Tension-dependent (TDH) and tension-independent heat (TIH) release were measured during single isovolumetric contractions in the arterially perfused rat ventricle. Under perfusion with 7 mM K-0.5 mM Ca, TDH showed only one component (H₃), whereas TIH could be divided into two components (H₁ and H₂) of short evolution (similar to the classically identified activation heat) and one component (H₄) of long duration (dependent on mitochondrial respiration). Under 25 mM K, TIH components (i.e., H₁, H₂, and H₄) increased with the increase in extracellular Ca concentration ([Ca]_o) from 0.5 to 4 mM, and H₃ correlated with pressure at all [Ca]_o, with regression parameters similar to those observed under 7 mM K. Under 25 mM K-2 mM Ca, peak pressure development (P), H₁, H₂, and H₃, plotted against the number of beats under 0.4 µM verapamil, exponentially decreased, but H₄ decreased to 5.5 ± 2.9% in the first contraction and remained constant thereafter. Under hypoxia, P, H₁, H₂, and H₃ progressively decreased for about six contractions, but H₄ was not detectable from the second contraction. The results suggest that increasing extracellular K concentration decreases contractile economy mainly by increasing energy expenditure related to a Ca-dependent (verapamil-sensitive) mitochondrial activity that is not related to force generation.