Ultrastructural changes and sarcoplasmic reticulum Ca²⁺ regulation in red vastus muscle following eccentric exercise in the rat

Abstract

This study examined the effects of a bout of low-intensity, prolonged downhill exercise on sarcoplasmic reticulum (SR) Ca(2+)-ATPase activity, Ca(2+) uptake and release in rat red vastus muscle. Ionophore stimulation was determined to assess vesicle integrity by measuring the ratio of Ca(2+)-ATPase activities in the presence and absence of A23187. Observations of the muscle ultrastructure were made to evaluate muscle damage at the level of the myofibrils and SR. Adult male Sprague-Dawley rats (weight, 395 +/- 5.9 g) were either assigned as non-exercise controls or subjected to 90 min of downhill treadmill exercise (-16 deg; 15 m min(-1)), and then killed immediately, 4, 24, 48, 72 or 144 h after exercise (n = 7). Calcium uptake was significantly lower (P < 0.05) compared with control values (19.25 +/- 1.38 nmol min(-1) (mg protein)(-1)), by 29 and 36% immediately and 4 h postexercise, respectively, and remained depressed (P < 0.05) 24 h postexercise. Calcium release was also significantly lower (P < 0.05) compared with control values (31.06 +/- 2.36 nmol min(-1) (mg protein)(-1)), by 37 and 39% immediately and 4 h postexercise, respectively, and remained depressed (P < 0.05) 24 h postexercise. Ca(2+)-ATPase activity measured with ionophore was 31% lower (P < 0.05) 4 h postexercise, and remained lower (P < 0.05) 24 h postexercise. The ratio of Ca(2+)-ATPase activities in the presence and absence of A23187 was not significantly changed after exercise, indicating that membrane integrity was not altered by the exercise. Focal dilatations of the SR were observed immediately and 4 h following exercise, implying that SR may be susceptible to damage in the localized regions of overstretched sarcomeres. The results demonstrate that a bout of low-intensity, prolonged downhill exercise results in a long-lasting depression of SR function that is not fully restored after 2 days of recovery, which may underlie some functional impairments induced by eccentric exercise.

Enhanced activity of eccentric contraction induces alterations in <i>in vitro</i> sarcoplasmic reticulum Ca²⁺ handling in rat hindlimb muscles

“…It has been suggested that this significant decrease at 300ECC or more may be attributed to the uncontrolled movement of Ca 2+ into the sarcoplasm, as activity changed with regard to the amount of ECC. Based on the principal findings of this study, we suggest that the differences in the amount of ECC caused increased or unchanged SR Ca 2+ -ATPase activity that occurred immediately after ECC in previous studies [8][9][10] .…”

“…Sixty-minutes of eccentric cycling *Correspondence: matsunaga@cc.miyazaki-u.ac.jp exercise 8) and 200 repeated electrical eccentric muscle extensions 9) elicited pronounced increases in SR Ca 2+ -ATPase activity. In contrast, some studies showed no detectable changes in SR Ca 2+ -ATPase activity immediately after eccentric downhill running 10) or ECC with electrical stimulation 11) . Although the reason for this discrepancy between the studies remains unclear, it is possible that SR Ca 2+ -ATPase activity could fluctuate with time of ECC, and differences in amounts of ECC to which muscles were exposed could yield conflicting results.…”

The impact of damaging exercise on electromechanical delay in biceps brachii

“…vided by microscopy (Fridén et al, 1983;Hortobágyi et al, 1996) and seems most prevalent in fast motor units (Fridén et al, 1983;Brockett et al, 2002). In addition to this initial mechanical stress, there is a secondary response which is a reflection of the loss in Ca 2+ homeostasis and subsequent cascade that exacerbates damage (Yasuda et al, 1997;Chen et al, 2007) and is followed by recovery McHugh, 2003). This investigation measured indirect indices of muscle damage which are commonly used to examine the magnitude and time course of damage and repair.…”

“…Muscle damage has also been reported to reduce cell membrane and sarcolemma integrity, which likely results from disturbances in Ca 2+ homeostasis (Yasuda et al, 1997;Chen et al, 2007) that may consequently negatively affect EMD. Data of this nature may provide additional information on muscle function and recovery following damaging exercise; despite this, no previous research has examined the impact of muscle damage on EMD.…”

Heat exposure does not alter eccentric exercise-induced increases in mitochondrial calcium and respiratory dysfunction

“…Although eccentric exercise is known to increase MCC (Duan et al 1990), the levels reached immediately post-exercise might not achieve magnitudes required for mitochondrial dysfunction (Brookes et al 2004;Gunter et al 2004;Szabadkai and Duchen 2008). By contrast, such levels may be reached in the following days (Duan et al 1990) due to depressed sarcoplasmic reticulum function (Chen et al 2007) and potentially leading to the opening of the mitochondrial permeability transition pore (mPTP) (Halestrap 2005;Halestrap et al 2002). mPTP opening will provoke the leak of protons across the inner membrane impairing respiratory indices.…”