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Physics

New discovery sheds light on how muscles respond to exercise

Researchers have found that activating a specific part of the AMPK protein is crucial for efficient energy use during physical activity.

Illustration: Blue Dot News

1 min read

In the quiet moments between breaths, our bodies whisper secrets to us. The whispers of tired muscles, creaking with fatigue, or the rush of endorphins as we push ourselves to new limits. These whispers are not just sounds; they're a language that tells us how our bodies work and what makes them tick.

A team of researchers recently unraveled one of these secrets using a powerful tool called CRISPR-Cas9. They created mice with a special mutation in their cells, which made it impossible for the protein Ampkα2 to be activated. This protein is like an energetic sensor that helps our muscles know when they need more energy and how to get it. The researchers found that these mice had trouble getting enough oxygen and energy during exercise, and their muscles didn't recover as quickly as usual.

What's remarkable about this discovery is not just the fact that scientists figured out what was going on in these mice, but also how it relates to our own bodies. It turns out that Ampkα2 T172 activation plays a crucial role in helping us perform exercise and get energy from the food we eat. This could have big implications for people with type 2 diabetes, who struggle with managing their blood sugar levels.

The people behind the work

  • Montalvo RN et al.

    Author

    Published in Science advances

Source: Science advances

Sources & Verification

Every statement in this story is drawn from the facts below. Each is linked to a primary or reputable source — follow any citation to check it for yourself.

  1. Adenosine 5'-monophosphate-activated protein kinase (AMPK) is an energetic sensor for metabolic regulation and integration. Science advances
  2. Here, we used CRISPR-Cas9 to generate nonactivatable Ampkα knock-in (KI) mice with mutation of threonine-172 phosphorylation site to alanine (T172A), circumventing the limitations of previous genetic interventions that disrupt the protein stoichiometry. Science advances
  3. KI mice of Ampkα2, but not Ampkα1, demonstrated phenotypic changes with increased fat-to-lean mass, impaired endurance exercise capacity, and diminished mitochondrial maximal respiration and conductance in skeletal muscle. Science advances
  4. Integrated temporal multiomics analysis (proteomics/phosphoproteomics/metabolomics) in skeletal muscle at rest and during exercise establishes a pleiotropic yet imperative role of Ampkα2 T172 activation for glycolytic and oxidative metabolism, mitochondrial respiration, and contractile function. Science advances
  5. There is a substantial overlap of skeletal muscle proteomic changes in Ampkα2 T172A KI mice with that of patients with type 2 diabetes. Science advances
  6. Our findings suggest that Ampkα2 T172 activation is critical for exercise performance and energy transduction in skeletal muscle and may serve as a therapeutic target for type 2 diabetes. Science advances

Part of the Blue Dot News 2026 retrospective — an archive reconstructed automatically from the published scientific record. The science is real and cited above; this is not original daily reporting, and it is deliberately kept out of the live news feed.

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