Ultrasound in medicine & biology · 2026
Low-Intensity Pulsed Ultrasound (LIPUS) Mitigates Exercise-Induced Myocardial Fatigue by Optimizing Glucose Oxidation Via the Aldolase/AMPK/PDH Signaling Axis.
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Liu Xindong, Liu Yuting, Gao Yushuo, Yi Ziyi, Zhao Nannan, Cai Hua, Li Min, Xu Lin
Аннотация
BACKGROUND: Myocardial energy deficiency is a key bottleneck limiting exercise endurance. Low-intensity pulsed ultrasound (LIPUS) has emerged as a non-invasive metabolic regulator. This study investigates whether LIPUS can activate glucose-centric pathways to alleviate exercise-induced myocardial fatigue.
METHODS: Sprague-Dawley rats were subjected to a 4-week exhaustive swimming protocol. LIPUS (1 MHz, 30 mW/cm², 20% duty cycle) was administered precordially for 30 min/day. We assessed exercise tolerance, cardiac injury markers (cTnI, NT-proBNP), mitochondrial ultrastructure, and metabolic flux. The activation of the Aldolase/AMPK/PDH axis was evaluated via Western blot and qPCR.
RESULTS: LIPUS treatment significantly prolonged exhaustive swimming time and reduced serum injury markers. Ultrastructural analysis revealed preserved mitochondrial cristae and myofiber alignment in LIPUS-treated hearts. Mechanistically, LIPUS promoted a metabolic switch from anaerobic glycolysis to efficient glucose aerobic oxidation by upregulating Aldolase and p-AMPK while reducing inhibitory PDH phosphorylation. Mitochondrial TCA cycle and respiratory chain activities (Complexes I-IV) were systematically restored.
CONCLUSIONS: LIPUS enhances myocardial glucose oxidation efficiency and exercise endurance by activating the Aldolase/AMPK/PDH signaling axis. These findings highlight LIPUS as a promising non-pharmacological strategy for exercise-induced cardioprotection.
METHODS: Sprague-Dawley rats were subjected to a 4-week exhaustive swimming protocol. LIPUS (1 MHz, 30 mW/cm², 20% duty cycle) was administered precordially for 30 min/day. We assessed exercise tolerance, cardiac injury markers (cTnI, NT-proBNP), mitochondrial ultrastructure, and metabolic flux. The activation of the Aldolase/AMPK/PDH axis was evaluated via Western blot and qPCR.
RESULTS: LIPUS treatment significantly prolonged exhaustive swimming time and reduced serum injury markers. Ultrastructural analysis revealed preserved mitochondrial cristae and myofiber alignment in LIPUS-treated hearts. Mechanistically, LIPUS promoted a metabolic switch from anaerobic glycolysis to efficient glucose aerobic oxidation by upregulating Aldolase and p-AMPK while reducing inhibitory PDH phosphorylation. Mitochondrial TCA cycle and respiratory chain activities (Complexes I-IV) were systematically restored.
CONCLUSIONS: LIPUS enhances myocardial glucose oxidation efficiency and exercise endurance by activating the Aldolase/AMPK/PDH signaling axis. These findings highlight LIPUS as a promising non-pharmacological strategy for exercise-induced cardioprotection.