Exercise hyperventilation in chronic heart failure is not caused by systemic lactic acidosis

Roland Wensel, Darrel P. Francis, Panagiota Georgiadou, Adam Scott, Sabine Genth-Zotz, Stefan D. Anker, Andrew J. S. Coats, Massimo F. Piepoli

Research output: Contribution to journalArticle

18 Citations (Scopus)


Background: Patients with heart failure have an abnormally high ventilatory response to exercise associated with gas exchange defects and reduced arterial pCO2.  

Aims: We examined the possibility of lactic acidosis as the stimulus to this increased ventilation that abnormally depresses pCO2 during exercise in heart failure.  

Method and results: We studied 18 patients with chronic heart failure. We measured VE/VCO2 slope during exercise, arterial blood gases and lactate concentrations during cardiopulmonary exercise testing (rest, peak exercise and one minute after the end of exercise). Neither VE/VCO2 slope nor arterial pCO2 were related to arterial lactate concentrations at peak exercise (r=–0.16, p=0.65 and r=–0.15, p=0.6). During early recovery, patients with a high VE/VCO2 slope had a particularly pronounced rise in arterial lactate and hydrogen ion concentrations (r=0.57, p<0.05 and r=0.84, p<0.0001) and yet their arterial pCO2 rose rather than fell (r=0.79, p<0.001). The rise in arterial pCO2 correlated with the increase in arterial hydrogen concentration (r=0.78, p<0.001) and with arterial pCO2 at peak exercise (r=–0.76, p<0.001).  

Conclusions: In heart failure VE/VCO2 slope and low arterial pCO2 at peak exercise are not related to the degree of systemic lactic acidosis. Lactic acidosis is therefore not a plausible mechanism of exercise induced hyperventilation.
Original languageEnglish
Pages (from-to)1105-1111
Number of pages7
JournalEuropean Heart Journal
Issue number7
Publication statusPublished - 2005

Cite this