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Onset exercise hyperaemia in humans: partitioning the contributors.
D Walter Wray1, Anthony J Donato, Abhimanyu Uberoi
1Department of Medicine, Physiology Division, 9500 Gilman Drive, University of California San Diego, La Jolla, CA 92093-0623, USA. dwray@ucsd.edu
The Journal of Physiology
|April 30, 2005
Summary
At exercise onset, heart rate increases and mechanical forces, not just the muscle pump, boost leg blood flow. Steady blood flow matches muscle needs during voluntary exercise.
Area of Science:
- Exercise Physiology
- Cardiovascular Regulation
- Skeletal Muscle Metabolism
Background:
- Understanding the mechanisms driving increased leg blood flow (LBF) at exercise onset is crucial for exercise physiology.
- Previous research has focused on the roles of cardiac output, vasodilation, and the skeletal muscle pump.
Purpose of the Study:
- To differentiate the contributions of mechanical, vasodilatory, and cardiac factors to the rapid increase in leg blood flow during dynamic knee-extensor exercise.
- To investigate the time course and magnitude of these contributions.
Main Methods:
- Utilized a reductionist approach comparing voluntary and passive knee-extensor exercise in seated and supine positions.
- Measured heart rate (HR) and leg blood flow (LBF) using ultrasound Doppler.
- Manipulated conditions to minimize the skeletal muscle pump and metabolic influences.
Main Results:
- Passive exercise, with minimized skeletal muscle pump, still elicited significant cardio-acceleration and leg hyperemia.
- Initial arterial inflow may exceed leg vasodilation in the first seconds of passive exercise.
- Steady-state LBF remained elevated during voluntary exercise but returned to baseline during passive movement.
Conclusions:
- Cardio-acceleration (tachycardia) and non-pump mechanical forces contribute to reduced vascular resistance and increased LBF at exercise onset.
- Steady-state LBF appears to be regulated by muscle metabolic demand during voluntary exercise.