Responses of human elbow flexor muscles to electrically stimulated forced lengthening exercise
Kazunori Nosaka, Michael David Newton, Paul Sacco
Abstract
Kazunori Nosaka, Michael David Newton, Paul Sacco
Abstract
This study developed an electrical stimulation model for human elbow flexors to examine eccentric exercise-induced muscle damage and adaptation. Male students (n=17) were randomly placed into one of two groups; isometric (ES-ISO, n=8) and eccentric (ES-ECC, n=9). The elbow joint was fixed at 90 degrees (1.57 rad) and the elbow flexors stimulated percutaneously by an electronic muscle stimulator for 5 s through two electrodes placed over the muscles for ES-ISO. In ES-ECC, the muscles were stimulated similarly to the ES-ISO, but the elbow joint was forcibly extended from an elbow flexed (90 degrees 1.57 rad) to a full-extended position (180 degrees, 3.14 rad) in 3 s. Maximal voluntary isometric force, range of motion, upper arm circumference, muscle thickness by ultrasonography, muscle soreness, plasma creatine kinase and aspartate aminotransferase activities were assessed before and for 4 days after exercise. ES-ECC produced significantly larger changes in all criterion measures compared with ES-ISO (P < 0.01). These findings confirmed that eccentric muscle actions induced muscle damage, but isometric contractions resulted in little or no damage. Six subjects from the ES-ECC group repeated the same eccentric exercise (ECC2) 2 weeks after the first bout (ECC1), and changes in the criterion measures were compared between the bouts. Changes in all criterion measures after ECC2 were significantly smaller than ECC1 (P < 0.01). These results suggest that the first eccentric exercise produced a protective effect against muscle damage in the subsequent eccentric exercise bout, which does not involve adaptations in the central nervous system.
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This study developed an electrical stimulation model for human elbow flexors to examine eccentric exercise-induced muscle damage and adaptation. Male students (n=17) were randomly placed into one of two groups; isometric (ES-ISO, n=8) and eccentric (ES-ECC, n=9). The elbow joint was fixed at 90 degrees (1.57 rad) and the elbow flexors stimulated percutaneously by an electronic muscle stimulator for 5 s through two electrodes placed over the muscles for ES-ISO. In ES-ECC, the muscles were stimulated similarly to the ES-ISO, but the elbow joint was forcibly extended from an elbow flexed (90 degrees 1.57 rad) to a full-extended position (180 degrees, 3.14 rad) in 3 s. Maximal voluntary isometric force, range of motion, upper arm circumference, muscle thickness by ultrasonography, muscle soreness, plasma creatine kinase and aspartate aminotransferase activities were assessed before and for 4 days after exercise. ES-ECC produced significantly larger changes in all criterion measures compared with ES-ISO (P < 0.01). These findings confirmed that eccentric muscle actions induced muscle damage, but isometric contractions resulted in little or no damage. Six subjects from the ES-ECC group repeated the same eccentric exercise (ECC2) 2 weeks after the first bout (ECC1), and changes in the criterion measures were compared between the bouts. Changes in all criterion measures after ECC2 were significantly smaller than ECC1 (P < 0.01). These results suggest that the first eccentric exercise produced a protective effect against muscle damage in the subsequent eccentric exercise bout, which does not involve adaptations in the central nervous system.
Key concepts: Isometric exercise, Elbow, Eccentric, Delayed onset muscle soreness, Creatine kinase, Medicine, Eccentric exercise, Range of motion