{'fraction_non_alphanumeric': 0.025384101536406144, 'fraction_numerical': 0.01736806947227789, 'mean_word_length': 5.320675105485232, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Sources of Intravascular ATP during Exercise in Man: Critical Role for Skeletal Muscle Perfusion

The origin of intravascular ATP resultant from exercise in humans is a matter of debate and is suggested to arise from sympathetic nerves, blood sources, endothelial cells, and skeletal myocytes, among others. We tested the hypothesis that acute activation of the sympathetic nervous system (SNA) increases plasma ATP draining skeletal muscle at rest, and that SNA superimposition during exercise further augments ATP. We show that augmenting SNA via −40mmHg lower body negative pressure does not increase ATP at rest (51±8 vs 58±7 nmol/L) nor in conjunction with forearm handgrip exercise (79±11 vs 71±8 nmol/L). Next, we tested the hypothesis that active perfusion of skeletal muscle is essential to increase intravascular ATP during exercise. We identify that complete obstruction of muscle perfusion abolishes exercise‐mediated increases in ATP (90±19 to 49±12 nmol/L), and further that cessation of blood flow prior to exercise completely inhibits the typical rise in ATP draining active muscle (3 vs 61%; obstructed vs intact perfusion). Our collective observations suggest that blood extracellular ATP is unlikely to originate from sympathetic nerves or the contacting muscle itself. We conclude that increased exercising blood flow per se is essential for a rise in plasma ATP and indicates an important role for red blood cells or endothelial cells in augmenting plasma ATP during exercise.