Improvement of alveolar-capillary membrane diffusing capacity with exercise training in chronic heart failure.

@article{Guazzi2004ImprovementOA,
  title={Improvement of alveolar-capillary membrane diffusing capacity with exercise training in chronic heart failure.},
  author={Marco Guazzi and Giuseppe Reina and Gabriele Tumminello and Maurizio D. Guazzi},
  journal={Journal of applied physiology},
  year={2004},
  volume={97 5},
  pages={1866-73}
}
Chronic heart failure (CHF) may impair lung gas diffusion, an effect that contributes to exercise limitation. We investigated whether diffusion improvement is a mechanism whereby physical training increases aerobic efficiency in CHF. Patients with CHF (n = 16) were trained (40 min of stationary cycling, 4 times/wk) for 8 wk; similar sedentary patients (n = 15) were used as controls. Training increased lung diffusion (DlCO, +25%), alveolar-capillary conductance (DM, +15%), pulmonary capillary… CONTINUE READING

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After detraining ( 8 wk ) , DlCO , DM , VC , peak VO2 , VO2 at AT , VE / VCO2 slope , cardiac output , stroke volume , pulmonary arteriolar resistance at peak exercise , and BAD reverted to levels similar to baseline and to levels similar to controls .
Training did not affect hemodynamics at rest and enhanced the increase of cardiac output ( + 226 vs. + 187% ) and stroke volume ( + 59 vs. + 49% ) and the decrease of pulmonary arteriolar resistance ( -28 vs. -13% ) at peak exercise .
After detraining ( 8 wk ) , DlCO , DM , VC , peak VO2 , VO2 at AT , VE / VCO2 slope , cardiac output , stroke volume , pulmonary arteriolar resistance at peak exercise , and BAD reverted to levels similar to baseline and to levels similar to controls .
After detraining ( 8 wk ) , DlCO , DM , VC , peak VO2 , VO2 at AT , VE / VCO2 slope , cardiac output , stroke volume , pulmonary arteriolar resistance at peak exercise , and BAD reverted to levels similar to baseline and to levels similar to controls .
After detraining ( 8 wk ) , DlCO , DM , VC , peak VO2 , VO2 at AT , VE / VCO2 slope , cardiac output , stroke volume , pulmonary arteriolar resistance at peak exercise , and BAD reverted to levels similar to baseline and to levels similar to controls .
Training did not affect hemodynamics at rest and enhanced the increase of cardiac output ( + 226 vs. + 187% ) and stroke volume ( + 59 vs. + 49% ) and the decrease of pulmonary arteriolar resistance ( -28 vs. -13% ) at peak exercise .
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