Muscle blood f low at onset of dynamic exercise in humans.

نویسندگان

  • G Rådegran
  • B Saltin
چکیده

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 ∼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 (∼15% of peak power output), two-component (∼40-70% of peak power output), or three-component exponential model (≥75% of peak power output), whereQ˙( t) =Q˙passive+ ΔQ˙1 ⋅ [1 - e -( t- TD1/τ1)] + ΔQ˙2 ⋅ [1 - e -( t - TD2/τ2)] + ΔQ˙3 ⋅ [1 - e -( t - TD3/τ3)]; Q˙passive, the blood flow during passive leg movement, equals 1.17 ± 0.11 l/min; TD is the onset latency; τ is the time constant; ΔQ˙ 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 ∼2.2-8.9 s. The blood flow leveled off after ∼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.

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عنوان ژورنال:
  • American journal of physiology. Heart and circulatory physiology

دوره 274 1  شماره 

صفحات  -

تاریخ انتشار 1998