Glutaminolysis Shapes Cardiac Resilience to Stress via Mitochondrial Glutathione.

Glutaminolysis rapidly mobilizes during acute β-adrenergic stress in mouse hearts to supply mitochondrial glutathione, preserving redox balance and sustaining contractile reserve.

• Why it matters: Cardiac reserve predicts cardiovascular outcomes, but the metabolic pathways that let the heart adapt to stress are not well defined.
• What they did: In mice with cardiomyocyte-specific glutaminase deletion, echocardiography under β-adrenergic stimulation and [U-13C] glutamine tracing in Langendorff-perfused hearts tested glutaminolysis’s role; a randomized double-blind placebo-controlled crossover trial assessed acute glutamine supplementation in healthy volunteers (ChiCTR2400082676).
• The result: Glutaminase-deficient mice showed impaired contractile reserve and exercise capacity with failure to raise mitochondrial glutathione and increased mitochondrial oxidative stress, while acute oral glutamine improved reserve on exercise stress echocardiography in humans.

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