Metabolic modulation of sympathetic vasoconstriction in human skeletal muscle: role of tissue hypoxia
Article first published online: 12 AUG 2004
The Journal of Physiology
Volume 527, Issue 2, pages 387–396, September 2000
How to Cite
Hansen, J., Sander, M., Hald, C. F., Victor, R. G. and Thomas, G. D. (2000), Metabolic modulation of sympathetic vasoconstriction in human skeletal muscle: role of tissue hypoxia. The Journal of Physiology, 527: 387–396. doi: 10.1111/j.1469-7793.2000.00387.x
- Issue published online: 12 AUG 2004
- Article first published online: 12 AUG 2004
- (Received 1 March 2000; accepted after revision 1 June 2000)
- 1Sympathetically evoked vasoconstriction is modulated by skeletal muscle contraction, but the underlying events are incompletely understood. During contraction, intramuscular oxygenation decreases with increasing exercise intensity. We therefore hypothesized that tissue hypoxia plays a crucial role in the attenuation of sympathetic vasoconstriction in contracting skeletal muscle.
- 2In 19 subjects, near-infrared spectroscopy was used to measure decreases in muscle oxygenation (ΔtHbO2+MbO2) as an estimate of the vasoconstrictor response to reflex sympathetic activation with lower body negative pressure (LBNP) in the microcirculation of resting and contracting forearm muscles. Oxygen delivery to the muscles was reduced by decreasing (a) arterial O2 content by breathing 10 % O2, or (b) muscle perfusion by applying forearm positive pressure (FPP, +40 mmHg).
- 3In resting forearm, reflex sympathetic activation decreased muscle oxygenation by 11 ± 1 %. Handgrip alone at 5 and 20 % of maximal voluntary contraction (MVC) decreased muscle oxygenation by 4 ± 1 and 28 ± 4 %, respectively. When superimposed on handgrip, LBNP-induced decreases in muscle oxygenation were preserved during handgrip at 5 % MVC, but were abolished during handgrip at 20 % MVC. Oral administration of aspirin (1 g) did not restore the latter response.
- 4When the decrease in forearm muscle oxygenation elicited by handgrip at 20 % MVC was mimicked by either (a) systemic hypoxia plus 5 % handgrip (ΔtHbO2+MbO2, −32 ± 3 %), or (b) hypoperfusion of resting muscle by FPP (ΔtHbO2+MbO2, −26 ± 6 %), LBNP-induced decreases in muscle oxygenation were greatly attenuated.
- 5These data suggest that local tissue hypoxia is involved in the metabolic attenuation of sympathetic vasoconstriction in the microcirculation of exercising human skeletal muscle. The specific underlying mechanism remains to be determined, although products of the cyclo-oxygenase pathway do not appear to be involved.