Endurance training: volume-dependent adaptational changes in myosin

The purpose of this study was to find the effect of different endurance training volumes on the composition and turnover of myosin. Sixteen-week-old male rats of the Wistar strain were divided into three different volume-based training groups. Changes in myosin heavy chain (MyHC), myosin light chain (MyLC) isoforms' composition, their synthesis rate, as well as myosin binding C-protein synthesis rate, and muscle protein degradation rate were measured. In slow-twitch (ST) soleus (Sol) muscle MyHC I isoform relative content increased and MyHC IIa isoform decreased during excessive increase in the volume of endurance training (ET). In plantaris (Pla) muscle excessive increase in ET volume decreased MyHC I and IIb isoforms, and increased MyHC IIa and IId relative content. In extensor digitorum longus (EDL) muscle the relative content of MyHC IId isoform increased during ET, but excessive increase in training volume decreased it. In Pla muscle the relative content of MyLC 1 (slow) isoform decreased during ET, but excessive increase in ET volume decreased the relative content of MyLC 3 (fast) isoform in both fast-twitch (FT) muscles. Decrease in MyHC and myosin binding C-protein synthesis rate in Pla muscle had significant correlation with ET volume (r = - 0.537, p < 0.05 and r = - 0.727, p < 0.001 subsequently). MyHC I and IIb isoforms and MyLC 3 (fast) isoform in Pla muscle and MyHC IIb, IId and MyLC 3 (fast) isoforms in EDL muscle are the most sensitive to the increase in ET volume. Excessive increase in ET volume leads to a decrease in physical working capacity. The degradation of muscle protein increased during ET in all groups.     

Composition and turnover of contractile proteins in volume-overtrained skeletal muscle

The purpose of this study was to find the composition shift of myosin heavy chain (MyHC) isoforms in overtraining in fast- and slow-twitch skeletal muscles and different changes in MyHC isofom composition, synthesis and turnover rate between 4-week and 6-week overtraining. Male Wistar rats were randomly assigned to 4-week and 6-week endurance training, 4-week and 6-week overtraining groups. Plantaris (Pla), extensor digitorum longus (EDL), and soleus (Sol) muscles were studied. Daily excretion of 3-methylhistidine (3-MeHis) pool as an indicator for protein degradation increased in the 4-week and 6-week overtraining group to 4.04 +/- 0.21 and 4.32 +/- 0.23 %/day subsequently in comparison with the control group (2.16 +/- 14 %/day, p < 0.001). In Pla muscle MyHC I isoform synthesis rate was 33 200 +/- 2150 (after 6-week overtraining 27 100 +/- 1800, p < 0.05), IIa 32 600 +/- 2100; IId 27 300 +/- 1890 and IIb isoform 20 100 +/- 1600 (after 6-week overtraining 15 500 +/- 1400, p < 0.05) dpm/M leucine/min. Actin synthesis rate increased in fast-twitch muscles during 4- and 6-week overtraining, and in soleus muscle during 6-week overtraining. In EDL and Sol muscle MyHC isoform composition during 6-week overtraining did not change significantly. During the 6-week overtraining the relative content of MyHC I and IIb isoforms decreased and IIa and IId isoforms increased in Pla muscle. The initial increase of MyHC IIb isoform after 4-week overtraining shows the higher stability of this isoform in comparison with MyHC I isoform in fast-twitch muscles during high volume exercise.     

Muscle protein turnover in endurance training: a review

There has been much debate about skeletal muscle capacity to adapt to long-lasting endurance exercise. Exercise in the aerobic zone of metabolism does not result in hypertrophy of skeletal muscle fibres but increases their oxidative capacity. The duration and intensity of an exercise session determines the time period of depressed muscle protein synthesis and increased degradation rate during the recovery period after exercise. Protein turnover characterizes the renewal processes of muscle proteins and the functional capacity of muscle. The turnover rate of myofibrillar proteins is slow in comparison with mitochondrial proteins and depends on the oxidative capacity of muscle fibres. The turnover rate of myofibrillar proteins in the same muscle is different and is also different within the myosin molecule between myosin heavy and light chain isoforms. The turnover rate of muscle proteins in endurance training shows the adaptation of skeletal muscle to long-lasting exercise via remodelling of muscle structures. Adaptational coordination between myofibrillar and mitochondrial compartments shows the physiological role and adaptational capacity of skeletal muscle to endurance training. It is challenging to use muscle protein turnover for the purposes of monitoring the training process of endurance athletes, optimizing training programs and preventing overtraining.     

Metabolic adaptations to short-term high-intensity interval training: a little pain for a lot of gain?

High-intensity interval training (HIT) is a potent time-efficient strategy to induce numerous metabolic adaptations usually associated with traditional endurance training. As little as six sessions of HIT over 2 wk or a total of only approximately 15 min of very intense exercise (approximately 600 kJ), can increase skeletal muscle oxidative capacity and endurance performance and alter metabolic control during aerobic-based exercise.     

The effect of mechanical loading on the MyHC synthesis rate and composition in rat plantaris muscle

The aim of this study was to investigate the response of protein synthesis rate, particularly myosin heavy chain (MyHC) isoforms synthesis and the magnitude of its isoform transformation in fast-twitch plantaris muscle, to different modes of prolonged mechanical loading. Different protocols of mechanical loading were used: resistance training (RT), compensatory hypertrophy (CH) of m. plantaris after tenotomy of m. gastrocnemius and a combination of the two previous loadings (RT + CH). During the different modes of loading, plantaris muscle hypertrophy in RT group was approximately 10 %, CH approximately 40 % and CH + RT approximately 44 %. MyHC I and IID isoform synthesis rate increased in all experimental groups, as well as their relative content. MyHC IIA relative content decreased during RT and RT + CH and increased during CH. MHC IIB isoform relative content decreased in all experimental groups, but compared with CH in CH + RT MyHC IIB isoform content increased in plantaris muscle. These results demonstrate that different modes of mechanical loading resulted in the selective up- and down-regulation of MyHC isoforms in fast-twitch skeletal muscle. The synthesis rate and relative content of the two fastest isoforms of MyHC IIB and IID are regulated to different directions during mechanical loading.     

Capillarization in skeletal muscle of rats with cardiac hypertrophy

PURPOSE: Exercise intolerance during chronic heart failure (CHF) is localized mainly in skeletal muscle. A decreased capillarization may impair exchange of oxygen between capillaries and muscle tissue and in this way contribute to exercise intolerance. We assessed changes in capillary supply in plantaris and diaphragm muscles of a rat aorta-caval fistula (ACF) preparation, a volume overload model for CHF. METHODS: An ACF was created under equithesin anesthesia. Plantaris and diaphragm muscles were removed 6 wk postsurgery and examined for myosin heavy chain (MyHC) content and capillary supply. RESULTS: Cardiac hypertrophy was 96% (P < 0.002) after ACF. The Type IIb MyHC content of the plantaris muscles increased (33.9 +/- 3.3 vs 49.8 +/- 3.8%; mean +/- SEM) at the expense of Type IIa MyHC (17.6 +/- 1.8 vs 11.2 +/- 1.7%) in ACF rats (P < 0.05). In the diaphragm, the number of Type I (32.1 +/- 2.3 vs 40.6 +/- 2.7%) and IIb fibers (40.6 +/- 1.9 vs 49.6 +/- 3.6%) increased at the expense of Type IIa fibers (26.8 +/- 2.5 vs 9.4 +/- 0.9%) (P < 0.05). The capillary number per fiber did not change, and this indicated that no capillary loss occurred with ACF. Also, the capillary density was maintained in the diaphragm and plantaris muscles of ACF rats. Furthermore, the coupling between fiber type, size, and metabolic type of surrounding fibers, with the capillary supply to a fiber, was maintained in rats with an ACF. CONCLUSION: The cardiac hypertrophy induced by volume overload seems adequate to prevent atrophy and changes in the microcirculation of limb and diaphragm muscles.     

Endurance training-induced increases in expiratory muscle oxidative capacity.

Recent evidence demonstrates that endurance exercise training improves the oxidative capacity of the major mammalian inspiratory muscle (e.g., costal diaphragm). In contrast, no data exist concerning the effects of exercise training on abdominal expiratory muscles. We tested the hypothesis that 12 wk of endurance exercise training would significantly increase the activity of selected beta oxidation and Krebs cycle enzymes of abdominal expiratory muscles of the rat. To test this hypothesis two groups of female Sprague-Dawley rats were studied: group 1, continuous exercise training (n = 13); and group 2, sedentary control (n = 6). Exercise trained animals ran 5 d.wk-1 on a motorized treadmill for 45 min.d-1 at approximately 75-80% VO2max. When compared with controls, exercise training resulted in elevated (P less than 0.05) activities of 3-hydroxy-acyl-Co-A dehydrogenase (HADH) and citrate synthase (CS) in two abdominal expiratory muscles (rectus abdominus and external obliques). In contrast, training did not alter (P greater than 0.05) CS or HADH activity in the internal obliques/transversus abdominus muscles. In general, the training-induced increases in expiratory muscles CS activity were relatively small (approximately 10-13%) when compared with the training-induced increase in CS activity in the plantaris muscle (approximately 44%). These data demonstrate that continuous exercise training results in small but statistically significant improvements in the oxidative and beta oxidation capacities of expiratory muscles.     

运动对衰老骨骼肌卫星细胞成肌分化中线粒体活性氧生成的影响及调控机制

目的:观察耐力运动训练对衰老骨骼肌卫星细胞成肌分化中线粒体活性氧(ROS)生成的影响,并探讨过氧化物酶体增殖物激活受体γ辅激活因子1(PGC-1α)对ROS生成调控的潜在机制。方法:C57BL/6小鼠分为青年对照组(YN组,2月龄,12只)、老年对照组(ON组,12月龄,12只)和老年运动训练组(OT组,12月龄,12只),其中OT组进行中等强度跑台训练(0°,17 m/min,25 min/天,5天/周)。12周后,HE染色鉴定骨骼肌萎缩程度。两步酶消化法分离骨骼肌卫星细胞,原代培养并体外诱导成肌分化24 h。倒置显微镜观察卫星细胞成肌分化程度,测定线粒体呼吸功能、细胞ROS水平、线粒体ROS生成速率、肌球蛋白重链(MyHC)各亚基mRNA表达,及MyHC、PGC-1α、Tfam、COXⅣ、MnSOD蛋白表达量。结果:与YN组比较,ON组肌纤维横截面积、肌管形成数量、My-HC蛋白表达、MyHCⅠ、MyHCⅡa、MyHCⅡx mRNA表达、态3呼吸速率(ST3)、呼吸控制比(RCR)和PGC-1α、Tfam、COXⅣ、MnSOD蛋白表达均显著降低(P<0.05～0.01),ON组态4呼吸速率(ST4)、细胞ROS水平、线粒体ROS生成速率及MyHCⅡb mRNA表达显著升高(P<0.05～0.01)。与ON组比较,OT组湿重/体重比值、肌纤维横截面积、肌管形成数量、MyHC蛋白表达、MyHCⅠ、MyHCⅡa、My-HCⅡx mRNA表达、ST3、RCR和PGC-1α、Tfam、COXⅣ、MnSOD蛋白表达均显著升高(P<0.05～0.01),OT组细胞ROS水平、线粒体ROS生成速率及MyHCⅡb mRNA表达显著降低(P<0.05～0.01)。结论:耐力运动训练提高衰老骨骼肌卫星细胞成肌分化中PGC-1α表达,继而通过上调Tfam和MnSOD提高线粒体能量代谢,减少线粒体ROS产生,以促进成肌分化。     

Acute and chronic responses of skeletal muscle to endurance and sprint exercise. A review

Skeletal muscle adapts to the stress of endurance and sprint exercise and training. There are 2 main types of skeletal muscle fibre--slow twitch (ST) and fast twitch (FTa, FTb, FTc). Exercise may produce transitions between FT and ST fibres. Sprint training has decreased the proportion of ST fibres and significantly increased the proportion of FTa fibres, while endurance training may convert FTb to FTa fibres, and increase the proportion of ST fibres (i.e. FTb----FTa----FTc----ST). However, the high proportion of ST fibres documented for elite endurance athletes may be simply the result of natural selection. ST fibres function predominantly during submaximal exercise, whereas FT fibres are recruited as exercise intensity approaches VO2max and/or glycogen stores are depleted. Long distance runners have greater ST and FT fibre areas than untrained controls. However, doubt remains as to whether the ST or FT fibre area is greatest in endurance athletes. Increases in FT fibre area seem to occur during the first 2 months of training whereas ST fibre areas appear to increase after 2 to 6 months of training. Sprint training leads to the preferential use of FT fibres and male, but not female sprinters have larger FT fibres than untrained controls. Mitochondrial proteins and oxidative enzymes, as opposed to VO2max, are important determinants of the duration of endurance exercise. Endurance training increases intramuscular glycogen stores in both FT and ST fibres and produces a 'glycogen-sparing' effect which is characterised by an increased free fatty acid (FFA) metabolism. The activity of glycogen synthase is also increased by endurance training. Sprint training increases glycogen concentrations similarly in all fibre types, reduces the rate of glycogen utilisation at submaximal workloads and allows supramaximal workloads to be maintained for longer periods of time. During endurance exercise the pattern of glycogen depletion varies between muscle fibre types and between muscle groups. Glycogen stores in ST fibres are utilised initially, followed by stores in FTa then FTb fibres. Sprint activities are associated with a much greater rate of glycogen depletion. However, it is unlikely that glycogen depletion causes fatigue during sprinting. Sprint work is associated with a preferential depletion of glycogen from FTb then FTa and ST fibres. Endurance training appears to increase triglyceride stores adjacent to mitochondria and ST fibres have greater triglyceride stores than FT fibres. Endurance exercise is associated with a preferential use of triglycerides from ST fibres and endogenous triglycerides may account for over 50% of the total lipid oxidised during exercise.(ABSTRACT TRUNCATED AT 400 WORDS)     

Calcium sensitivity of human single muscle fibers following plyometric training

PURPOSE: To study the effect of plyometric training on Ca2+ sensitivity and the influence of troponin T (TnT) isoforms on Ca2+ -activation properties in skinned human muscle fibers. METHODS: Biopsies were obtained from the vastus lateralis of eight men before and after the training period. Chemically skinned fibers were evaluated regarding their Ca2+ -activation properties and were classified according to their myosin heavy chain (MHC) contents and analyzed regarding their slow and fast TnT isoforms. RESULTS: After training, significant improvements (P < 0.05) were found for static jump, countermovement jump, 6 x 5-m shuttle-run test, and leg-press performances. An 8% increase in the proportion of type IIa fibers (P < 0.05) was observed. Single-fiber diameters increased by 11% in type I (P < 0.01), 10% in type IIa (P < 0.001), and 15% in type IIa/IIx fibers (P < 0.001). Peak fiber force increased by 35% in type I (P < 0.001), 25% in type IIa (P < 0.001), and 57% in type IIa/IIx fibers (P < 0.01). The Ca2+ -activation threshold was not altered by training, but the Ca2+ concentration required to elicit half-maximal activation showed a decreasing trend, with significant changes in type I fibers (P < 0.001). Cooperativity at low Ca2+ concentrations was increased in type I and type IIa/IIx fibers (P < 0.05). Type I fibers exclusively expressed slow TnT isoforms, and type II fibers were always associated with fast TnT isoforms, independent of training status. Therefore, changes in Ca2+ sensitivity after training could not be explained by differential fast or slow TnT isoform expression. CONCLUSION: Plyometric training increased single-fiber Ca2+ sensitivity, especially in type I fibers. These changes could not be explained by a modified TnT isoform expression pattern.     

Development of aerobic power in relation to age and training in cross-country skiers.

In most of the training studies on different populations the effects of training have been investigated up to a frequency of five to six times per week and a duration of 45 min per session. These correspond to the training regimens of 15-yr-old cross-country skiers and, consequently, the results cannot be applied to older athletes. The maximal oxygen uptake (VO2max) of cross-country skiers increases with age and training from about 55-60 to 75-80 ml.kg-1.min-1 between 15 and 25 yr of age. After 20 yr of age VO2max starts to level off, but elite skiers are able to increase VO2max further concomitantly with an increase in the volume of training and the volume of intensive training. The activity of oxidative enzymes in muscles of skiers is increased with training, but distance runners have had a higher oxidative capacity in their leg muscles. Although widely used by cross-country skiers, the training effects of roller skiing, skiwalking-skistriding, and long-distance training on skis are to a large extent unknown. However, intensive training at the intensity of "anaerobic threshold" or higher seems to be most effective in inducing improvements in maximal oxygen uptake; distance training at relatively low intensity seems to be most effective in producing improvements in the determinants of submaximal endurance.     

Exercise training-induced alterations in skeletal muscle antioxidant capacity: a brief review.

Cellular oxidants include a variety of reactive oxygen, nitrogen, and chlorinating species. It is well established that the increase in metabolic rate in skeletal muscle during contractile activity results in an increased production of oxidants. Failure to remove these oxidants during exercise can result in significant oxidative damage of cellular biomolecules. Fortunately, regular endurance exercise results in adaptations in the skeletal muscle antioxidant capacity, which protects myocytes against the deleterious effects of oxidants and prevents extensive cellular damage. This review discusses the effects of chronic exercise on the up-regulation of both antioxidant enzymes and the glutathione antioxidant defense system. Primary antioxidant enzymes superoxide dismutase, glutathione peroxidase, and catalase will be discussed as well as glutathione, which is an important nonenzymatic antioxidant. Growing evidence indicates that exercise training results in an elevation in the activities of both superoxide dismutase and glutathione peroxidase along with increased cellular concentrations of glutathione in skeletal muscles. It seems plausible that increased cellular concentrations of these antioxidants will reduce the risk of cellular injury, improve performance, and delay muscle fatigue.     

Endurance training reduces the rate of diaphragm fatigue in vitro

PURPOSE: The present study examined the effects of endurance training on the contractile and biochemical properties of the rat costal diaphragm in vitro. METHODS: Sixty-four rats were divided into two groups: exercise trained (T) and control (C). Training consisted of treadmill running 5 d x wk(-1), 60 min x d(-1) at approximately 70% of VO2max, over a 10-wk period. RESULTS: Control diaphragm strips produced an average of 12% less force from minute 15 to 50 of a 60-min in vitro fatigue protocol, compared with the T diaphragm strips (P < 0.01). T diaphragms had 10.1% higher citrate synthase (CS) and 12.1% higher superoxide dismutase (SOD) activities compared with the C (P < 0.05). Despite a significant decrease (P < 0.05) in Type IIb myosin heavy chains (MHC) and an increase (P < 0.05) in Type I MHC in T diaphragms, maximal shortening velocity (Vmax) in the diaphragm was not different between T and C animals. No differences were observed in specific force or the relative proportions of myosin light chains between groups. CONCLUSIONS: These findings suggest that endurance training reduces the rate of diaphragm fatigue in vitro but has no effect on Vmax or specific force.     

Specific muscle adaptations in type II fibers after high‐intensity interval training of well‐trained runners

High‐intensity interval training (HIIT) forms an important component of endurance athletes' training, but little is known on intramuscular metabolic and fiber type adaptations. This study investigated physiological and skeletal muscle adaptations in endurance runners subjected to 6 weeks HIIT. Eighteen well‐trained endurance athletes were subjected to 6 weeks HIIT. Maximal and submaximal exercise tests and muscle biopsies were performed before and after training. Results indicated that peak treadmill speed (PTS) increased (21.0 ± 0.8 vs 22.1 ± 1.2 km/h, P<0.001) and plasma lactate decreased at 64% and 80% PTS (P<0.05) after HIIT. Cross‐sectional area of type II fibers tended to have decreased (P=0.06). No changes were observed in maximal oxygen consumption, muscle fiber type, capillary supply, citrate synthase and 3‐hydroxyacetyl CoA dehydrogenase activities. Lactate dehydrogenase (LDH) activity increased in homogenate (P<0.05) and type IIa fiber pools (9.3%, P<0.05). The change in the latter correlated with an absolute interval training speed (r=0.65; P<0.05). In conclusion, HIIT in trained endurance runners causes no adaptations in muscle oxidative capacity but increased LDH activity, especially in type IIa fibers and in relation to absolute HIIT speed.     

Effects of resistance training on endurance capacity and muscle fiber composition in young top-level cyclists

Equivocal findings exist on the effect of concurrent strength (S) and endurance (E) training on endurance performance and muscle morphology. Further, the influence of concurrent SE training on muscle fiber-type composition, vascularization and endurance capacity remains unknown in top-level endurance athletes. The present study examined the effect of 16 weeks of concurrent SE training on maximal muscle strength (MVC), contractile rate of force development (RFD), muscle fiber morphology and composition, capillarization, aerobic power (VO2max), cycling economy (CE) and long/short-term endurance capacity in young elite competitive cyclists (n=14). MVC and RFD increased 12-20% with SE (P<0.01) but not E. VO2max remained unchanged. CE improved in E to reach values seen in SE. Short-term (5-min) endurance performance increased (3-4%) after SE and E (P<0.05), whereas 45-min endurance capacity increased (8%) with SE only (P<0.05). Type IIA fiber proportions increased and type IIX proportions decreased after SE training (P<0.05) with no change in E. Muscle fiber area and capillarization remained unchanged. In conclusion, concurrent strength/endurance training in young elite competitive cyclists led to an improved 45-min time-trial endurance capacity that was accompanied by an increased proportion of type IIA muscle fibers and gains in MVC and RFD, while capillarization remained unaffected.     

Exercise and beta-adrenergic regulation of rat cardiac myosin isoforms

BACKGROUND: The purpose of this experiment was to examine the effects of both exercise and beta-adrenergic receptor blockade on the expression of native cardiac myosin isoforms. Specifically, this experiment tested two hypotheses: 1) treatment of sedentary rats with the beta blocker, propranolol, will promote increased ventricular V3 (slow) native myosin content with a concomitant reduction of V1 (fast) myosin isoforms; and 2) endurance exercise training will result in an increased sympathetic drive and therefore will retard the propranolol-induced shift in cardiac myosin isoform expression. METHODS: Adult, male Sprauge-Dawley rats (120 days old) were randomly divided into 4 groups: 1) exercise-sham (ES); 2) exercise-propranolol (EP); 3) sedentary-sham (SS); and 4) sedentary-propranolol (SP). Propranolol (30 mg drug/kg body wt) and sham (saline) injections (i.p.) were administered 30 minutes prior to daily exercise. Both ES and EP groups completed six weeks (5 day/wk) of treadmill running at approximately 65-70% VO2max. RESULTS: Data analysis revealed that exercise training did not alter (p > 0.05) ventricular myosin isoforms in the sham injected animals. In contrast, propranolol treatment resulted in a significant (p < 0.05) increase in the slow (V3) myosin isoform and a concomitant decrease in the V1 isoform in both sedentary and exercise trained animals. CONCLUSIONS: The observed increase in V3 myosin isoform in propranolol treated rats supports the notion that beta-adrenergic stimulation is an important regulator of cardiac myosin isoform expression. However, our hypothesis that exercise training would retard the propranolol-induced shift in cardiac myosin was not supported.     

The profile and distribution of myosin heavy chain isoforms in middle-aged sedentary persons

AIM: Human lifestyle has drastically changed during the past century as the share of physical work in daily life has decreased. The purpose of the present study was to examine the distribution of myosin heavy chain (MHC) isoforms in middle-aged sedentary persons, to compare the proportion of MHC isoforms of middle-aged and young sedentary persons and to demonstrate the effect of physical activity of MHC isoforms in middle-aged sedentary persons. METHODS: Eighty-nine middle-aged sedentary and 13 young sedentary persons volunteered for the study. Thirty middle-aged sedentary subjects participated in strength-conditional exercise program during 9 months. Vertical jumping height and maximal anaerobic work capacity were measured. Muscle samples were taken from vastus lateralis muscle. MHC isoform composition was determined by SDS-PAGE. RESULTS: Variation of MHC I and MHC IIa isoforms in middle-age sedentary persons demonstrated normal distribution. Significant differences of MHC isoform proportions between middle-aged and young sedentary participants were not observed. The proportion of MHC IIx decreased significantly after the exercise period that significantly improved the maximal anaerobic power and jumping height of participants. CONCLUSIONS: Normal distribution illustrated the proportion of MHC I and MHC IIa isoforms in 89 middle-aged sedentary persons while significant differences of MHC isoforms proportion between young and middle-aged sedentary persons were not observed. Even small increase of physical activity improved physical performance and decrease the MHC IIx proportion of middle-aged sedentary persons. Physically active lifestyle in middle age, when age-related changes have not started yet, may delay age-related changes in skeletal muscle.     

Erythropoietin induces a shift of muscle phenotype from fast glycolytic to slow oxidative

Sedentary and trained rat groups were studied. Each of these groups was either erythropoietin or placebo treated. Erythropoietin treatment increased significantly all haematological parameters studied. Training per se failed to modify haematological parameters. In a second time, we studied the specific activity of several oxidative enzymes in three different muscles. In sedentary rats, erythropoietin treatment increased significantly the specific activities of cytochrome c oxidase and L-3-hydroxyacyl CoA dehydrogenase in the soleus and those of L-3-hydroxyacyl CoA dehydrogenase and phosphofructokinase in both locomotor muscles. Training increased the oxidative enzymes activities in all muscles studied. In trained rats, effects of erythropoietin and training on oxidative enzymes activities were additive. In all erythropoietin treated muscles, the expression of slow twitch myosin light chains and oxidative myosin heavy chains increased. A similar phenomenon took place in all trained groups for light chains and in placebo treated trained rats for heavy chains. In trained groups, the effects of the hormone and of training were additive. Our results suggest strongly that two different mechanisms are involved in the response of skeletal muscles to erythropoietin treatment and to endurance training and probably whole body endurance is affected by erythropoietin treatment by an increase of oxygenation of all tissues.