Effect of endurance training and acute exercise on sarcoplasmic reticulum function in rat fast- and slow-twitch skeletal muscles

Abstract

Following 10 weeks of endurance training and in age-matched sedentary rats, sarcoplasmic reticulum (SR) Ca(2+)-uptake, Ca(2+)-release, and Ca(2+)-stimulated adenosinetriphosphatase (ATPase) activity were examined in homogenates of the plantaris and soleus muscles from rats subjected to moderate-intensity treadmill running to exhaustion. In order to examine the effects of acute exercise and/or training on SR Ca(2+)-handling capacity, comparisons between exhausted and non-exercised rats and between trained and untrained rats were performed. Our data confirm that Ca(2+)-sequestration by the SR from fast-twitch muscles is depressed after training. Immediately after exhaustive running, decreases in SR function occurred in both muscles, but were more pronounced in the soleus. In the plantaris, reductions in SR Ca(2+)-uptake rate and Ca(2+)-ATPase activity were observed in untrained rats only, while in the soleus they were adversely affected irrespective of training status. Although the average run time to exhaustion varied markedly between untrained and trained animals (untrained: 253.0 min; trained: 559.4 min), no differences existed with regard to the magnitude of decreases in SR function in the soleus after exercise. The mean rate of decline in SR Ca(2+)-handling capacity during acute exercise, as estimated from the run time and the extent of the decline, was more than twofold higher in untrained than in trained soleus. From the present study, it is unclear whether there exists a causal relationship between muscular fatigue and SR function because the run time to exhaustion was not significantly correlated with any of parameters indicative of SR Ca(2+)-handling capacity, but suggested that endurance training may be capable of delaying a progression of the deterioration in SR function that occurs during exercise.

Maximal voluntary contraction force, SR function and glycogen resynthesis during the first 72 h after a high-level competitive soccer game

“…Thus, we have previously demonstrated that high-intensity training induced an enhanced peak SR Ca 2+ release, due to an enhanced total volume of SR, whereas SR Ca 2+ sequestration function was not altered (Ørtenblad et al 2000b). However, SR function is depressed to a similar extent with fatigue in trained and untrained subjects, despite that trained subjects exercise at a higher intensity or longer (Inashima et al 2003;Li et al 2002), indicating that training may delay the exercise-induced progressive deterioration of SR function. However, little is known about the eVect of a soccer match on SR function and the recovery of the SR system in the days after a match.…”

Skeletal Muscle Fatigue: Cellular Mechanisms

“…A number of studies have reported that Ca 2ϩ release from isolated SR is reduced by ϳ20 -40% following prolonged or intense exercise in humans (210,284,285) and rodents (161), although some studies found no change (111,396) or a reduction in slow-twitch but not fast-twitch muscle (161,221). It is unclear how long this effect persists after exercise, as this was only examined in one study to date, and the results were somewhat equivocal at the one recovery time examined (3.5 h) (210 ] i also greatly prolongs PCD in Xenopus fast-twitch fibers (69,70,269).…”

Detailed Characterization of a Long-Term Rodent Model of Critical Illness and Recovery

“…Treadmill exercise capacity has been assessed in animal models of heart failure (48, 49), diabetes (50), aging (51,52) and skeletal muscle pathophysiology (53)(54)(55)(56). Motorised rodent treadmills have been used in sepsis models though as a means of determining the impact of endurance training on outcomes (57)(58)(59)(60).…”