Key result
High aerobic capacity in rats fails to reduce infarct size after ischemia-reperfusion due to mitochondrial loss.
Why the study?
Does the High Capacity Aerobic Running (HCR) phenotype protect against ischemia reperfusion injury compared to the Low Capacity Running (LCR) phenotype?
Does the High Capacity Aerobic Running (HCR) phenotype protect against ischemia reperfusion injury compared to the Low Capacity Running (LCR) phenotype?
Absolute Event Rate: 49.2% vs 53.7%
The intrinsic high capacity aerobic running phenotype does not appear to protect against acute tissue stressors like ischemia reperfusion, as the loss of respiratory capacity was greater than in low capacity runners.
High-capacity running phenotype confers no infarct size protection after ischemia-reperfusion in rats; leaves open mitochondrial resilience as a therapeutic target.
retention capacity, infarct size, and arrhythmogenicity, despite the increased mitochondrial capacity in the HCRs before ischemia. Relatively, the loss of respiratory capacity was actually greater in HCR than LCR. These data could suggest limits in the extent to which the HCR phenotype might be "protective" against acute tissue stressors. The extent to which any of these deficits could be "rescued" by adding an active exercise component to the intrinsic phenotype is unknown.
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Alsahly et al. (2021) studied Ischemia-reperfusion injury (n=34). High capacity aerobic running (HCR) phenotype vs. Low capacity aerobic running (LCR) phenotype was evaluated on Infarct size. Following ischemia-reperfusion injury, the augmented baseline cardiac mitochondrial capacity in high capacity aerobic running rats was lost, resulting in similar infarct sizes compared to low capacity rats.
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