Chemoreceptor hyperactivity in heart failure: is lactate the culprit?

we propose that in patients with HF, the blunted cardiac output during exercise results in inadequate oxygen delivery to working muscle, and earlier anaerobic metabolism which increase both lactate production and H+ and both are stimulus that augment the ventilatory drive and induce an early reduction of PaCO2 tensions.

The link between lactate and hyperventilation is further supported by the demonstration that a reduction of arterial lactate concentration throughout exercise is associated with a reduction of ventilatory response to exercise in patients with HF after 2 months of exercise training.10 Also, reduction of blood lactate concentrations by dichloroacetate administration is associated with an improvement of myocardial function in patients with HF.

We recognize that the documentation of the correlation between blood lactate concentration and VE/VCO2 slope during exercise in HF does not prove a cause-effect relationship. Accordingly, the present report should be considered only as hypothesis generating but this fascinating hypothesis has a strong physiological background but needs to be confirmed by dedicated studies.