Estrogen and gender do not affect fatigue resistance of extensor digitorum longus muscle in rats.

The effects of estrogen on skeletal muscle fatigue are controversial. To determine the effects of estrogen and gender on rat extensor digitorum longus (EDL) muscle, we either injected 40 microg beta-estradiol 3/benzoate.kg BW(-1) to female rats or sham injected male or female rats for 14 days. Subsequently a 90 min fatigue protocol consisting of electrical stimulation at 10 Hz delivered in 500 ms trains was administered. Force was recorded for a 5 s period at the start of the protocol (0 min) and at 5 min intervals until completion following 90 min of stimulation. After 90 min, EDL force generation at 10 Hz stimulation declined in all groups to between 50-60 % of initial values. However, no significant difference in fatigue rate or final 10 Hz stimulated force was seen between females administered estrogen, sham injected females or males. Hence, estrogen administration and gender did not significantly affect EDL muscle fatigue in this model.

Increased force development rates of fatigued mouse skeletal muscle are graded to myosin light chain phosphate content.

Phosphorylation of myosin regulatory light chain (R-LC) increases the Ca2+ sensitivity of cross-bridge transitions, which determine rate of force development in skinned skeletal muscle fibers. The purpose of this study was to determine whether phosphorylation of R-LC is the molecular basis for the increased force development rates (+dF/dtmax) observed in fatigued mouse extensor digitorum longus muscle (EDL) (stimulated in vitro at 25 degrees C). Parameters of twitch and tetanic force were obtained after the application of different-frequency conditioning stimuli (CS), which were used to vary R-LC phosphorylation and reduce peak tetanic force (Po). Without CS, R-LC phosphorylation (in moles phosphate per mole R-LC) was not elevated above rest (0.11 +/- 0.02 vs. 0.13 +/- 0.02, respectively), and no aspect of the twitch (Pt) Po was altered. Stimulating muscles at 2.5-20 Hz increased R-LC phosphorylation in a frequency-dependent manner, from 0.23 +/- 0.04 to 0.82 +/- 0.03, respectively. Moreover, stimulation at 2.5-20 Hz potentiated Pt (range: 4 +/- 2-28 +/- 2%), increased the +dF/dtmax of potentiated twitches (range: 5 +/- 1-28 +/- 2%), and reduced Po (range: 6 +/- 1-21 +/- 1%). Higher-frequency stimulation (40 or 100 Hz) did not phosphorylate R-LC or potentiate Pt or twitch +dF/dtmax further. Stimulation at 40 and 100 Hz did, however, have different effects on Po compared with 20-Hz data (Po reduced 27 +/- 2 and 11 +/- 2%, respectively). The increased +dF/dtmax of potentiated twitches observed after different CS procedures were graded to R-LC phosphorylation (r = 0.97, P < 0.001). It is concluded that phosphorylation of R-LC increases extent of twitch force development in mouse EDL muscle fatigued by CS.

Elevated catalase activity in red and white muscles of MyoD gene-inactivated mice.

MyoD is a myogenic transcription factor responsible for skeletal muscle differentiation during development. Muscle antioxidant enzyme status was determined in transgenic MyoD deactivated mice. While catalase activity was significantly (P < 0.05) elevated in soleus and extensor digitorum longus muscles from MyoD deactivated mice, superoxide dismutase and glutathione peroxidase activities were not. While this may imply a greater propensity for inherent oxidative stress, soleus glutathione status was similar between MyoD deactivated mouse and control soleus muscles. Catalase activity is localized primarily in peroxisomes. Therefore elevated catalase activity may also indicate the presence of factors associated with peroxisome proliferation in muscles from MyoD gene-inactivated mice.