Sympathetic outflow to the skeletal muscle in humans increases during prolonged light exercise

M Saito, R Sone, M Ikeda… - Journal of Applied …, 1997 - journals.physiology.org
M Saito, R Sone, M Ikeda, T Mano
Journal of Applied Physiology, 1997journals.physiology.org
Saito, Mitsuru, Ryoko Sone, Masao Ikeda, and Tadaaki Mano. Sympathetic outflow to the
skeletal muscle in humans increases during prolonged light exercise. J. Appl. Physiol. 82
(4): 1237–1243, 1997.—To investigate the effects of exercise duration on muscle
sympathetic nerve activity (MSNA), heart rate, blood pressure (BP), tympanic temperature,
blood lactate concentration, and thigh electromyogram were measured in eight volunteers
during 30 min of cycling in the sitting position at an intensity of 40% of maximal oxygen …
Saito, Mitsuru, Ryoko Sone, Masao Ikeda, and Tadaaki Mano.Sympathetic outflow to the skeletal muscle in humans increases during prolonged light exercise. J. Appl. Physiol. 82(4): 1237 – 1243, 1997.—To investigate the effects of exercise duration on muscle sympathetic nerve activity (MSNA), heart rate, blood pressure (BP), tympanic temperature, blood lactate concentration, and thigh electromyogram were measured in eight volunteers during 30 min of cycling in the sitting position at an intensity of 40% of maximal oxygen uptake. MSNA burst frequency increased 18 min after exercise was begun (25 ± 4 bursts/min at baseline and 36 ± 5 bursts/min at 21 min of exercise), reaching 41 ± 5 bursts/min at the end of exercise. Heart rate and systolic BP increased during exercise. Twenty minutes after commencement of exercise, however, both systolic and diastolic BP values tended to drop compared with the initial period of exercise. Tympanic temperature increased in a time-dependent manner, and the increment was significant 12 min after exercise was begun. Blood lactate concentration and integrated electromyogram showed no significant changes during exercise. The increased MSNA during prolonged light-intensity exercise may be a secondary effect of the drop in BP as a result of blood redistribution caused by thermoregulation rather than by metaboreflex.
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