Year: 1998
Type: article
Abstract: To evaluate the temporal relationship between blood flow, blood pressure, and muscle contractions, we continuously measured femoral arterial inflow with ultrasound Doppler at onset of passive exercise and voluntary, one-legged, dynamic knee-extensor exercise in humans. Blood velocity and inflow increased (P < 0.006) with the first relaxation of passive and voluntary exercise, whereas the arterial-venous pressure difference was unaltered [P = not significant (NS)]. During steady-state exercise, and with arterial pressure as a superimposed influence, blood velocity was affected by the muscle pump, peaking (P < 0.001) at approximately 2.5 +/- 0.3 m/s as the relaxation coincided with peak systolic arterial blood pressure; blood velocity decreased (P < 0.001) to 44.2 +/- 8.6 and 28.5 +/- 5.5% of peak velocity at the second dicrotic and diastolic blood pressure notches, respectively. Mechanical hindrance occurred (P < 0.001) during the contraction phase at blood pressures less than or equal to that at the second dicrotic notch. The increase in blood flow (Q) was characterized by a one-component (approximately 15% of peak power output), two-component (approximately 40-70% of peak power output), or three-component exponential model (> or = 75% of peak power output), where Q(t) = Qpassive + delta Q1.[1 - e-(t - TD1/tau 1)]+ delta Q2.[1 - e-(t - TD2/tau 2)]+ delta Q3.[1 - e-(t - TD3/tau 3)]; Qpassive, the blood flow during passive leg movement, equals 1.17 +/- 0.11 l/min; TD is the onset latency; tau is the time constant; delta Q is the magnitude of blood flow rise; and subscripts 1-3 refer to the first, second, and third components of the exponential model, respectively. The time to reach 50% of the difference between passive and voluntary asymptotic blood flow was approximately 2.2-8.9 s. The blood flow leveled off after approximately 10-150 s, related to the power outputs. It is concluded that the elevation in blood flow with the first duty cycle(s) is due to muscle mechanical factors, but vasodilators initiate a more potent amplification within the second to fourth contraction.
Authors: G. Rådegran, B. Saltin
Institutions: Rigshospitalet, Copenhagen Muscle Research Centre
Language: English
Subfield: Physiology (medical)
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
Funder: Rigshospitalet
OpenAlex ID: W2158696769