Acute exercise is not cardioprotective and may induce apoptotic signalling in heart surgery: a randomized controlled trial

Abstract

OBJECTIVES During open-heart surgery, the myocardium experiences ischaemia–reperfusion injury. A single bout of moderate, 30-min exercise induces preconditioning and protects the heart from ischaemia–reperfusion injury in rats, but this has never been investigated in humans. We aimed to investigate whether 1 bout of moderate exercise 24 h prior to surgery protects against mitochondrial and cardiac damage.

METHODS Patients scheduled for elective coronary artery bypass were eligible for this pilot study. Twenty were included and randomized to the treadmill exercise group (the EX group, n = 10) 24 h preoperatively or to standard presurgical procedures (control n = 10). Right atrial (RA) and left ventricular (LV) biopsies were collected immediately before and as long as possible after aortic cross-clamping to assess the primary outcome of mitochondrial respiration by respirometry, in addition to reactive oxygen species production by fluorometry and apoptotic transcripts. Cardiac troponin T and creatine kinase myocardial brain were measured in plasma at arrival, before surgery and 6 and 24 h postoperatively.

RESULTS Mitochondrial respiration was lower in the EX group after surgery in the LV (Complex I −22%, P < 0.05 and maximal −23%, P < 0.05) and the right atrium (Complex I −25%, P < 0.05). Transcript level of the apoptosis-related marker caspase 3 was increased 1.5-fold in the LV prior to surgery in the EX group when compared with the control group, P < 0.05. Cardiac troponin T was 45% higher in the EX group than in the control group 6 h postoperatively (P = 0.03), although not significant when corrected for aortic cross-clamping time.

CONCLUSIONS Results indicate that exercise did not precondition the heart against surgery-related damage. Exercise may render the myocardium and mitochondria more vulnerable to perioperative damage.