Chronic psychological stressors and overconsumption of hyperpalatable foods are major risk factors in the development of cardiovascular disease, mood, and metabolic disorders. This energetic imbalance overtime results in mitochondrial dysfunction, reportedly causing reduced infarct tolerance and response to cardioprotection in the heart. However, implications of low-level and possible synergistic effects of mood and metabolic disturbances have yet to be fully elucidated in cardiac mitochondrial analyses. The study aims to investigate the effects of subclinical exposure to both chronic psychological stress (CS) and a Western diet (WD) on the cardiac mitochondrial functional response and associated mitochondrial targets.
Male C57Bl/6 mice received a control or WD (32%/57%/11% calories from fat/carbohydrates/protein) for 16 weeks, with chronic restraint stress (2 hr restraint/day) implemented in sub-sets throughout the final 2 weeks. Langendorff perfusions were performed on hearts under ischemia preconditioning (IPC) protocol or an ischemia-reperfusion protocol (non-IPC) to assess post-ischaemic myocardial functional responses. Left ventricular myocardium was homogenised and loaded into an Oroboros 02k-oxygraph to measure mitochondrial respiration or used for western blotting to assess mitochondrial protein expression.
The WD increased body weight alone and combined with CS, while CS alone had no effect. WD+CS alone worsened recovery from ischemia and limited cardioprotection, evidenced by elevated lactate dehydrogenase and reduced contractile function. IPC increased non-phosphorylating mitochondrial respiration which was attenuated by CS. This was coupled with a decrease in maximal and spare respiratory capacity although outer mitochondrial membrane was preserved in IPC treated CS hearts. Mitochondrial respiration was unchanged with WD in non- and IPC.
The combined effects of WD and CS exhibited significant myocardial injury in IPC hearts while CS appears to decrease mitochondrial functional capacity. Investigation of select mitochondrial proteins are needed to further justify the results.