.1 mL/kg per minute vs 27.9 mL/kg per minute and 17.0 +/- 4.7 mL/kg per minute vs 18.3 mL/kg per minute; both P<0.001). The improvement in muscle capillary-to-fiber (C/F) ratio was significantly greater in CSs vs COPD patients (+11%+/- 9% vs +23%+/- 21%; P<0.05). Although maximal exercise BP was reduced in CSs (DP: 89 +/- 10 mmHg vs 85 +/- 9 mmHg; P<0.001/SP: 204 +/- 25 mmHg vs 196 +/- 27 mmHg; P<0.05), it did not change in COPD patients (DP: 94 +/- 14 mmHg vs 97 +/- 16 mmHg; P=0.46/SP: 202 +/- 27 mmHg vs 208 +/- 24 mmHg; P=0.13). The change in muscle C/F ratio was negatively correlated with maximal exercise SP in CSs and COPD patients (r=-0.41; P=0.02). Conclusion: COPD patients showed impaired training-induced BP adaptation related to a change in muscle capillarization, suggesting the possibility of blunted angiogenesis.