Résumé
Muthalib M, Lee H, Millet GY, Ferrari M, Nosaka K. Comparison between maximal lengthening and shortening contractions for biceps brachii muscle oxygenation and hemodynamics. J Appl Physiol 109: 710-720, 2010. First published July 1, 2010; doi: 10.1152/japplphysiol.01297.2009.-Eccentric contractions (ECC) require lower systemic oxygen (O-2) and induce greater symptoms of muscle damage than concentric contractions (CON); however, it is not known if local muscle oxygenation is lower in ECC than CON during and following exercise. This study compared between ECC and CON for changes in biceps brachii muscle oxygenation [tissue oxygenation index (TOI)] and hemodynamics [total hemoglobin volume (tHb) = oxygenated-Hb + deoxy-genated-Hb], determined by near-infrared spectroscopy over 10 sets of 6 maximal contractions of the elbow flexors of 10 healthy subjects. This study also compared between ECC and CON for changes in TOI and tHb during a 10-s sustained and 30-repeated maximal isometric contraction (MVC) task measured immediately before and after and 1-3 days following exercise. The torque integral during ECC was greater (P < 0.05) than that during CON by similar to 30%, and the decrease in TOI was smaller (P < 0.05) by similar to 50% during ECC than CON. Increases in tHb during the relaxation phases were smaller (P < 0.05) by similar to 100% for ECC than CON; however, the decreases in tHb during the contraction phases were not significantly different between sessions. These results suggest that ECC utilizes a lower muscle O-2 relative to O-2 supply compared with CON. Following exercise, greater (P < 0.05) decreases in MVC strength and increases in plasma creatine kinase activity and muscle soreness were evident 1-3 days after ECC than CON. Torque integral, TOI, and tHb during the sustained and repeated MVC tasks decreased (P < 0.01) only after ECC, suggesting that muscle O-2 demand relative to O-2 supply during the isometric tasks was decreased after ECC. This could mainly be due to a lower maximal muscle mass activated as a consequence of muscle damage; however, an increase in O-2 supply due to microcirculation dysfunction and/or inflammatory vasodilatory responses after ECC is recognized.