In heart failure (HF), elevated blood lactate levels, particularly during exercise or in advanced disease stages, reflect impaired tissue perfusion and altered metabolic regulation. Beyond its traditional role as a marker of anaerobic metabolism, lactate has emerged as a dynamic indicator of metabolic reserve and ventilatory control. This narrative review summarizes current evidence on lactate dynamics at rest and during exercise, highlighting their pathophysiological and clinical relevance. In HF patients, exercise-induced lactate accumulation occurs earlier and at lower workloads, reflecting impaired oxidative capacity and reduced peripheral oxygen utilization. This phenomenon is closely associated with ventilatory inefficiency, as demonstrated by the relationship between lactate levels and the VE/VCO2 slope during cardiopulmonary exercise testing (CPET). Emerging data suggest that lactate is not only a marker of disease severity but also a potential mediator of chemoreflex activation and abnormal ventilatory responses. Furthermore, both pharmacologic and non-pharmacologic interventions may influence lactate production and utilization, supporting its role as a potential tool for therapeutic monitoring. Overall, the integration of lactate assessment, particularly during exercise, into clinical evaluation may provide additional insight into disease mechanisms, improve risk stratification, and contribute to personalized therapeutic optimization in patients with HF.
Resting and Exercise Lactate Dynamics in Heart Failure: Guiding Therapeutic Optimization
Fossati, Chiara;Pigozzi, Fabio;
2026-01-01
Abstract
In heart failure (HF), elevated blood lactate levels, particularly during exercise or in advanced disease stages, reflect impaired tissue perfusion and altered metabolic regulation. Beyond its traditional role as a marker of anaerobic metabolism, lactate has emerged as a dynamic indicator of metabolic reserve and ventilatory control. This narrative review summarizes current evidence on lactate dynamics at rest and during exercise, highlighting their pathophysiological and clinical relevance. In HF patients, exercise-induced lactate accumulation occurs earlier and at lower workloads, reflecting impaired oxidative capacity and reduced peripheral oxygen utilization. This phenomenon is closely associated with ventilatory inefficiency, as demonstrated by the relationship between lactate levels and the VE/VCO2 slope during cardiopulmonary exercise testing (CPET). Emerging data suggest that lactate is not only a marker of disease severity but also a potential mediator of chemoreflex activation and abnormal ventilatory responses. Furthermore, both pharmacologic and non-pharmacologic interventions may influence lactate production and utilization, supporting its role as a potential tool for therapeutic monitoring. Overall, the integration of lactate assessment, particularly during exercise, into clinical evaluation may provide additional insight into disease mechanisms, improve risk stratification, and contribute to personalized therapeutic optimization in patients with HF.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

