Ultrastructural changes and sarcoplasmic reticulum Ca2+ regulation in red vastus muscle following eccentric exercise in the rat.
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.
Chen
Wan
W
School of Exercise & Sport Science, The University of Sydney, Sydney, NSW 1825, Australia.
Ruell
Patricia A
PA
Ghoddusi
Majid
M
Kee
Anthony
A
Hardeman
Edna C
EC
Hoffman
Kylie M
KM
Thompson
Martin W
MW
D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D006706:Homeostasis; D007476:Ionophores / Q000494:pharmacology; D008297:Male; D018656:Muscle Fibers, Fast-Twitch / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D018482:Muscle, Skeletal / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D010805:Physical Conditioning, Animal; D005082:Physical Exertion / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function; D012519:Sarcoplasmic Reticulum / Q000187:drug effects / Q000201:enzymology* / Q000648:ultrastructure; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases / Q000378:metabolism*; D013997:Time Factors
D007476:Ionophores; D000001:Calcimycin; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D002118:Calcium