Passive leg movement-induced vasodilation and exercise-induced sympathetic vasoconstriction

Area of Science:

• Physiology
• Cardiovascular Regulation
• Skeletal Muscle Metabolism

Background:

• Nitric oxide (NO) plays a role in regulating blood vessel dilation.
• The interaction between NO-mediated vasodilation and sympathetic vasoconstriction in skeletal muscle is not fully understood.
• Evidence suggests sympathetic activity can limit NO-mediated vasodilation.

Purpose of the Study:

• To investigate if exercise-induced muscle sympathetic nerve activity (MSNA) attenuates passive leg movement (PLM)-induced vasodilation.
• To determine the relationship between MSNA and leg vascular conductance (LVC) during PLM with concurrent exercise.
• To clarify the role of MSNA in modulating NO-mediated vasodilation in skeletal muscle.

Main Methods:

• Nine healthy subjects performed incremental arm-cranking exercise (ACE) at 25%, 50%, and 75% of maximal capacity.
• Muscle sympathetic nerve activity (MSNA), leg blood flow (LBF), and mean arterial blood pressure (MAP) were measured.
• Leg vascular conductance (LVC) was calculated during PLM with and without ACE.

Main Results:

• MSNA significantly increased with increasing ACE intensity.
• LVC during PLM was markedly reduced with each increment in ACE intensity.
• A strong inverse relationship was observed between the increase in MSNA and the decrease in peak LVC.

Conclusions:

• Exercise-induced MSNA significantly and proportionally attenuates NO-mediated vasodilation during PLM.
• This study highlights the dominant role of MSNA in regulating skeletal muscle vascular conductance.
• Sympathetic vasoconstriction restrains NO-mediated vasodilation in skeletal muscle during exercise.