DIFFERENTIAL SYMPATHETIC NEURAL CONTROL OF OXYGENATION IN RESTING ANDEXERCISING HUMAN SKELETAL-MUSCLE

Metabolic products of skeletal muscle contraction activate metaborecep tor muscle afferents that reflexively increase sympathetic nerve activ ity (SNA) targeted to both resting and exercising skeletal muscle. To determine effects of the increased sympathetic vasoconstrictor drive o n muscle oxygenation, we measured changes in tissue oxygen stores and mitochondrial cytochrome a,a(3) redox state in rhythmically contractin g human forearm muscles with near infrared spectroscopy while simultan eously measuring muscle SNA with microelectrodes. The major new findin g is that the ability of reflex-sympathetic activation to decrease mus cle oxygenation is abolished when the muscle is exercised at an intens ity > 10% of maximal voluntary contraction (MVC). During high intensit y handgrip (45% MVC), contraction-induced decreases in muscle oxygenat ion remained stable despite progressive metaboreceptor-mediated reflex increases in SNA, During mild to moderate handgrips (20-33% MVC) that do not evoke reflex-sympathetic activation, experimentally induced in creases in muscle SNA had no effect on oxygenation in exercising muscl es but produced robust decreases in oxygenation in resting muscles. Th e latter decreases were evident even during maximal metabolic vasodila tion accompanying reactive hyperemia. We conclude that in humans sympa thetic neural control of skeletal muscle oxygenation is sensitive to m odulation by metabolic events in the contracting muscles. These events are different from those involved in either metaboreceptor muscle aff erent activation or reactive hyperemia.