The Claim

In L6 rat myoblasts, sodium-dependent creatine uptake is inhibited by the Na,K-ATPase inhibitors ouabain or digoxin, and creatine influx increases above baseline levels following the removal of these inhibitors, indicating a potential up-regulation of creatine transport after transient inhibition.

Source: Regulation of intracellular creatine in erythrocytes and myoblasts: Influence of uraemia and inhibition of Na, K‐ATPase

What the research says

Supports is higher

Support is ahead, but a single strong opposing study can change this.

Supports
27score
Challenges
0score

These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.

How it works
1 study reviewed
In plain English

When certain heart medications are removed from rat muscle cells in a lab, the cells start taking in more creatine than before — like they're bouncing back stronger after a pause.

See the scientific wording

In L6 rat myoblasts, sodium-dependent creatine uptake is inhibited by ouabain or digoxin, but creatine influx increases above control levels after removal of these Na,K-ATPase inhibitors, suggesting up-regulation of creatine transport following transient inhibition.

What the research says

1 study

  1. Study: Regulation of intracellular creatine in erythrocytes and myoblasts: Influence of uraemia and inhibition of Na, K‐ATPase

    The study shows that when certain drugs block a cell pump in rat muscle cells, creatine uptake stops, but after removing the drugs, the cells take in even more creatine than before—just like the claim says.

Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting studies

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