Aims: This study aimed to evaluate the kinetics of lactate and lactate dehydrogenase B (LDH-B) protein levels as well as the maximum effort capacity of spontaneously hypertensive rats (SHRs) with experimental acute myocardial infarction (AMI). Methods: thirty-two SHRs were divided into (n=8/group): S (sham), SE (sham+exercise), I (AMI), and IE (AMI+exercise). A maximum exercise test (treadmill) was evaluated before AMI or sham surgery. Echocardiography was performed 48h after the surgery. Lactacidemia was assessed at rest and during an intense exercise bout (48h after echocardiography). A two-way ANOVA followed by the post-hoc (Bonferroni) test was used, p<0.05. Results: In the end, the heart was removed for analysis of LDH-B. AMI resulted in lower cardiac output (S vs I: ∆51.3%, p<0.001), ejection fraction (S vs I: ∆60.5%, p<0.001) and shortening fraction (S vs I: ∆72.4%, p<0.001). The IE showed a reduction in exercise capacity when compared with pre-AMI values (1.50±0.1 vs 1.38±0.2 km/h; p=0.030) but not when compared with SE (1.41±0.3 vs 1.38±0.2 km/h; p=0.208). During the exhaustion exercise session, IE group showed lower lactacidemia at 12 min (∆9.7%, p=0.042) and 18 min (∆8.3%, p=0.038). No differences were observed in the protein level of LDH-B among the groups (p=0.573). However, when the AMI factor was considered alone, LDH-B expression was lower (sham vs AMI rats, p=0.040). Conclusion: LDH-B protein levels in cardiac tissue appear to be associated with AMI only. Furthermore, AMI induced a reduction in exercise capacity but did not affect lactacidemia during the intense exercise bout.
