Muscle deoxygenation in aerobic and anaerobic exercise

Abstract

It has been generally accepted that the use of oxygen is a major contributor of ATP synthesis in endurance exercise but not in short sprints. In anaerobic exercise, muscle energy is thought to be initially supported by the PCr-ATP system followed by glycolysis, not through mitochondrial oxidative phosphorylation. However, in real exercise practice, we do not know how much of this notion is true when an athlete approaches his/her maximal capacity of aerobic and anaerobic exercise, such as during a graded VO2(max) test. This study investigates the use of oxygen in aerobic and anaerobic exercise by monitoring oxygen concentration of the vastus lateralis muscle at maximum intensity using Near Infra-red Spectroscopy (NIRS). We tested 14 sprinters from the University of Penn track team, whose competitive events are high jump, pole vault, 100 m, 200 m, 400 m, and 800 m. The Wingate anaerobic power test was performed on a cycle ergometer with 10% body weight resistance for 30 seconds. To compare oxygenation during aerobic exercise, a steady-state VO2(max) test with a cycle ergometer was used with 25 watt increments every 2 min. until exhaustion. Results showed that in the Wingate test, total power reached 774 ± 86 watt, about 3 times greater than that in the VO2(max) test (270 ± 43 watt). In the Wingate test, the deoxygenation reached approximately 80 % of the established maximum value, while in the VO2(max) test resulted in approximately 36 % deoxygenation. There was no delay in onset of deoxygenation in the Wingate test, while in the VO2(max) test, deoxygenation did not occur under low intensity work. The results indicate that oxygen was used from the beginning of sprint test, suggesting that the mitochondrial ATP synthesis was triggered after a surprisingly brief exercise duration. One explanation is that prior warm-up (unloaded exercise) was enough to provide the mitochondrial substrates; ADP and Pi to activate oxidative phosphorylation by the type II a and type I myocytes. In addition, transmural pressure created by the muscle contraction reduces blood flow, causing relative hypoxia.