Relationships between skeletal muscle characteristics and aerobic performance in sedentary and active subjects

Forty-eight sedentary and 39 quite active or well-trained men participated in this study. Muscle biopsy samples were taken from the vastus lateralis for the determination of fiber type composition (I, IIa, IIb), fiber type area, and assay of the following enzymes: malate dehydrogenase (MDH), 3-hydroxyacyl CoA dehydrogenase (HADH) and oxoglutarate dehydrogenase (OGDH). Maximal oxygen uptake (VO2max) was determined with a progressive cycle ergometer test, while endurance performance or maximal aerobic capacity (MAC) was defined as the total work output during a 90-min cycle ergometer test. Correlation analysis revealed no evidence of association between fiber type composition and VO2max kg-1 or MAC kg-1 in sedentary subjects, while active men exhibited significant correlation between % type I (r = 0.52), % type IIb (r = 0.31) and VO2max kg-1. Enzyme activities were not significantly correlated with MAC kg-1 and VO2max kg-1 in sedentary men while active men exhibited significant correlation for the three enzymes (0.37 less than or equal to r less than or equal to 0.51) with VO2max kg-1. These results show that the contribution of muscle fiber type and enzyme activities to aerobic performance may be inflated from a statistical point of view by the training status heterogeneity of subjects. They also suggest that variation in these muscle characteristics does not account for the individual differences in aerobic performance of subjects who have never trained before. Therefore, the assessment of muscle characteristics is not as useful as originally thought for the detection of individuals with a high potential for endurance performance among untrained subjects.     

H1 and H2 receptors mediate postexercise hyperemia in sedentary and endurance exercise-trained men and women.

In sedentary individuals, H(1) receptors mediate the early portion of postexercise skeletal muscle hyperemia, whereas H(2) receptors mediate the later portion. It is not known whether postexercise hyperemia also presents in endurance-trained individuals. We hypothesized that the postexercise skeletal muscle hyperemia would also exist in endurance-trained individuals and that combined blockade of H(1) and H(2) receptors would abolish the long-lasting postexercise hyperemia in trained and sedentary individuals. We studied 28 sedentary and endurance trained men and women before and through 90 min after a 60-min bout of cycling at 60% peak O(2) uptake on control and combined H(1)- and H(2)-receptor antagonist days (fexofenadine and ranitidine). We measured arterial pressure (brachial auscultation) and femoral blood flow (Doppler ultrasound). On the control day, femoral vascular conductance (calculated as flow/pressure) was elevated in all groups 60 min after exercise (sedentary men: Delta86 +/- 35%, trained men, Delta65 +/- 18%; sedentary women, Delta61 +/- 19%, trained women: Delta59 +/- 23%, where Delta is change; all P < 0.05 vs. preexercise). In contrast, on the histamine antagonist day, femoral vascular conductance was not elevated in any of the groups after exercise (sedentary men: Delta21 +/- 17%, trained men: Delta9 +/- 5%, sedentary women: Delta19 +/- 4%, trained women: Delta11 +/- 11%; all P > 0.16 vs. preexercise; all P < 0.05 vs. control day). These data suggest postexercise skeletal muscle hyperemia exists in endurance trained men and women. Furthermore, histaminergic mechanisms produce the long-lasting hyperemia in sedentary and endurance-trained individuals.     

Creatine kinase MB and citrate synthase in type I and type II muscle fibres in trained and untrained men

Total creatine kinase (CK), creatine kinase MB (CK-MB) and citrate synthase (CS) were determined in isolated and pooled type I and type II skeletal muscle fibres. Determinations were made on biopsies from 3 sedentary men, 3 junior cyclists and 2 elite cyclists. CS and CK-MB activities were higher in the trained groups in both fibre types. The total CK activity was not related to training status, although it was lower in type I fibres than in type II fibres (p less than 0.05). The reverse relation was observed for CS and CK-MB activities (p less than 0.01). The ratio of type I/type II for CS was not related to training status, while the corresponding ratio for CK-MB increased with a greater degree of endurance training. For a given increase in CS activity, the increase in CK-MB activity was greater in type I fibres than in type II fibres (p less than 0.01). Thus, with endurance training there seems to be a specific adaptation for CK-MB, particularly in type I fibres.     

5'-AMP-activated protein kinase activity and subunit expression in exercise-trained human skeletal muscle.

5'-AMP-activated protein kinase (AMPK) has been proposed to be a pivotal factor in cellular responses to both acute exercise and exercise training. To investigate whether protein levels and gene expression of catalytic (alpha(1), alpha(2)) and regulatory (beta(1), beta(2), gamma(1), gamma(2), gamma(3)) AMPK subunits and exercise-induced AMPK activity are influenced by exercise training status, muscle biopsies were obtained from seven endurance exercise-trained and seven sedentary young healthy men. The alpha(1)- and alpha(2)-AMPK mRNA contents in trained subjects were both 117 +/- 2% of that in sedentary subjects (not significant), whereas mRNA for gamma(3) was 61 +/- 1% of that in sedentary subjects (not significant). The level of alpha(1)-AMPK protein in trained subjects was 185 +/- 34% of that in sedentary subjects (P < 0.05), whereas the levels of the remaining subunits (alpha(2), beta(1), beta(2), gamma(1), gamma(2), gamma(3)) were similar in trained and sedentary subjects. At the end of 20 min of cycle exercise at 80% of peak O(2) uptake, the increase in phosphorylation of alpha-AMPK (Thr(172)) was blunted in the trained group (138 +/- 38% above rest) compared with the sedentary group (353 +/- 63% above rest) (P < 0.05). Acetyl CoA-carboxylase beta-phosphorylation (Ser(221)), which is a marker for in vivo AMPK activity, was increased by exercise in both groups but to a lower level in trained subjects (32 +/- 5 arbitrary units) than in sedentary controls (45 +/- 1 arbitrary units) (P < 0.01). In conclusion, trained human skeletal muscle has increased alpha(1)-AMPK protein levels and blunted AMPK activation during exercise.     

Physiological and biochemical correlates of increased work in trained iron-deficient rats

We investigated physiological and biochemical factors associated with the improved work capacity of trained iron-deficient rats. Female 21-day-old rats were assigned to one of four groups, two dietary groups (50 and 6 ppm dietary iron) subdivided into two levels of activity (sedentary and treadmill trained). Iron deficiency decreased hemoglobin (61%), maximal O2 uptake. (VO2max) (40%), skeletal muscle mitochondrial oxidase activities (59-90%), and running endurance (94%). In contrast, activities of tricarboxylic acid (TCA) cycle enzymes in skeletal muscle were largely unaffected. Four weeks of mild training in iron-deficient rats resulted in improved blood lactate homeostasis during exercise and increased VO2max (15%), TCA cycle enzymes of skeletal muscle (27-58%) and heart (29%), and liver NADH oxidase (34%) but did not affect any of these parameters in the iron-sufficient animals. In iron-deficient rats training affected neither the blood hemoglobin level nor any measured iron-dependent enzyme pathway of skeletal muscle but substantially increased endurance (230%). We conclude that the training-induced increase in endurance in iron-deficient rats may be related to cardiovascular improvements, elevations in liver oxidative capacity, and increases in the activities of oxidative enzymes that do not contain iron in skeletal and cardiac muscle.     

Skeletal muscle adaptations to endurance training in 60- to 70-yr-old men and women.

Previous studies of endurance exercise training in older men and women generally have found only minimal skeletal muscle adaptations to training. To evaluate the possibility that this may have been due to an inadequate training stimulus, we studied 23 healthy older (64 +/- 3 yr) men and women before and after they had trained by walking/jogging at 80% of maximal heart rate for 45 min/day 4 days/wk for 9-12 mo. This training program resulted in a 23% increase in maximal O2 consumption. Needle biopsy samples of the lateral gastrocnemius muscle were obtained before and after training and analyzed for selected histochemical and enzymatic characteristics. The percentage of type I muscle fibers did not change with training. The percentage of type IIb fibers, however, decreased from 19.1 +/- 9.1 to 15.1 +/- 8.1% (P less than 0.001), whereas the percentage of type IIa fibers increased from 22.1 +/- 7.7 to 29.6 +/- 9.1% (P less than 0.05). Training also induced increases in the cross-sectional area of both type I (12%; P less than 0.001) and type IIa fibers (10%; P less than 0.05). Capillary density increased from 257 +/- 43 capillaries/mm2 before training to 310 +/- 48 capillaries/mm2 after training (P less than 0.001) because of increases in the capillary-to-fiber ratio and in the number of capillaries in contact with each fiber. Lactate dehydrogenase activity decreased by 21% (P less than 0.001), whereas the activities of the mitochondrial enzymes succinate dehydrogenase, citrate synthase, and beta-hydroxyacyl-CoA dehydrogenase increased by 24-55% in response to training (P less than 0.001-0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of beta 1- vs. beta 1- beta 2-blockade on training adaptations in rat skeletal muscle

The effect of selective vs. nonselective beta-blockade on fast-twitch [extensor digitorum longus (EDL)] and slow-twitch [soleus (SOL)] muscle enzyme activities following endurance training were characterized. Citrate synthase (CS), lactate dehydrogenase (LDH), and beta-hydroxyacyl-CoA dehydrogenase (HAD) activities were compared in SOL and EDL muscles of trained (T), metoprolol-trained (MT), propranolol-trained (PT), and sedentary (C) rats. Following 8 wk of treadmill running (1 h/day, 5 days/wk at approximately 30 m/min), LDH activity was depressed approximately 20% (P less than 0.05) in both SOL and EDL in only the PT rats, indicating inhibition of beta 2-mediated anaerobic glycolysis. EDL CS activity was similarly elevated in all three trained groups compared with sedentary controls. In SOL muscle, however, a drug attenuation effect was observed so that CS activity was increased only in the T (P less than 0.01) and MT (P less than 0.05) groups. HAD enzyme activity was increased somewhat (P less than 0.10) in SOL muscle in only the T group, but more so (P less than 0.05) in EDL in all three trained groups. The above findings suggest a training-induced selectivity effect not only with respect to beta 1-vs. beta 1-beta 2-blockers, but also with respect to muscle fiber type.     

Effects of iron deficiency and training on mitochondrial enzymes in skeletal muscle

We measured mitochondrial enzyme activities in skeletal muscle under conditions of iron deficiency and endurance training to assess the effects of these interventions on the contents and proportions of non-iron-containing and iron-dependent enzymes and proteins. Male Sprague-Dawley rats, 21 days of age, received a diet containing either 6 (iron deficient) or 50 mg iron/kg diet (iron sufficient). At 35 days of age animals were subdivided into sedentary and endurance training groups (running at 0.7 mph, 0% grade, 45 min/day, 6 days/wk). By 70 days of age, iron deficiency had decreased gastrocnemius muscle cytochrome c by 62% in sedentary animals. In contrast, the activities of tricarboxylic acid cycle enzymes were increased, remained unchanged or were slightly decreased, indicating that iron deficiency markedly altered mitochondrial composition. Endurance training increased cytochrome c (35%), tricarboxylic acid cycle enzymes (approximately 15%), and manganese superoxide dismutase (33%) in iron-deficient rats, whereas the same exercise regimen had no effect on the skeletal muscle of iron-sufficient animals. The interactive effect of dietary iron deficiency and mild exercise on mitochondrial enzymes suggests that adaptation to a training stimulus is, to some extent, geared to the relationship between the energy demand of exercise and the capacity for O2 transport and utilization.     

Adrenal medulla and exercise training

The adrenaline release from the adrenal medulla increases during exercise, but at a given absolute work intensity the magnitude of this response is less pronounced in endurance trained vs sedentary individuals most likely due to a lower sympathetic stimulation of the adrenal medulla. However, when trained and untrained subjects are compared at identical relative work loads as well as in response to numerous non-exercise stimuli, endurance trained athletes have a higher epinephrine secretion capacity compared to sedentary individuals. This indicates a development of a so-called “sports adrenal medulla” as a result of a long term adaption of an endocrine gland to physical training. Such an adaptation is parallel to adaptations taking place in other tissues like skeletal muscle and the heart, and can be advantageous in relation to both exercise performance in the competing athlete and cause a biological rejuvenation in relation to aging. Accepted: 4 September 1997     

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.     

Aging and respiratory muscle metabolic plasticity: effects of endurance training.

We examined the oxidative and antioxidant enzyme activities in respiratory and locomotor muscles in response to endurance training in young and aging rats. Young adult (4-mo-old) and old (24-mo-old) female Fischer 344 rats were divided into four groups: 1) young trained (n = 12), 2) young untrained (n = 12), 3) old trained (n = 10), and 4) old untrained (n = 6). Both young and old endurance-trained animals performed the same training protocol during 10 wk of continuous treadmill exercise (60 min/day, 5 days/wk). Compared with young untrained animals, the young trained group had significantly elevated (P less than 0.05) activities of 3-hydroxyacyl-CoA dehydrogenase (HADH), glutathione peroxidase (GPX), and citrate synthase (CS) in both the costal diaphragm and the plantaris muscle. In contrast, training had no influence (P greater than 0.05) on the activity of lactate dehydrogenase within the costal diaphragm in young animals. In the aging animals, training did not alter (P greater than 0.05) activities of CS, HADH, GPX, or lactate dehydrogenase in the costal diaphragm but significantly (P less than 0.05) increased CS, HADH, and GPX activities in the plantaris muscle. Furthermore, training resulted in higher activities of CS and HADH in the intercostal muscles in the old trained than in the old untrained animals. Finally, activities of CS, HADH, and GPX were significantly (P less than 0.05) lower in the plantaris in the old untrained than in the young untrained animals; however, CS, HADH, and GPX activities were greater (P less than 0.05) in the costal diaphragm in the old sedentary than in the young untrained animals.(ABSTRACT TRUNCATED AT 250 WORDS)     

The respiratory system as an exercise limiting factor in normal sedentary subjects.

The present study was undertaken to investigate the respiratory system as an exercise limiting factor. Breathing and cycle endurance (i.e. the time until exhaustion at a given performance level) as well as physical working capacity 170 (i.e. the exercise intensity corresponding to a heart rate of 170 beats.min-1 on a cycle ergometer) were determined in four healthy sedentary subjects. Subsequently, the subjects trained their respiratory system for 4 weeks by breathing daily about 90 l.min-1 for 30 min. Otherwise they continued their sedentary lifestyle. Immediately after the respiratory training and 18 months later, all performance tests carried out at the beginning of the study were repeated. The respiratory training increased breathing endurance from 4.2 (SD 1.9) min to 15.3 (SD 3.8) min. Cycle endurance was improved from 26.8 (SD 5.9) min to 40.2 (SD 9.2) min whereas physical working capacity 170 remained essentially the same. During the endurance cycling test in the respiratory untrained state, the subjects continuously increased their ventilation up to hyperventilation [ventilation at exhaustion = 96.9 (SD 23.6) l.min-1] while after the respiratory training they reached a respiratory steady-state without hyperventilation [ventilation at exhaustion = 63.3 (SD 14.5) l.min-1]. The absence of this marked hyperventilation was the cause of the impressive increase of cycle endurance in normal sedentary subjects after respiratory training. The effects gained by the respiratory training were completely lost after 18 months. Our results indicated that the respiratory system was an exercise limiting factor during an endurance test in normal sedentary subjects.     

Effects of detraining on responses to submaximal exercise

Seven endurance-trained subjects were studied 12, 21, 56, and 84 days after cessation of training. Heart rate, ventilation, respiratory exchange ratio, and blood lactate concentration during submaximal exercise of the same absolute intensity increased (P less than 0.05) progressively during the first 56 days of detraining, after which a stabilization occurred. These changes paralleled a 40% decline (P less than 0.001) in mitochondrial enzyme activity levels and a 21% increase in total lactate dehydrogenase (LDH) activity (P less than 0.05) in trained skeletal muscle. After 84 days of detraining, the experimental subjects' muscle mitochondrial enzyme levels were still 50% above, and LDH activity was 22% below, sedentary control levels. The blood lactate threshold of the detrained subjects occurred at higher absolute and relative (i.e., 75 +/- 2% vs. 62 +/- 3% of maximal O2 uptake) exercise intensities in the subjects after 84 days of detraining than in untrained controls (P less than 0.05). Thus it appears that a portion of the adaptation to prolonged and intense endurance training that is responsible for the higher lactate threshold in the trained state persists for a long time (greater than 85 days) after training is stopped.     

Age- and training-related changes in the collagen metabolism of rat skeletal muscle

The effects of ageing and life-long endurance training on the collagen metabolism of skeletal muscle were evaluated in a longitudinal study. Wistar rats performed treadmill running 5 days a week for 2 years. The activities of collagen biosynthesis enzymes, prolyl-4-hydroxylase and galactosylhydroxylysyl glucosyltransferase, were highest in the muscles of the youngest animals, decreased up to the age of 2 months and from then on remained virtually unchanged. The enzyme activity in young animals was higher in the slow collagenous soleus muscle than in the rectus femoris muscle. The enzyme activity in the soleus muscle was higher for older trained rats than older untrained rats. The relative proportion of type I collagen increased and that of type III collagen decreased with age, suggesting a more marked contribution by type I collagen to the age-related accumulation of total muscular collagen. The results show that collagen biosynthesis decreases with maturation and that life-long endurance training maintains a higher level of biosynthesis in slow muscles.     

Phosphorylation of pig brain microtubule proteins. General properties and partial characterization of endogenous substrate and cyclic AMP-dependent protein kinase.

Collagen synthesis and the activities of prolyl hydroxylase, lysyl hydroxylase, collagen galactosyltransferase and collagen glucosyltransferase were studied in isolated chick-embryo tendon cells after the administration of cortisol acetate to the chick embryos. When the steroid was injected 1 day before isolation of the tendon cells, collagen synthesis was decreased, even though the enzyme activities were not changed. When cortisol acetate was given as repeated injections over a period of 4 days, both collagen synthesis and the enzyme activities decreased. The hydroxylase activities decreased even more than the two collagen glycosyltransferase activities, both in isolated cells and in whole chick embryos. The amount of prolyl hydroxylase protein diminished to the same extent as the enzyme activity, indicating that cortisol acetate inhibits enzyme synthesis. The inhibitory effect of cortisol acetate on collagen synthesis and on the enzyme activities was partially reversible in 3 days. Total protein synthesis was completely restored within this time. Only massive doses of cortisol acetate inhibited collagen synthesis in vitro. Additional experiments indicated that cortisol acetate did not decrease the rate of the enzyme reactions when added directly to the enzyme incubation mixtures. The results suggest that cortisol acetate decreases collagen synthesis both by its direct effect on collagen polypeptide-chain synthesis and by decreasing the activities of enzymes involved in post-translational modifications.     

Collagen biosynthesis. Characterization of subcellular fractions from embryonic chick fibroblasts and the intracellular localization of protocollagen prolyl and protocollagen lysyl hydroxylases

1. Subcellular fractions of freshly isolated matrix-free embryonic chick tendon and sternal cartilage cells have been characterized by chemical analysis, electron microscopy and the location of specific marker enzymes. These data indicate the fractions to be of a high degree of purity comparable with those obtained from other tissues, e.g. liver and kidney. 2. When homogenates were assayed for protocollagen prolyl hydroxylase and protocollagen lysyl hydroxylase activities, addition of Triton X-100 (0.1%, w/v) was found to stimulate enzyme activities by up to 60% suggesting that the enzymes were probably membrane-bound. 3. Assay of subcellular fractions obtained by differential centrifugation for protocollagen prolyl hydroxylase activity indicated the specific activity to be highest in the microsomal fraction. Similar results were obtained for protocollagen lysyl hydroxylase activity. 4. Submicrosomal fractions obtained by discontinuous sucrose-gradient centrifugation were assayed for the two enzymes and protocollagen prolyl hydroxylase and protocollagen lysyl hydroxylase were found to be associated almost exclusively with the rough endoplasmic reticulum fraction in both tendon and cartilage cells.     

Regulation of collagen post-translational modification in transformed human and chick-embryo cells.

Changes in the regulation of collagen post-translational modification in transformed cells were studied in three established human sarcoma cell lines and in chick-embryo fibroblasts freshly transformed by Rous sarcoma virus. The collagens synthesized by all but one of these and by all the control human and chick-embryo cell lines were almost exclusively of types I and/or III. The relative rate of collagen synthesis and the amounts of prolyl hydroxylase activity and immunoreactive protein were markedly low in all the transformed human cell lines. The other enzymes studied, lysyl hydroxylase, hydroxylysyl galactosyltransferase and galactosylhydroxylysyl glucosyltransferase, never showed as large a decrease in activity as did prolyl hydroxylase, suggesting a more efficient regulation of the last enzyme than of the three others. The chick-embryo fibroblasts freshly transformed by Rous sarcoma virus differed from the human sarcoma cells in that prolyl hydroxylase activity was distinctly increased, whereas the decreases in immunoreactive prolyl hydroxylase protein and the three other enzyme activities were very similar to those in the simian-virus-40-transformed human fibroblasts. It seems possible that this increased prolyl hydroxylase activity is only a temporary phenomenon occurring shortly after the transformation, and may be followed by a decrease in activity later. The newly synthesized collagens of all the transformed cells that produced almost exclusively collagen types I and/or III had high extents of lysyl hydroxylation, and there was also an increase in the ratio of glycosylated to non-glycosylated hydroxylysine. The data suggest that one critical factor affecting modification is the rate of collagen synthesis, which affects the ratio of enzyme to substrate in the cell.     

Adaptation of mitochondrial ATP production in human skeletal muscle to endurance training and detraining.

The adaptation of mitochondrial ATP production rate (MAPR) to training and detraining was evaluated in nine healthy men. Muscle samples (approximately 60 mg) were obtained before and after 6 wk of endurance training and after 3 wk of detraining. MAPR was measured in isolated mitochondria by a bioluminometric method. In addition, the activities of mitochondrial and glycolytic enzymes were determined in skeletal muscle. In response to training, MAPR increased by 70%, with a substrate combination of pyruvate + palmitoyl-L-carnitine + alpha-ketoglutarate + malate, by 50% with only pyruvate + malate, and by 92% with palmitoyl-L-carnitine + malate. With detraining MAPR decreased by 12-28% from the posttraining rate (although not significantly for all substrates). No differences were found when MAPR was related to the protein content in the mitochondrial fraction. The largest increase in mitochondrial enzyme activities induced by training was observed for cytochrome-c oxidase (78%), whereas succinate cytochrome c reductase showed only an 18% increase. The activity of citrate synthase increased by 40% and of glutamate dehydrogenase by 45%. Corresponding changes in maximal O2 uptake were a 9.6% increase by training and a 6.0% reversion after detraining. In conclusion, both MAPR and mitochondrial enzyme activities are shown to increase with endurance training and to decrease with detraining.     

Skeletal muscle enzymes and fiber composition in male and female track athletes.

Muscle samples were obtained from the gastrocnemius of 17 female and 23 male track athletes, 10 untrained women, and 11 untrained men. Portions of the specimen were analyzed for total phosphorylase, lactic dehydrogenase (LDH), and succinate dehydrogenase (SDH) activities. Sections of the muscle were stained for myosin adenosine triphosphatase, NADH2 tetrazolium reductase, and alpha-glycerophosphate dehydrogenase. Maximal oxygen uptake (VO2max) was measured on a treadmill for 23 of the volunteers (6 female athletes, 11 male athletes, 10 untrained women, and 6 untrained men). These measurements confirm earlier reports which suggest that the athlete's preference for strength, speed, and/or endurance events is in part a matter of genetic endowment. Aside from differences in fiber composition and enzymes among middle-distance runners, the only distinction between the sexes was the larger fiber areas of the male athletes. SDH activity was found to correlate 0.79 with VO2max, while muscle LDH appeared to be a function of muscle fiber composition. While sprint- and endurance-trained athletes are characterized by distinct fiber compositions and enzyme activities, participants in strength events (e.g., shot-put) have relatively low muscle enzyme activities and a variety of fiber compositions.     

Increased atypical PKC activity in endurance-trained human skeletal muscle

Exercise training may modulate protein content and enzyme activities in skeletal muscle. However, it is not known whether atypical protein kinase C (aPKC) is affected by training. Thus, we investigated aPKC, extracellular-regulated protein kinase 1/2 (ERK 1/2), and P38 mitogen-activated protein kinase (P38 MAPK) activities and expression in skeletal muscle from untrained and endurance-trained subjects at rest and after 20min of cycle exercise (80% of VO(2peak)). Activities of aPKC (P<0.05) and ERK 1/2 (P=0.06), but not phosphorylation of P38 MAPK, were higher in trained than in sedentary subjects at rest. Exercise increased the activities of ERK 1/2 (P<0.01) and aPKC (P<0.05) and the phosphorylation (Thr180/Tyr182) of P38 MAPK (P<0.01) similarly in muscle from trained and sedentary subjects. Protein expression of the kinases was similar in trained and sedentary muscle. The increased aPKC activity in exercise-trained subjects could be important in explaining the enhanced insulin action in these individuals.