Key result
Mechanical effects of muscle contraction independently elevated intravascular ATP and further augmented ATP effluent when superimposed with mild exercise compared to rest (11.6 vs 1.2 nmol/min, P<0.05).
Why the study?
Do the mechanical effects of muscle contraction increase intravascular ATP draining quiescent and active skeletal muscle in young healthy adults?
Do the mechanical effects of muscle contraction increase intravascular ATP draining quiescent and active skeletal muscle in young healthy adults?
Absolute Event Rate: 11.6% vs 1.2%
p-value: p=<0.05
Mechanical compression of skeletal muscle independently elevates intravascular ATP and further augments ATP release during mild exercise, suggesting mechanical forces contribute to exercise-induced vasodilation.
No clinical change warranted in healthy adults; leaves open mechanical ATP release as contributor to exercise vasodilation in disease.
Intravascular adenosine triphosphate (ATP) evokes vasodilation and is implicated in the regulation of skeletal muscle blood flow during exercise. Mechanical stresses to erythrocytes and endothelial cells stimulate ATP release in vitro. How mechanical effects of muscle contractions contribute to increased plasma ATP during exercise is largely unexplored. We tested the hypothesis that simulated mechanical effects of muscle contractions increase [ATP](venous) and ATP effluent in vivo, independent of changes in tissue metabolic demand, and further increase plasma ATP when superimposed with mild-intensity exercise. In young healthy adults, we measured forearm blood flow (FBF) (Doppler ultrasound) and plasma [ATP](v) (luciferin-luciferase assay), then calculated forearm ATP effluent (FBF×[ATP](v)) during rhythmic forearm compressions (RFC) via a blood pressure cuff at three graded pressures (50, 100, and 200 mmHg; Protocol 1; n = 10) and during RFC at 100 mmHg, 5% maximal voluntary contraction rhythmic handgrip exercise (RHG), and combined RFC + RHG (Protocol 2; n = 10). [ATP](v) increased from rest with each cuff pressure (range 144-161 vs. 64 ± 13 nmol/l), and ATP effluent was graded with pressure. In Protocol 2, [ATP](v) increased in each condition compared with rest (RFC: 123 ± 33; RHG: 51 ± 9; RFC + RHG: 96 ± 23 vs. Mean Rest: 42 ± 4 nmol/l; P < 0.05), and ATP effluent was greatest with RFC + RHG (RFC: 5.3 ± 1.4; RHG: 5.3 ± 1.1; RFC + RHG: 11.6 ± 2.7 vs. Mean Rest: 1.2 ± 0.1 nmol/min; P < 0.05). We conclude that the mechanical effects of muscle contraction can 1) independently elevate intravascular ATP draining quiescent skeletal muscle without changes in local metabolism and 2) further augment intravascular ATP during mild exercise associated with increases in metabolism and local deoxygenation; therefore, it is likely one stimulus for increasing intravascular ATP during exercise in humans.
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Crecelius et al. (2013) studied Healthy adults (n=20). Rhythmic forearm compressions and rhythmic handgrip exercise vs. Rest was evaluated on Forearm ATP effluent (p=<0.05). Mechanical effects of muscle contraction independently elevated intravascular ATP and further augmented ATP effluent when superimposed with mild exercise compared to rest (11.6 vs 1.2 nmol/min, P<0.05).