Increased oxidative capacity does not protect skeletal muscle fibers from eccentric contraction-induced injury

1  Departments of Orthopaedics, Medicine, and Bioengineering, Biomedical Sciences Graduate Group, University of California and Veterans Affairs Medical Centers, San Diego, California 92161; and 2  Department of Hand Surgery, Göteborg University, Göteborg, Sweden S-412 Isometric electrical stimulatio...

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Published inAmerican journal of physiology. Regulatory, integrative and comparative physiology Vol. 274; no. 5; pp. 1300 - R1308
Main Authors Patel, T. J, Cuizon, D, Mathieu-Costello, O, Friden, J, Lieber, R. L
Format Journal Article
LanguageEnglish
Published United States 01.05.1998
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Summary:1  Departments of Orthopaedics, Medicine, and Bioengineering, Biomedical Sciences Graduate Group, University of California and Veterans Affairs Medical Centers, San Diego, California 92161; and 2  Department of Hand Surgery, Göteborg University, Göteborg, Sweden S-412 Isometric electrical stimulation was delivered to rabbit dorsiflexor muscles at 10 Hz for 1 s on and 1 s off over 30 min, 5 days/wk for 3 wk to induce an increase in muscle oxidative capacity. Stimulation-trained muscles as well as untrained muscles were then subjected to a 30-min eccentric exercise bout to test whether increased oxidative capacity provided a protective effect against muscle injury. Electrical stimulation resulted in significant training of both the extensor digitorum longus (EDL) and tibialis anterior (TA) muscles, with EDL citrate synthase (CS) activity increasing an average of 67% ( P  < 0.0001) and TA CS activity increasing by 27% ( P  < 0.05). For all parameters measured, the magnitude of change was much greater for EDL than for TA muscle. Dorsiflexor fatigability decreased significantly during the 3-wk training period ( P  < 0.0001), whereas the EDL and TA individually showed strong decreasing trends in fatigability after training. TA and EDL capillary density measured histomorphometrically increased from 839 ± 56 to 1,026 ± 71 mm 2 ( P  = 0.07) and from 589 ± 37 to 792 ± 66 mm 2 ( P  < 0.05), respectively. TA and EDL capillary-to-fiber ratio increased from 1.32 ± 0.10 to 1.55 ± 0.16 ( P  > 0.2) and 1.08 ± 0.07 to 1.36 ± 0.14 ( P  > 0.1), respectively. Type 2A fiber type percentage increased after stimulation training by 68% ( P  < 0.0001) for the EDL and by 32% ( P  > 0.1) for the TA at the expense of type 2D fibers. Despite the large training effect for the EDL and the modest training effect for the TA, no differences were observed between stimulation-trained and untrained groups for maximum dorsiflexion torque ( P  > 0.3) or maximum tetanic tension ( P  > 0.3) after eccentric contraction-induced injury. Additionally, no significant correlation was observed between CS activity and maximum tetanic tension after eccentric contraction-induced injury for either muscle ( P  > 0.2). Thus we conclude that increasing muscle oxidative capacity by isometric electrical stimulation training did not protect muscle against eccentric contraction-induced injury. muscle metabolism; fiber type; muscle mechanics
ISSN:0363-6119
0002-9513
1522-1490
DOI:10.1152/ajpregu.1998.274.5.r1300