Noradrenaline spillover during exercise in active versus resting skeletal muscle in man

Abstract

Increases in plasma noradrenaline (NA) concentration occur during moderate to heavy exercise in man. This study was undertaken to examine the spillover of NA from both resting and contracting skeletal muscle during exercise. Six male subjects performed one-legged knee-extension so that all measurements could be made both in the exercising and in the resting leg. Subjects exercised for 10 min at each of 50% and 100% of the peak performance capacity of the leg. Leg blood flow was measured by thermodilution and blood samples were drawn for the determination of plasma NA and adrenaline, first in the resting leg and then in the exercising leg. To calculate NA spillover, the extraction of NA (NAe) or of adrenalin (Ae) is required: NAe was measured by repeating the experiment under constant [3H]NA infusion following a 40-min rest period. During exercise, NA spillover was significantly larger in the exercising leg than in the resting leg both during 50% and 100% leg exercise. These results suggest that contracting skeletal muscle may contribute to a larger extent than resting skeletal muscle to increasing the level of plasma NA during exercise. Contractile activity may influence the NA spillover from skeletal muscle by a presynaptic and/or postsynaptic influence on the sympathetic nervous activity to this tissue.

Coherence between the sympathetic drives to relaxed and contracting muscles of different limbs of human subjects.

“…There has been no previous study of changes in MSA to contracting muscles, but one study of noradrenaline spillover led to the opposite conclusions (Savard et al 1987). However, that study involved dynamic (rather than static) contractions of a large muscle mass performed at 50-100 % of maximal power for 10-20 min.…”

“…Strong dynamic contractions of thigh muscles to 50-100% of maximum result in increased noradrenaline spillover to blood from the working muscle (e.g. Savard, Strange, Kiens, Richter, Christensen & Saltin, 1987), suggesting an increase in sympathetically mediated vasoconstrictor tone. Similarly, studies in intact rats and following acute sympathectomy suggest that, during locomotion, hindlimb blood flow and the flow to individual exercising muscles are under active sympathetic control (Peterson, Armstrong & Laughlin, 1988).…”

Transient hyperpolarization of non‐contracting muscle fibres in anaesthetized rats.

“…This signal cannot be extracellular [K+], since raising the latter in a resting muscle does not induce HRs , and it would appear that some other signal must be involved (see also Savard et al 1987). In addition, it is possible that there are pump stimulants other than intracellular [Na+], in the contracting fibres, and noradrenaline; in this context, Clausen & Andersen (1991) have recently suggested that calcitonin gene-related peptide, released from motor nerve terminals, may be a factor.…”

Neural control of muscle blood flow during exercise

“…This resetting occurs without a change in sensitivity so that the baroreflex continues to modulate SNA in response to changes in blood pressure during exercise (25,63,76). These respective signaling pathways evoke specific changes in regional autonomic outflows during exercise, such that central command increases sympathetic discharge to skin and the heart (96, 97), whereas stimulation of the muscle metaboreceptors increases sympathetic discharge to both resting and exercising skeletal muscle (36,48,75,96). Taken together, these findings raise an important question: what is the functional consequence of increased sympathetic nerve activity in exercising muscle?…”