Literature DB >> 20595540

Comparison between maximal lengthening and shortening contractions for biceps brachii muscle oxygenation and hemodynamics.

Makii Muthalib1, Hoseong Lee, Guillaume Y Millet, Marco Ferrari, Kazunori Nosaka.   

Abstract

Eccentric contractions (ECC) require lower systemic oxygen (O2) 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+deoxygenated-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 approximately 30%, and the decrease in TOI was smaller (P<0.05) by approximately 50% during ECC than CON. Increases in tHb during the relaxation phases were smaller (P<0.05) by approximately 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 O2 relative to O2 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 O2 demand relative to O2 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 O2 supply due to microcirculation dysfunction and/or inflammatory vasodilatory responses after ECC is recognized.

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Year:  2010        PMID: 20595540     DOI: 10.1152/japplphysiol.01297.2009

Source DB:  PubMed          Journal:  J Appl Physiol (1985)        ISSN: 0161-7567


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