TY - JOUR

T1 - Creatine kinase release from regenerated muscles after eccentric contractions in rats

AU - Sakamoto, Kei

AU - Nosaka, Kazunori

AU - Shimegi, Satoshi

AU - Ohmori, Hajime

AU - Katsuta , Shigeru

PY - 1996/1/1

Y1 - 1996/1/1

N2 - The purpose of this study was to test the hypothesis that an increase in plasma creatine kinase (CK) activity after eccentric contractions (ECC) would be attenuated in regenerated muscle fibres. Adult male Wistar rats (aged 12-14 weeks) were randomly assigned to a treatment group (n = 14) or a control group (n = 10). In the treatment group, 1.2% barium chloride solution (BaCl2) was injected into the tibialis anterior (TA) and extensor digitorum longus (EDL) muscles to induce degeneration and subsequent regeneration. The same amount of isotonic saline solution was injected into TA and EDL for the control group. Histological observation showed that approximately 50% of the fibres in the transverse sections of both muscles underwent necrosis 2 days after BaCl2, injection. The CK activity increased about tenfold at 2-4 h after BaCl2 injection. At 4 weeks after BaCl2 injection, when the regeneration process was almost complete, the TA and EDL of anaesthetized rats from both groups were subjected to ECC in which maximal dorsiflexion was caused by nerve electrical stimulation and the flexed foot was forcibly extended by a lever arm connected to a motor. This action was performed in 2 sets of 30 repetitions. Maximal isometric torque of the dorsiflexors decreased to about 15% (P < 0.01) of the pre-ECC value immediately after the exercise. Blood samples were collected before and 2, 4, 12, 24, 48 h after ECC. The CK activity increased significantly (P < 0.01) and peaked at 2-4 h after ECC, and there was no significant difference in the amount of CK increase between the treatment [1007 (SEM 120) IU·l-1] and the control [1064 (SEM 120) IU·l-1] group. Contrary to the hypothesis, CK release after ECC was not attenuated in muscle regenerated from BaCl2-induced myonecrosis.

AB - The purpose of this study was to test the hypothesis that an increase in plasma creatine kinase (CK) activity after eccentric contractions (ECC) would be attenuated in regenerated muscle fibres. Adult male Wistar rats (aged 12-14 weeks) were randomly assigned to a treatment group (n = 14) or a control group (n = 10). In the treatment group, 1.2% barium chloride solution (BaCl2) was injected into the tibialis anterior (TA) and extensor digitorum longus (EDL) muscles to induce degeneration and subsequent regeneration. The same amount of isotonic saline solution was injected into TA and EDL for the control group. Histological observation showed that approximately 50% of the fibres in the transverse sections of both muscles underwent necrosis 2 days after BaCl2, injection. The CK activity increased about tenfold at 2-4 h after BaCl2 injection. At 4 weeks after BaCl2 injection, when the regeneration process was almost complete, the TA and EDL of anaesthetized rats from both groups were subjected to ECC in which maximal dorsiflexion was caused by nerve electrical stimulation and the flexed foot was forcibly extended by a lever arm connected to a motor. This action was performed in 2 sets of 30 repetitions. Maximal isometric torque of the dorsiflexors decreased to about 15% (P < 0.01) of the pre-ECC value immediately after the exercise. Blood samples were collected before and 2, 4, 12, 24, 48 h after ECC. The CK activity increased significantly (P < 0.01) and peaked at 2-4 h after ECC, and there was no significant difference in the amount of CK increase between the treatment [1007 (SEM 120) IU·l-1] and the control [1064 (SEM 120) IU·l-1] group. Contrary to the hypothesis, CK release after ECC was not attenuated in muscle regenerated from BaCl2-induced myonecrosis.

KW - Barium chloride

KW - Creatine kinase

KW - Eccentric contraction

KW - Myonecrosis

KW - Regeneration

UR - http://www.scopus.com/inward/record.url?scp=0030055957&partnerID=8YFLogxK

U2 - 10.1007/BF00357673

DO - 10.1007/BF00357673

M3 - Journal article

C2 - 8817121

AN - SCOPUS:0030055957

VL - 73

SP - 516

EP - 520

JO - European Journal of Applied Physiology and Occupational Physiology

JF - European Journal of Applied Physiology and Occupational Physiology

SN - 0301-5548

IS - 6

ER -