The Claim
In human skeletal muscle mitochondria during prolonged aerobic exercise, the specific inhibitor sulfo-N-succinimidyl oleate (SSO) reduces palmitate oxidation by approximately 80%, demonstrating that fatty acid translocase CD36 is functionally required for long-chain fatty acid transport into mitochondria.
What the research says
Supports is higher
Support is ahead, but a single strong opposing study can change this.
These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.
During prolonged aerobic exercise, blocking the CD36 protein in human muscle mitochondria reduces the breakdown of palmitate, a long-chain fatty acid, by about 80%, indicating that CD36 is necessary for transporting this fatty acid into mitochondria.
See the scientific wording
In human skeletal muscle mitochondria during prolonged aerobic exercise, the specific inhibitor sulfo-N-succinimidyl oleate (SSO) reduces palmitate oxidation by approximately 80%, demonstrating that fatty acid translocase CD36 is functionally required for long-chain fatty acid transport into mitochondria.
During prolonged aerobic exercise, fat molecules move into the energy-producing parts of muscle cells by hitching a ride on a protein called CD36 that moves to the surface of those energy factories. This protein grabs the fat and delivers it to the machinery that breaks it down for energy. When this protein is blocked, fat burning drops by 80%, proving it is essential for the process.
What the research says
1 studyWhen scientists blocked a protein called CD36 in muscle cells during exercise, fat burning dropped by about 80%, proving that CD36 is needed to move fat into the cell’s energy factories. Without it, the muscles can’t burn fat as well.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting studies
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