2002•Acta Physiologica ScandinavicaRequires access

Responses of human elbow flexor muscles to electrically stimulated forced lengthening exercise

Kazunori Nosaka, Michael David Newton, Paul Sacco

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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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What this paper is about

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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Available 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.

Key concepts: Isometric exercise, Elbow, Eccentric, Delayed onset muscle soreness, Creatine kinase, Medicine, Eccentric exercise, Range of motion

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