title: Skeletal muscle blood flow in humans and its regulation during exercise.
abstract: Regional limb blood flow has been measured with dilution techniques (cardio-green or thermodilution) and ultrasound Doppler. When applied to the femoral artery and vein at rest and during dynamical exercise these methods give similar reproducible results. The blood flow in the femoral artery is approximately 0.3 L min(-1) at rest and increases linearly with dynamical knee-extensor exercise as a function of the power output to 6-10 L min[-1] (Q= 1.94 + 0.07 load). Considering the size of the knee-extensor muscles, perfusion during peak effort may amount to 2-3 L kg(-1) min(-1), i.e. approximately 100-fold elevation from rest. The onset of hyperaemia is very fast at the start of exercise with T 1/2 of 2-10 s related to the power output with the muscle pump bringing about the very first increase in blood flow. A steady level is reached within approximately 10-150 s of exercise. At all exercise intensities the blood flow fluctuates primarily due to the variation in intramuscular pressure, resulting in a phase shift with the pulse pressure as a superimposed minor influence. Among the many vasoactive compounds likely to contribute to the vasodilation after the first contraction adenosine is a primary candidate as it can be demonstrated to (1) cause a change in limb blood flow when infused i.a., that is similar in time and magnitude as observed in exercise, and (2) become elevated in the interstitial space (microdialysis technique) during exercise to levels inducing vasodilation. NO appears less likely since NOS blockade with L-NMMA causing a reduced blood flow at rest and during recovery, it has no effect during exercise. Muscle contraction causes with some delay (60 s) an elevation in muscle sympathetic nerve activity (MSNA), related to the exercise intensity. The compounds produced in the contracting muscle activating the group IIl-IV sensory nerves (the muscle reflex) are unknown. In small muscle group exercise an elevation in MSNA may not cause vasoconstriction (functional sympatholysis). The mechanism for functional sympatholysis is still unknown. However, when engaging a large fraction of the muscle mass more intensely during exercise, the MSNA has an important functional role in maintaining blood pressure by limiting blood flow also to exercising muscles.
authors.affiliation: The Copenhagen Muscle Research Centre, Rigshospitalet, Tagensvei, Denmark.
authors.forename: B
authors.initials: B
authors.lastname: Saltin
authors.forename: G
authors.initials: G
authors.lastname: Rådegran
authors.forename: M D
authors.initials: MD
authors.lastname: Koskolou
authors.forename: R C
authors.initials: RC
authors.lastname: Roach
mesh_terms: D006801:Humans; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000294:innervation / Q000502:physiology*; D005082:Physical Exertion / Q000502:physiology*; D012039:Regional Blood Flow / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology; D014664:Vasodilation / Q000502:physiology*