ArticleFrontiers in physiology2013
Have we missed that neural vasodilator mechanisms may contribute to exercise hyperemia at onset of voluntary exercise?
Article in Frontiers in physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Effect of contralateral limb exercise on peripheral perfusion index in a resting limb.The Indian journal of medical research · 2025Article
- Local alternating heat and cold stimulation affects hemodynamics and oxygenation in fatigued muscle tissue and autonomic nervous activity: a single-arm interventional study.Journal of physiological anthropology · 2024Article
- Central command increases muscular oxygenation of the non-exercising arm at the early period of voluntary one-armed cranking.Physiological reports · 2017Article
- Acetylcholine released by endothelial cells facilitates flow-mediated dilatation.The Journal of physiology · 2016Article
- Regulation of increased blood flow (hyperemia) to muscles during exercise: a hierarchy of competing physiological needs.Physiological reviews · 2015Review
- Differential contribution of ACh-muscarinic and β-adrenergic receptors to vasodilatation in noncontracting muscle during voluntary one-legged exercise.Physiological reports · 2014Article
- Evidence for centrally induced cholinergic vasodilatation in skeletal muscle during voluntary one-legged cycling and motor imagery in humans.Physiological reports · 2013Article
- Neural control of the circulation during exercise in health and disease.Frontiers in physiology · 2013Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Whether neurally-mediated vasodilatation may contribute to exercise hyperemia has not been completely understood. Bülbring and Burn (1935) found for the first time the existence of sympathetic cholinergic nerve to skeletal muscle contributing to vasodilatation in animals. Blair et al. (1959) reported that atropine-sensitive vasodilatation in skeletal muscle appeared during arousal behavior or mental stress in humans. However, such sympathetic vasodilator mechanism for muscle vascular bed in humans is generally denied at present, because surgical sympathectomy, autonomic blockade, and local anesthesia of sympathetic nerves cause no substantial influence on vasodilatation in muscle not only during mental stress but also during exercise. On the other hand, neural mechanisms may play an important role in regulating blood flow to non-contracting muscle. Careful consideration of the neural mechanisms may lead us to an insight about a possible neural mechanism responsible for exercise hyperemia in contracting muscle. Referring to our recent study measuring muscle tissue blood flow with higher time resolution, this review has focused on whether or not central command may transmit vasodilator signal to skeletal muscle especially at the onset of voluntary exercise.
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