Abstract
This study investigated the role of opioid receptor (OR) subtypes as a mechanism by which endurance exercise promotes cardioprotection against myocardial ischemia-reperfusion (IR) injury. Wistar rats were randomly divided into one of seven experimental groups: 1) control; 2) exercise-trained; 3) exercise-trained plus a non-selective OR antagonist; 4) control sham; 5) exercise-trained plus a kappa OR antagonist; 6) exercise-trained plus a delta OR antagonist; and 7) exercise-trained plus a mu OR antagonist. The exercised animals underwent 4 consecutive days of treadmill training (60 min/day at ∼70% of maximal oxygen consumption). All groups except the sham group were exposed to an in vivo myocardial IR insult, and the myocardial infarct size (IS) was determined histologically. Myocardial capillary density, OR subtype expression, heat shock protein 72 (HSP72) expression, and antioxidant enzyme activity were measured in the hearts of both the exercised and control groups. Exercise training significantly reduced the myocardial IS by approximately 34%. Pharmacological blockade of the kappa or mu OR subtypes did not blunt exercise-induced cardioprotection against IR-mediated infarction, whereas treatment of animals with a non-selective OR antagonist or a delta OR antagonist abolished exercise-induced cardioprotection. Exercise training enhanced the activities of myocardial superoxide dismutase (SOD) and catalase but did not increase the left ventricular capillary density or the mRNA levels of HSP72, SOD, and catalase. In addition, exercise significantly reduced the protein expression of kappa and delta ORs in the heart by 44% and 37%, respectively. Together, these results indicate that ORs contribute to the cardioprotection conferred by endurance exercise, with the delta OR subtype playing a key role in this response.
Highlights
The concept that regular exercise is cardioprotective against ischemia-reperfusion (IR) cardiac injury is well established in animal models [1], [2], and human epidemiological studies suggest that physically active individuals are protected against IR-induced myocardial injury [3,4,5]
Ischemia produced a significant decrease in systolic, mean and diastolic arterial pressure 5 min after coronary ligation in all groups compared with the sham group (Table 2)
It is well established that regular bouts of endurance exercise result in cardioprotection against IR injury, the mechanisms responsible for this cardioprotection remain under debate
Summary
The concept that regular exercise is cardioprotective against ischemia-reperfusion (IR) cardiac injury is well established in animal models [1], [2], and human epidemiological studies suggest that physically active individuals are protected against IR-induced myocardial injury [3,4,5]. Specific mechanisms that may be responsible for exercise-induced cardioprotection include the following: (a) increased nitric oxide production and cardiac antioxidant capacity [2], [7,8,9,10,11]; (b) expansion of the coronary capillary network and enlargement of the coronary artery diameter [2], [7]; (c) increased production of heat shock proteins (HSP) [2], [7], [8]; (d) reduced production of reactive oxygen species (ROS) in myocardial mitochondria during IR [7], [12]; and (e) improved function of sarcolemmal and/or mitochondrial ATP-sensitive potassium channels (sarco/mito K+ ATP channels) [7], [8]
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