Elsevier

Cell Calcium

Volume 22, Issue 5, November 1997, Pages 373-383
Cell Calcium

Quantitative measurement of resting skeletal muscle [Ca2+]i following acute and long-term downhill running exercise in mice

https://doi.org/10.1016/S0143-4160(97)90022-1Get rights and content

Abstract

Alteration of resting free intracellular [Ca2+] ([Ca2+]i) homeostasis has been implicated in the aetiology of skeletal muscle fibre injury following damaging pliometric (lengthening or 'eccentric') contractions. Quantitative measurements of resting [Ca2+]i in skeletal muscles following acute or long-term exercise involving such injurious contractions have not been performed. We tested the hypothesis that, following an acute bout of pliometric exercise, the maximum force production (Po) of isolated skeletal muscles would be significantly reduced and that this deficit in force would be accompanied by an elevation in resting skeletal muscle [Ca2+]i. Further, we tested whether long-term pliometric exercise training would protect skeletal muscles from contraction-induced injury. Adult male mice were randomly assigned to either: control, 24-hour, 48-hour, or trained groups. The 24-hour and 48-hour group animals were subjected to a single acute downhill treadmill running bout (decline 16°, at a rate of 13 m/min, for 60 min) and sacrificed at 24 or 48 h, respectively. Trained animals underwent a 14 week endurance training program consisting of a daily (5 days/week) downhill running session, under identical conditions to that of the acutely exercised groups. The sedentary control animals remained in their cages. For each animal, Po was determined in the fast-twitch EDL and slow-twitch soleus muscles from one hindlimb and quantitative measurements of [Ca2+]i were made in the contralateral muscles using fluorescence digital imaging microscopy in conjunction with Fura-2. Po was lower in the EDL and soleus muscles from the 48-hour group compared with the control group animals. Po was higher in the EDL muscles of the trained group compared with the 48-hour group. No significant difference in Po was detected in either muscle from the 24-hour or trained groups compared with muscles from control mice. In EDL muscles, [Ca2+]i was elevated in the 48-hour group compared with the control and trained group animals, but was not different between the 24-hour group compared with control mice. [Ca2+]i was not different in the soleus muscles among the 48-hour, trained or control group mice, but was increased in muscles from the 48-hour group compared with the 24-hour group. Endurance downhill running training conferred protection to recruited skeletal muscles against the effects of an acute bout of repeated pliometric contractions, as evidenced by [Ca2+], and Po values similar to muscles from unexercised control mice.

References (46)

  • R.B. Armstrong et al.

    Mechanisms of exercise-induced muscle fibre injury

    Sports Med

    (1991)
  • J.H. Van der Meulen et al.

    Relationship between exercise-induced muscle damage and enzyme release in rats

    J Appl Physiol

    (1991)
  • C.J. Duncan et al.

    Different mechanisms mediate structural changes and intracellular enzyme efflux following damage to skeletal muscle

    J Cell Sci

    (1987)
  • R.L. Lieber et al.

    Muscle damage is not a function of muscle force but active muscle strain

    J Appl Physiol

    (1993)
  • P.L. McNeil et al.

    Disruptions of muscle fiber plasma membranes

    Am J Pathol

    (1992)
  • J. Fridén et al.

    Structural and mechanical basis of exerciseinduced muscle injury

    Med Sci Sports Exerc

    (1992)
  • P.M. Clarkson et al.

    Muscle function after exercise-induced muscle damage and rapid adaptation

    Med Sci Sports Exerc

    (1992)
  • P. Sacco et al.

    The protective effect of damaging eccentric exercise against repeated bouts of exercise in the mouse tibialis anterior muscle

    Exp Physiol

    (1992)
  • R.B. Armstrong

    Initial events in exercise-induced muscular injury

    Med Sci Sports Exerc

    (1990)
  • C. Duan et al.

    Rat skeletal muscle mitochondrial [Ca 2+] and injury from downhill walking

    J Appl Physiol

    (1990)
  • G.L. Warren et al.

    Excitation failure in eccentric contractioninduced injury of mouse soleus muscle

    J Physiol

    (1993)
  • C.D. Balnave et al.

    Intracellular calcium and force in single mouse muscle fibres following repeated contractions with stretch

    J Physiol

    (1995)
  • J.A. Schwane et al.

    Effect of training on skeletal muscle injury from downhill running in rats

    J Appl Physiol

    (1983)
  • Cited by (67)

    • Capillarisin attenuates exercise-induced muscle damage through MAPK and NF-κB signaling

      2017, Phytomedicine
      Citation Excerpt :

      The treadmill had an electrical shock grid at the end of the rail to keep the mice running. The exercise groups (Group 2–4) were experimented on the treadmill 24 h after CAP administration according to the eccentric exercise protocol (13 m/min for 60 min, −16° downhill) (Haramizu et al., 2011; Lynch et al., 1997). The level of ROS was quantified using the fluorescent probe 2′,7′-dichlorofluorescein-diacetate (DCFH-DA), according to the method of Driver et al., with a slight modification (Driver et al., 2000).

    • Combined aerobic exercise and enzyme replacement therapy rejuvenates the mitochondrial-lysosomal axis and alleviates autophagic blockage in Pompe disease

      2015, Free Radical Biology and Medicine
      Citation Excerpt :

      We have previously shown an increased abundance of glycogen-laden lysosomes in close proximity to the sarcolemma in SO versus FOG/FG muscle fibers in GAA-KO mice [8] and proposed that contractile activity (acute exercise) and/or fiber-type transition from a glycolytic to an oxidative phenotype (long-term aerobic training) may enhance Ca2+-induced lysosomal exocytosis and cellular clearance. Excitation–contraction coupling instantly raises resting [Ca2+]i (50 nM) ∼100-fold locally in skeletal muscle [96, 97], and it stays significantly elevated for 24–48 h following eccentric exercise [98]. While contractile activity-induced Ca2+ release may facilitate vesicle fusion and membrane resealing, recent research suggests that trafficking and nucleation of intracellular vesicles at injury sites are mainly driven by changes in the oxidative environment in striated muscle.

    • Des-aspartate-angiotensin I attenuates ICAM-1 formation in hydrogen peroxide-treated L6 skeletal muscle cells and soleus muscle of mice subjected to eccentric exercise

      2013, Regulatory Peptides
      Citation Excerpt :

      Preliminary experiment with an early batch of 4 mice showed that the two-day training session did not cause any significant increase in superoxide level in the soleus muscle of these mice as compared to untrained mice (data not shown), and was unlikely to cause adaptation. Adaptation had been reported to occur when mice ran at a speed of 13 m/min for 60 min per day for 4 weeks [24] and at a speed of 12–17 cm/s for 75–135 min per day for 9 days [25]. The study was carried out as described earlier [16].

    View all citing articles on Scopus
    View full text