Regulation of the skeletal muscle blood flow in humans.
Level 5 - mechanism / opinion, no new human data
Narrative review of physiological mechanisms without systematic methodology or primary human data.
PubMed 25192730 · doi:10.1113/expphysiol.2014.081620
What was done
This narrative review summarizes existing evidence on the mechanisms governing human skeletal muscle blood flow regulation during exercise, focusing on the interplay between locally generated vasodilators (nitric oxide and prostaglandins) and purinergic signaling via ATP and adenosine in both plasma and the interstitial space.
What was found
The abstract reports no numerical values or effect sizes. It qualitatively describes that plasma ATP rises in both arterial inflow and venous outflow of contracting muscle, where it stimulates nitric oxide and prostaglandin formation and counteracts sympathetic vasoconstriction. Interstitial concentrations of both ATP and adenosine increase in close correlation with blood flow changes, though plasma adenosine does not increase during exercise. ATP in the interstitium may additionally trigger vasoconstriction and stimulate afferent nerves that increase sympathetic outflow. The exact contribution of ATP remains unconfirmed because specific purinergic receptor antagonists for human administration are unavailable.
Why it matters
It outlines how local vascular signaling coordinates exercise hyperemia and metabolic sympatholysis, clarifying the physiological roles and site-specific actions of adenosine and ATP in human muscle.
Limits
The paper is a non-systematic narrative review providing no quantitative synthesis, sample sizes, or study selection criteria. Inferences regarding interstitial and intravascular ATP mechanisms in humans are constrained by the absence of selective purinergic receptor blockers safe for human experimentation.
Cited by
- supports During intense dynamic exercise, red blood cells, blood vessels, and skeletal muscle release ATP and ADP, which act as potent vasodilators causing local functional sympatholysis.