Eccentric exercise-induced injury to rat skeletal muscle

These experiments were designed to study skeletal muscle pathology resulting from eccentric-biased exercise in rats. The effects on the muscles of running on a treadmill on a 0 degrees incline (similar amounts of concentric and eccentric contractions), down a 16 degrees incline (primarily eccentric contractions), and up a 16 degrees incline (primarily concentric contractions) at 16 m . min-1 for 90 min were assessed by following postexercise changes in 1) plasma creatine kinase and lactate dehydrogenase activities, 2) glucose-6-phosphate dehydrogenase (G-6-PDase) activity (bio- and histochemically) in the physiological extensor muscles, and 3) histological appearance of the muscles. The data indicate the following. 1) Whereas all exercise protocols resulted in elevations of plasma enzymes immediately after running, only eccentric exercise caused late phase elevations 1.5-2 days postexercise. 2) Significant increases in muscle G-6-PDase activity, which were always associated with accumulations of mononuclear cells, always occurred within some muscles of each extensor group 1-3 days following downhill and uphill running and did not occur following level running; the increases in activity were usually of lower magnitude in the muscles of uphill runners than in those of downhill runners; the deeply located, predominantly slow-twitch muscles were most affected by both down- and uphill running. 3) Muscle histology demonstrated localized disruption of normal banding patterns of some fibers immediately after exercise and accumulations of macrophages in the interstitium and in some (less than 5%) muscle fibers by 24 h postexercise in the deep slow muscles of the antigravity groups. Although the data generally indicated that eccentric exercise causes greater injury to the muscles, questions remain.     

Postexercise muscle and liver glycogen metabolism in male and female rats

Male and female Wistar rats were run for 5 min at 1.7 mph at a 17% grade to determine whether a sex difference exists in the rate of glycogen resynthesis during recovery in fast-twitch red muscle, fast-twitch white muscle, and liver. Rats were killed at one of three time points: immediately after the exercise bout, and at 1 or 4 h later. Males had significantly higher resting muscle glycogen levels (P less than 0.05). Exercise resulted in significant glycogen depletion in both sexes (P less than 0.01). Males utilized approximately 50% more glycogen during the exercise bout than females (P less than 0.05). During the food-restricted 4-h recovery period, muscle glycogen was repleted significantly during the 1st h (P less than 0.05). Liver glycogen was not depleted as a result of the exercise bout, but fell during the first h of recovery (P less than 0.05) and remained low during the subsequent 3 h. The greater glycogen utilization in red and white fast-twitch muscle during exercise by males could represent a true sex difference but could also be attributable in part to the males having performed more work as a result of 20% greater body mass. We conclude that no sex difference was observed in the rates of muscle glycogen repletion after exercise or in liver glycogen metabolism during and after exercise, and rapid postexercise muscle glycogen repletion occurred at a time of accelerated liver glycogen depletion.     

Postexercise muscle glycogen resynthesis in obese insulin-resistant Zucker rats.

We determined the effect of an acute bout of swimming (8 x 30 min) followed by either carbohydrate administration (0.5 mg/g glucose ip and ad libitum access to chow; CHO) or fasting (Fast) on postexercise glycogen resynthesis in soleus muscle and liver from female lean (ZL) and obese insulin-resistant (ZO) Zucker rats. Resting soleus muscle glycogen concentration ([glycogen]) was similar between genotypes and was reduced by 73 (ZL) and 63% (ZO) after exercise (P < 0.05). Liver [glycogen] at rest was greater in ZO than ZL (334 +/- 31 vs. 247 +/- 16 micromol/g wet wt; P < 0.01) and fell by 44 and 94% after exercise (P < 0.05). The fractional activity of glycogen synthase (active/total) increased immediately after exercise (from 0.22 +/- 0.05 and 0.32 +/- 0.04 to 0.63 +/- 0.08 vs. 0.57 +/- 0.05; P < 0.01 for ZL and ZO rats, respectively) and remained elevated above resting values after 30 min of recovery. During this time, muscle [glycogen] in ZO increased 68% with CHO (P < 0.05) but did not change in Fast. Muscle [glycogen] was unchanged in ZL from postexercise values after both treatments. After 6 h recovery, GLUT-4 protein concentration was increased above resting levels by a similar extent for both genotypes in both fasted (approximately 45%) and CHO-supplemented (approximately 115%) rats. Accordingly, during this time CHO refeeding resulted in supercompensation in both genotypes (68% vs. 44% for ZL and ZO). With CHO, liver [glycogen] was restored to resting levels in ZL but remained at postexercise values for ZO after both treatments. We conclude that the increased glucose availability with carbohydrate refeeding after glycogen-depleting exercise resulted in glycogen supercompensation, even in the face of muscle insulin-resistance.     

Curcumin effects on inflammation and performance recovery following eccentric exercise-induced muscle damage

Downhill running is associated with fiber damage, inflammation, delayed-onset muscle soreness, and various functional deficits. Curcumin, a constituent of the Indian spice turmeric has been investigated for its anti-inflammatory activity and may offset some of the damage and functional deficits associated with downhill running. This study examined the effects of curcumin on inflammation and recovery of running performance following downhill running in mice. Male mice were assigned to downhill placebo (Down-Plac), downhill curcumin (Down-Cur), uphill placebo (Up-Plac), or uphill curcumin (Up-Cur) groups and run on a treadmill at 22 m/min at -14% or +14% grade, for 150 min. At 48 h or 72 h after the up/downhill run, mice (experiment 1) underwent a treadmill performance run to fatigue. Another subset of mice was placed in voluntary activity wheel cages following the up/downhill run (experiment 2) and their voluntary activity (distance, time and peak speed) was recorded. Additional mice (experiment 3) were killed at 24 h and 48 h following the up/downhill run, and the soleus muscle was harvested for analysis of inflammatory cytokines (IL-1beta, IL-6, and TNF-alpha), and plasma was collected for creatine kinase analysis. Downhill running decreased both treadmill run time to fatigue (48 h and 72 h) and voluntary activity (24 h) (P < 0.05), and curcumin feedings offset these effects on running performance. Downhill running was also associated with an increase in inflammatory cytokines (24 h and 48 h) and creatine kinase (24 h) (P < 0.05) that were blunted by curcumin feedings. These results support the hypothesis that curcumin can reduce inflammation and offset some of the performance deficits associated with eccentric exercise-induced muscle damage.     

Enhanced Glycogen Storage of a Subcellular Hot Spot in Human Skeletal Muscle during Early Recovery from Eccentric Contractions

Unaccustomed eccentric exercise is accompanied by muscle damage and impaired glucose uptake and glycogen synthesis during subsequent recovery. Recently, it was shown that the role and regulation of glycogen in skeletal muscle are dependent on its subcellular localization, and that glycogen synthesis, as described by the product of glycogen particle size and number, is dependent on the time course of recovery after exercise and carbohydrate availability. In the present study, we investigated the subcellular distribution of glycogen in fibers with high (type I) and low (type II) mitochondrial content during post-exercise recovery from eccentric contractions. Analysis was completed on five male subjects performing an exercise bout consisting of 15 x 10 maximal eccentric contractions. Carbohydrate-rich drinks were subsequently ingested throughout a 48 h recovery period and muscle biopsies for analysis included time points 3, 24 and 48 h post exercise from the exercising leg, whereas biopsies corresponding to prior to and at 48 h after the exercise bout were collected from the non-exercising, control leg. Quantitative imaging by transmission electron microscopy revealed an early (post 3 and 24 h) enhanced storage of intramyofibrillar glycogen (defined as glycogen particles located within the myofibrils) of type I fibers, which was associated with an increase in the number of particles. In contrast, late in recovery (post 48 h), intermyofibrillar, intramyofibrillar and subsarcolemmal glycogen in both type I and II fibers were lower in the exercise leg compared with the control leg, and this was associated with a smaller size of the glycogen particles. We conclude that in the carbohydrate-supplemented state, the effect of eccentric contractions on glycogen metabolism depends on the subcellular localization, muscle fiber’s oxidative capacity, and the time course of recovery. The early enhanced storage of intramyofibrillar glycogen after the eccentric contractions may entail important implications for muscle function and fatigue resistance.     

L-arginine Supplementation Protects Exercise Performance and Structural Integrity of Muscle Fibers after a Single Bout of Eccentric Exercise in Rats

Eccentric exercise is known to disrupt sarcolemmal integrity and induce damage of skeletal muscle fibers. We hypothesized that L-arginine (L-Arg; nitric oxide synthase (NOS) substrate) supplementation prior to a single bout of eccentric exercise would diminish exercise-induced damage. In addition, we used N-nitro-L-arginine methyl ester hydrochloride (L-NAME; NOS inhibitor) to clarify the role of native NOS activity in the development of exercise-induced muscle damage. Rats were divided into four groups: non-treated control (C), downhill running with (RA) or without (R) L-Arg supplementation and downhill running with L-NAME supplementation (RN). Twenty four hours following eccentric exercise seven rats in each group were sacrificed and soleus muscles were dissected and frozen for further analysis. The remaining seven rats in each group were subjected to the exercise performance test. Our experiments showed that L-Arg supplementation prior to a single bout of eccentric exercise improved subsequent exercise performance capacity tests in RA rats when compared with R, RN and C rats by 37%, 27% and 13%, respectively. This outcome is mediated by L-Arg protection against post-exercise damage of sarcolemma (2.26- and 0.87-fold less than R and RN groups, respectively), reduced numbers of damaged muscle fibers indicated by the reduced loss of desmin content in the muscle (15% and 25% less than R and RN groups, respectively), and diminished µ-calpain mRNA up-regulation (42% and 30% less than R and RN groups, respectively). In conclusion, our study indicates that L-Arg supplementation prior to a single bout of eccentric exercise alleviates muscle fiber damage and preserves exercise performance capacity.     

大负荷运动诱导大鼠骨骼肌损伤对其自噬超微结构及Beclin1和LC3-II/I的影响*

目的: 观察大负荷离心运动对大鼠骨骼肌自噬超微结构及自噬相关蛋白Beclin1和LC3II/I的影响。方法: 48只SD雄性大鼠适应性训练后随机分成对照组(C,n=8)和大负荷离心运动组(E,n=40)。E组于跑台进行90 min下坡跑,运动后0 h、12 h、24 h、48 h和72 h取比目鱼肌,透射电镜观察其自噬体超微结构变化;Western blot检测Beclin1和LC3II/I蛋白表达;免疫荧光观测LC3的定位及含量变化。结果: E组比目鱼肌自噬体数量在运动后0 h、12 h和24 h均有增加,并伴LC3自噬荧光明显增强(P＜0.01),同时运动后48 h自噬荧光仍有显著性升高(P＜0.05);Beclin1和LC3II/I在大负荷离心干预后表达升高(P＜0.05),运动后12 h～24 h达到峰值(P＜0.01),直至运动后72 h完全恢复。结论: 大负荷离心运动可诱导骨骼肌自噬超微结构变化,自噬蛋白表达增强,以上可能是运动损伤的骨骼肌功能下降的原因之一。     

Lesions in the rat soleus muscle following eccentrically biased exercise

Morphological changes in skeletal muscle related to lengthening (eccentric) contractions have been noted by several laboratories. However, a systematic examination of skeletal muscle following repetitive eccentric contractions is lacking. This study was undertaken to study lesions and determine their relative densities in rat soleus muscle 30 min following level or downhill treadmill exercise. Following fixation in situ by vascular perfusion, toluidine-blue-stained 1-micron sections of the muscle samples selected at 73-micron intervals were scanned with a light microscope. Three types of lesions were noted: focal disruptions in the A-band, localized dissolution of Z-lines, and clotting of muscle fibers. Soleus muscle from the caged controls and the tibialis anterior muscle from downhill-exercised rats were essentially free of lesions. Eighty-nine percent of the soleus m. lesions in the downhill runner group and 97% of those in the level runner group were A-band disruptions. A-band lesion density was significantly higher in the soleus muscle of the downhill runners compared to level runners with the highest incidence in the distal half. A-band lesion density was lower in soleus muscles from level runners; however, the highest intramuscular incidence was in the proximal rather than the distal end. The results indicate that a disruption of the A-band is a principal change within some skeletal muscle fibers 30 min following repetitive eccentric contractions.     

Protective effect of nitric oxide on cytoskeletal proteins in rat soleus under eccentric exercise

An in vivo study was performed to see whether deterioration of the muscle cytoskeleton caused by eccentric exercise could be counteracted by raising the tissue content of nitric oxide. In Wistar rats that ran downhill on a treadmill inclined at 16° for 40 min at 20 m/min, the desmin content in m. soleus measured 24 h later declined by 15%, and the percentage of ruptures in the dystrophin layer was three times higher than in the control. Destruction of cytoskeletal proteins was also pronounced in rats pretreated with a blocker of NO synthase before exercise. By contrast, animals that received a nitric oxide donor (L-arginine) prior to running had control levels of desmin and dystrophin. It was concluded that nitric oxide can protect muscle cytoskeletal proteins in a single eccentric exercise.     

Exercise-induced muscle glycogen depletion and repletion in diabetic rats.

The purpose of this experiment was to examine glycogen depletion in muscles of chronic diabetic rats during treadmill running of moderate intensity and glycogen repletion following the exercise bouts. Diabetes was induced with a single intravenous injection of streptozotocin (70 mg × kg^?1). Glycogen concentrations in muscles from diabetic and normal animals were determined at rest, after running either 10 or 30 min at 23 m × min^?1 (5% incline), or 2, 4, or 8 hr following 30 min of running at the same speed and incline. With the exception of soleus muscle after 30 min of running, there were no differences in muscle glycogen contents between normal and diabetic rats before exercise, immediately after exercise, or during the recovery period. All muscles showed a significant loss of glycogen during exercise, and most muscles had completely restored their glycogen by 2 hr following exercise. Blood lactate concentrations were also similar for normal and diabetic rats at rest and after exercise. It is concluded that the diabetic condition studied in this experiment did not significantly alter muscle glycogen metabolism during exercise of moderate intensity or during recovery from the activity.     

Effect of hepatic vagotomy on postexercise substrate levels in food-restricted rats

The metabolic effects of a selective hepatic vagotomy (HV) were investigated at rest and immediately after a 50-min exercise period (26 m/min, 0% grade) in rats subjected to an overnight 50% food restriction. This dietary restriction reduced liver glycogen content to 50% of normal resting concentrations (2.2-2.8 g/100 g). No significant differences between HV and sham-operated rats were found in resting and exercising beta-hydroxybutyrate, glucose, glycerol, and insulin concentrations. Postexercise liver glycogen concentrations were reduced to approximately 1.0 g/100 g in both HV and sham-operated groups. This decrease was associated with significantly (P less than 0.01) lower postexercise glycogen levels in the soleus muscle of HV rats (2.6 times) along with higher plasma free fatty acid concentrations (P less than 0.01). These data provide evidence that HV combined with a progressive decrease in liver glycogen content may influence substrate regulation during exercise. They also support the concept of the existence of hepatic glucoreceptors responsive to a decrease in liver glycogen content.     

Adaptive response of hypertrophied skeletal muscle to endurance training

The response of hypertrophied soleus and plantaris muscle of rats to endurance training was studied. Hypertrophy was produced by bilateral extirpation of the gastrocnemius muscle. A 13-wk training program of treadmill running initiated 30 days after removal of the gastrocnemius muscle accentuated (P less than 0.01) the hypertrophy. Succinate dehydrogenase activities of the enlarged muscles of sedentary rats were similar to those of normal animals, as were the increases associated with training. Phosphorylase and hexokinase activities were unaltered as a result of the experimental perturbations. Rates of glycogen depletion during exercise were lower (P less than 0.01) in the liver and soleus and plantaris muscles of endurance-trained animals. No difference existed in the rate of glycogen depletion of normal and hypertrophied muscle within the sedentary or trained groups. These data demonstrate that extensively hypertrophied muscle responds to training and exercise in a manner similar to that of normal muscle.     

Downhill running preferentially increases CGRP in fast glycolytic muscle fibers.

Calcitonin gene-related peptide (CGRP) is present in some spinal cord motoneurons and at neuromuscular junctions in skeletal muscle. We previously reported increased numbers of CGRP-positive (CGRP+) motoneurons supplying hindlimb extensors after downhill exercise (Homonko DA and Theriault E, Inter J Sport Med 18: 1-7, 1997). The present study identifies the responding population with respect to muscle and motoneuron pool and correlates changes in CGRP with muscle fiber type-identified end plates. Twenty seven rats were divided into the following groups: control and 72 h and 2 wk postexercise. FluoroGold was injected into the soleus, lateral gastrocnemius, and the proximal (mixed fiber type) or distal (fast-twitch glycolytic) regions of the medial gastrocnemius (MG). Untrained animals ran downhill on a treadmill for 30 min. The number of FluoroGold/CGRP+ motoneurons within proximal and distal MG increased by 72 h postexercise (P<0.05). No significant changes were observed in soleus or lateral gastrocnemius motoneurons postexercise. The number of alpha-bungarotoxin/CGRP+ motor end plates in the MG increased exclusively at fast-twitch glycolytic muscle fibers 72 h and 2 wk postexercise (P<0.05). One interpretation of these results is that unaccustomed exercise preferentially activates fast-twitch glycolytic muscle fibers in the MG.     

Post-exercise glycogen resynthesis in trained high-protein or high-fat-fed rats after glucose feeding

This study examined the effect on glycogen resynthesis during recovery from exercise of feeding glucose orally to physically trained rats which had been fed for 5 weeks on high-protein low fat (HP), high-protein/long-chain triglyceride (LCT) or high carbohydrate (CHO) diets. Muscle glycogen remained low and hepatic gluconeogenesis was stimulated by long-term fat or high-protein diets. The trained rats received, via a stomach tube, 3 ml of a 34% glucose solution immediately after exercise (2 h at 20 m.min-1), followed by 1-ml portions at hourly intervals until the end of the experiments. When fed glucose soleus muscle glycogen overcompensation occurred rapidly in the rats fed all three diets following prolonged exercise. In LCT- and CHO-fed rats, glucose feeding appeared more effective for soleus muscle repletion than in HP-fed rats. The liver demonstrated no appreciable glycogen overcompensation. A complete restoration of liver glycogen occurred within a 2- to 4-h recovery period in the rats fed HP-diet, while the liver glycogen store had been restored by only 67% in CHO-fed rats and 84% in LCT-fed rats within a 6-h recovery period. This coincides with low gluconeogenesis efficiency in these animals.     

Exercise-induced satellite cell activation in growing and mature skeletal muscle

The time course and extent of satellite cell activation were studied in the soleus (m-SOL) and extensor digitorum longus (m-EDL) muscles of untrained growing and mature rats after a single bout of prolonged eccentric treadmill running. At 24, 48, 72, and 120 h postexercise, satellite cell mitotic activity was quantitated in autoradiographs of whole-fiber segments after injection of [3H]thymidine. Fiber damage and localization of labeled cells were also examined in muscle cross sections. Labeling in growing muscles progressively increased to peak levels (approximately 250% of control) at 72 h postexercise, whereas mature muscles exhibited an earlier peak (approximately 250% of control) at 24 (m-SOL) and 48 (m-EDL) h, followed by a more rapid decline to control levels by 120 h postexercise. In all exercised muscles the calculated satellite cell activation was far greater than required to repair the small number (less than 3.0%) of necrotic fibers identified at the light-microscopic level. These results suggest that satellite cells were activated not only on fibers exhibiting overt necrosis but also on those with lesions not discernible with light microscopy.     

Glycogen overload by postexercise insulin administration abolished the exercise-induced increase in GLUT4 protein

Summary To elucidate the role of muscle glycogen storage on regulation of GLUT4 protein expression and whole-body glucose tolerance, muscle glycogen level was manipulated by exercise and insulin administration. Sixty Sprague-Dawley rats were evenly separated into three groups: control (CON), immediately after exercise (EX0), and 16 h after exercise (EX16). Rats from each group were further divided into two groups: saline- and insulin-injected. The 2-day exercise protocol consisted of 2 bouts of 3-h swimming with 45-min rest for each day, which effectively depleted glycogen in both red gastrocnemius (RG) and plantaris muscles. EX0 rats were sacrificed immediately after the last bout of exercise on second day. CON and EX16 rats were intubated with 1 g/kg glucose solution following exercise and recovery for 16 h before muscle tissue collection. Insulin (0.5 μU/kg) or saline was injected daily at the time when glucose was intubated. Insulin injection elevated muscle glycogen levels substantially in both muscles above saline-injected group at CON and EX16. With previous day insulin injection, EX0 preserved greater amount of postexercise glycogen above their saline-injected control. In the saline-injected rats, EX16 significantly increased GLUT4 protein level above CON, concurrent with muscle glycogen supercompensation. Insulin injection for EX16 rats significantly enhanced muscle glycogen level above their saline-injected control, but the increases in muscle GLUT4 protein and whole-body glucose tolerance were attenuated. In conclusion, the new finding of the study was that glycogen overload by postexercise insulin administration significantly abolished the exercise-induced increases in GLUT4 protein and glucose tolerance.     

Acute effect of physical exercise on glycogen content and lipoprotein lipase activity in untrained diabetic rats

The effect of acute physical exercise on skeletal muscle glycogen content and on lipoprotein lipase activity of muscle, adipose and lung tissues was studied in streptozotocin diabetic and control rats. Rats were accustomed to treadmill running for two weeks after streptozotocin treatment. For an exercise bout of moderate intensity rats were randomly divided into two groups: one was sacrificed immediately after exercise and the other 24 hours afterwards. In addition there was a nonexercised sedentary group. No depletion of glycogen was observed after exercise in the vastus lateralis muscle of control (nondiabetic) rats. No difference in glycogen utilization was found in soleus muscle between diabetic and control rats. In diabetic rats a slight decrease occurred in the lipoprotein lipase activity in adipose tissue immediately after exercise, while in control rats there was a significant decline 24 hours after exercise. In soleus muscle a slight but significant increase of lipoprotein lipase activity occurred 24 hours after exercise in diabetic rats but not in control rats. The results suggest that nonketotic streptozotocin diabetes of short duration does not influence muscle glycogen in the resting state, but glycogen utilization is disturbed in white muscle during moderate treadmill running in untrained diabetic rats. The increase in lipoprotein lipase activity after physical exercise in red muscle of diabetic rats occurs during the recovery phase.     

Glycogen concentrations and endurance capacity of rats with chronic heart failure

The endurance capacities of rats with myocardial infarctions (MI) and of rats having undergone sham operations (SHAM) were tested during a submaximal exercise regimen that consisted of swimming to exhaustion. During this test, a decrement in the endurance capacity of the MI rat was demonstrated as the SHAM rat swam 25% longer than the MI rat (65 +/- 4 vs. 52 +/- 4 min). Glycogen concentrations were measured in the liver and the white gastrocnemius, plantaris, and soleus muscles of SHAM and MI rats that were randomly divided into four subgroups, which consisted of resting control, swim to exhaustion, swim to exhaustion + 24 h recovery, and swim to exhaustion + 24 h recovery + a second swim to exhaustion. The results demonstrated that the glycogen concentrations found in the liver, white gastrocnemius, plantaris, and soleus muscles of the SHAM and MI rats belonging to the resting control groups were similar. After swimming to exhaustion the glycogen concentrations in these tissues were significantly reduced compared with those found in the resting control groups of rats, and after 24 h of recovery the glycogen concentrations in these tissues were again similar to those found in the resting control groups of rats. Since the magnitude of the glycogen depletion in the liver and the white gastrocnemius, plantaris, and soleus muscles was similar in the SHAM and MI rats and because the SHAM rats consistently swam for longer periods of time in each of the experimental groups, it would be logical to assume that the rates of glycogen utilization for the various tissues may have been greater in the MI rat during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Estrogen influences satellite cell activation and proliferation following downhill running in rats.

To investigate the influence of estrogen on postexercise muscle repair processes, we examined the effects of estrogen supplementation (0.25-mg pellet) on numbers of myofibers positive for markers of total, activated, and proliferating satellite cells in rat skeletal muscles 72 h following downhill running. Ovariectomized female rats (n = 44) were divided into four groups (n = 11 per group): sham (no estrogen) controls (SC); sham, exercised (SE); estrogen-supplemented controls (EC); and estrogen-supplemented, exercised (EE). After 8 days of estrogen exposure, animals were exposed to 90 min of treadmill running at 17 m/min (-13.5 degrees ). Seventy-two hours later, soleus and white vastus muscles were removed and immunostained for total [paired box homeotic gene 7 (Pax7)], [activated myogenic differentiation factor D (MyoD)], and proliferating [5-bromo-2'-deoxyuridine (BrdU)] satellite cells. beta-Glucuronidase activity was increased (P < 0.05) in both muscles following exercise; however, the postexercise elevations in enzyme activity were attenuated in the EE group compared with the SE group in the soleus (P < 0.05). Immunohistochemical analysis revealed that exercised groups displayed increased numbers of myofibers containing total, activated, and proliferating satellite cells compared with control groups (P < 0.05). Furthermore, greater numbers of fibers positive for markers of total, activated, and proliferating satellite cells were observed postexercise in EE animals compared with SE animals for both muscles (P < 0.05). The results demonstrate that estrogen may potentially influence post-damage repair of skeletal muscle through activation of satellite cells.     

Carbohydrate metabolism in fructose-fed and food-restricted running rats

In chronically catheterized rats hepatic glycogen was increased by fructose (approximately 10 g/kg) gavage (FF rats) or lowered by overnight food restriction (FR rats). [3-3H]- and [U-14C]glucose were infused before, during, and after treadmill running. During exercise the increase in glucose production (Ra) was always directly related to work intensity and faster than the increase in glucose disappearance, resulting in increased plasma glucose levels. At identical work-loads the increase in Ra and plasma glucose as well as liver glycogen breakdown were higher in FF and control (C) rats than in FR rats. Breakdown of muscle glycogen was less in FF than in C rats. Incorporation of [14C]glucose in glycogen at rest and mobilization of label during exercise partly explained that 14C estimates of carbohydrate metabolism disagreed with chemical measurements. In some muscles glycogen depletion was not accompanied by loss of 14C and 3H, indicating futile cycling of glucose. In FR rats a postexercise increase in liver glycogen was seen with 14C/3H similar to that of plasma glucose, indicating direct synthesis from glucose. In conclusion, in exercising rats the increase in glucose production is subjected to feedforward regulation and depends on the liver glycogen concentration. Endogenous glucose may be incorporated in glycogen in working muscle and may be used directly for liver glycogen synthesis rather than after conversion to trioses. Fructose ingestion may diminish muscular glycogen breakdown. The [14C]glucose infusion technique for determination of muscular glycogenolysis is of doubtful value in rats.