Sympathetic influence on cerebral blood flow and metabolism during exercise in humans

Activation-induced increase in cerebral blood flow is coupled to enhanced metabolic activity, maybe with brain tissue redox state and oxygen tension as key modulators. To evaluate this hypothesis at the onset of exercise in humans, blood was sampled at 0.1 to 0.2 Hz from the radial artery and right internal jugular vein, while middle cerebral artery mean flow velocity (MCA Vmean) was recorded. Both the arterial and venous lactate-to-pyruvate ratio increased after 10 s ( P < 0.05), and the arterial ratio remained slightly higher than the venous ( P < 0.05). The calculated average cerebral capillary oxygen tension decreased by 2.7 mmHg after 5 s ( P < 0.05), while MCA Vmean increased only after 30 s. Furthermore, there was an unaccounted cerebral carbohydrate uptake relative to the uptake of oxygen that became significant 50 s after the onset of exercise. These findings support brain tissue redox state and oxygenation as potential modulators of an increase in cerebral blood flow at the onset of exercise.

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Partial pharmacologic blockade demonstrates sympathetic influence on the phase angle between oscillations in blood pressure and cerebral blood flow modulation

Autonomic Neuroscience ◽

10.1016/j.autneu.2015.07.135 ◽

2015 ◽

Vol 192 ◽

pp. 96

Author(s):

M.J. Hilz ◽

H. Marthol ◽

A. Tillmann ◽

S. Riss ◽

P. Hauck ◽

...

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Phase Angle ◽

Flow Modulation ◽

Sympathetic Influence

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Cerebral blood flow during submaximal and maximal dynamic exercise in humans

Journal of Applied Physiology ◽

10.1152/jappl.1989.67.2.744 ◽

1989 ◽

Vol 67 (2) ◽

pp. 744-748 ◽

Cited By ~ 73

Author(s):

S. N. Thomas ◽

T. Schroeder ◽

N. H. Secher ◽

J. H. Mitchell

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Mean Arterial Pressure ◽

Cycle Ergometer ◽

Dynamic Exercise ◽

Initial Slope ◽

O2 Uptake ◽

Male And Female ◽

Median Increase ◽

Exercise In Humans

Cerebral blood flow (CBF) in humans was measured at rest and during dynamic exercise on a cycle ergometer corresponding to 56% (range 27–85) of maximal O2 uptake (VO2max). Exercise bouts were performed by 16 male and female subjects, lasted 15 min each, and were carried out in a semisupine position. CBF (133Xe clearance) was expressed as the initial slope index (ISI) and as the first compartment flow (F1). CBF at rest [ISI, 58 (range 45–73); F1, 76 (range 55–98) ml.100 g-1.min-1] increased during exercise [ISI to 79 (57–94) and F1 to 118 (75–164) ml.100 g-1.min-1, P less than 0.01]. CBF did not differ significantly between work loads from 32 (24–33) to 86% (74–96) of VO2max (n = 10). During exercise, mean arterial pressure increased from 84 (60–100) to 101 (78–124) Torr (P less than 0.01) and PCO2 remained unchanged [5.1 (4.6–5.6) vs. 5.4 (4.4–6.3) kPa, n = 6]. These results demonstrate a median increase of 31% (0–87) in CBF by ISI and a median increase of 58% (0–133) in CBF by F1 during dynamic exercise in humans.

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Effects of hyperthermia on cerebral blood flow and metabolism during prolonged exercise in humans

Journal of Applied Physiology ◽

10.1152/japplphysiol.00049.2002 ◽

2002 ◽

Vol 93 (1) ◽

pp. 58-64 ◽

Cited By ~ 127

Author(s):

Lars Nybo ◽

Kirsten Møller ◽

Stefanos Volianitis ◽

Bodil Nielsen ◽

Niels H. Secher

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Metabolic Rate ◽

Core Temperature ◽

Prolonged Exercise ◽

Cerebral Metabolism ◽

Cycle Ergometer ◽

Carbon Dioxide Tension ◽

Cerebral Metabolic Rate ◽

Exercise In Humans

The development of hyperthermia during prolonged exercise in humans is associated with various changes in the brain, but it is not known whether the cerebral metabolism or the global cerebral blood flow (gCBF) is affected. Eight endurance-trained subjects completed two exercise bouts on a cycle ergometer. The gCBF and cerebral metabolic rates of oxygen, glucose, and lactate were determined with the Kety-Schmidt technique after 15 min of exercise when core temperature was similar across trials, and at the end of exercise, either when subjects remained normothermic (core temperature = 37.9°C; control) or when severe hyperthermia had developed (core temperature = 39.5°C; hyperthermia). The gCBF was similar after 15 min in the two trials, and it remained stable throughout control. In contrast, during hyperthermia gCBF decreased by 18% and was therefore lower in hyperthermia compared with control at the end of exercise (43 ± 4 vs. 51 ± 4 ml · 100 g−1· min−1; P < 0.05). Concomitant with the reduction in gCBF, there was a proportionally larger increase in the arteriovenous differences for oxygen and glucose, and the cerebral metabolic rate was therefore higher at the end of the hyperthermic trial compared with control. The hyperthermia-induced lowering of gCBF did not alter cerebral lactate release. The hyperthermia-induced reduction in exercise cerebral blood flow seems to relate to a concomitant 18% lowering of arterial carbon dioxide tension, whereas the higher cerebral metabolic rate of oxygen may be ascribed to a Q10(temperature) effect and/or the level of cerebral neuronal activity associated with increased exertion.

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