INCREASED OXIDATIVE CAPACITY DOES NOT PROTECT SKELETAL-MUSCLE FIBERS FROM ECCENTRIC CONTRACTION-INDUCED INJURY

Isometric electrical stimulation was delivered to rabbit dorsiflexor m uscles 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-train ed muscles as well as untrained muscles were then subjected to a 30-mi n eccentric exercise bout to test whether increased oxidative capacity provided a protective effect against muscle injury. Electrical stimul ation resulted in significant training of both the extensor digitorum longus (EDL) and tibialis anterior (TA) muscles, with EDL citrate synt hase (CS) activity increasing an average of 67% (P < 0.0001) and TA CS activity increasing by 27% (P < 0.05). For all parameters measured, t he magnitude of change was much greater for EDL than for TA muscle. Do rsiflexor fatigability decreased significantly during the 3-wk trainin g period (P < 0.0001), whereas the EDL and TA individually showed stro ng decreasing trends in fatigability after training. TA and EDL capill ary density measured histomorphometrically increased from 839 +/- 56 t o 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 incr eased 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 percentag e 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. Des pite the large training effect for the EDL and the modest training eff ect for the TA, no differences were observed between stimulation-train ed and untrained groups for maximum dorsiflexion torque (P > 0.3) or m aximum tetanic tension (P > 0.3) after eccentric contraction-induced i njury. Additionally, no significant correlation was observed between C S activity and maximum tetanic tension after eccentric contraction-ind uced injury for either muscle (P > 0.2). Thus we conclude that increas ing muscle oxidative capacity by isometric electrical stimulation trai ning did not protect muscle against eccentric contraction-induced inju ry.