PubMed HealthSearch

PubMed · 6748930

Peripheral limitations to exercise.

Abstract

We present a computer simulation of a two-compartment model of the systemic circulation which demonstrates how this model can be used to understand the mechanism(s) for the maximal exercise cardiac output (Q). The model consists of two parallel vascular channels, the splanchnic channel (all blood draining through the hepatic veins) and the peripheral channel (all other vascular beds). The distinguishing characteristic of each channel is the product of its venous compliance and venous resistance. Model parameters for the human circulation were estimated from similar parameters obtained directly from animal experiments. "Exercise" was achieved by decreasing the compliance of both channels to 40% of their initial value and by redistributing the Q such that the fraction of Q perfusing the splanchnic channel fell from 38 to 5%, while that perfusing the peripheral channel (skeletal muscles) increased from 62 to 95%. These combined changes increased Q from 4.4 to 22.0 l X min-1 and suggest that maximal adjustments of the two-compartment model parameters lead to a prediction of a maximal Q that approaches the maximal Q usually obtained by humans during exercise.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J F Green, A P Jackman. 1984. Peripheral limitations to exercise.. https://pubmed.ncbi.nlm.nih.gov/6748930/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Advanced glycosylation end products in diabetic renal and vascular disease.

An increasing body of experimental data supports the important, etiologic role of advanced glycosylation end products (AGEs) in the development of the renal and vascular complications of diabetes. Advanced glycosylation end products arise from glucose-derived Amadori products and act to increase vascular permeability, enhance protein and lipoprotein deposition, inactivate nitric oxide, and promote matrix protein synthesis and glomerular sclerosis. Loss of normal renal function increases the level of circulating plasma AGEs and contributes markedly to their ultimate tissue toxicity. Aminoguanidine, a recently developed pharmacologic inhibitor of advanced glycosylation, is presently undergoing phase II/III clinical trials in diabetic nephropathy and may offer a specific therapeutic modality for diminishing the formation and toxicity of AGEs.

Blood Circulation