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ممنون

[banel87]

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ممنون

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[javad2625]

سوالم خیلی سخته؟..شاید نامفهومه؟!! ...توضیح بیشتری میخواد؟
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ببخشید که دیر به دیر سر می زنم چون وقتم کمه.

[javad2625]

سلام
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[Davood_titan]

کسی میتونه  با برنامه یه سایت  خبرگذاری درست کنه 

[javad2625]

کسی میتونه  با برنامه یه سایت  خبرگذاری درست کنه 

آره. چطور مگه؟

[Davood_titan]

آره. چطور مگه؟

ممنون میشم  سایت  itna.ir  رو  برام  درست کنید  حدود  10  صفحه

[masoud_cmp]

we employed single-leg submaximal cycle training, conducted overa 10-wk period, to investigate adaptations in sarcoplasmic reticulum(SR) Ca 2+ -regulatory proteins and processes of the vastuslateralis. During the final weeks, the untrained volunteers (age21.4 ± 0.3 yr; means ± SE, n = 10) wereexercising 5 times/wk and for 60 min/session. Analyses were performedon tissue extracted by needle biopsy ~4 days after the last trainingsession. Compared with the control leg, the trained leg displayed a19% reduction ( P maximalCa 2+ -ATPase activity (192 ± 11 vs. 156 ± 18 µmol · gprotein 1 · min 1 ), a4.3% increase ( P 50,defined as the Ca 2+ concentration at half-maximal activity(6.01 ± 0.05 vs. 6.26 ± 0.07), and no change in the Hillcoefficient (1.75 ± 0.15 vs. 1.76 ± 0.21). Western blotanalysis using monoclonal antibodies (7E6 and A52) revealed a 13%lower ( P reticulumCa 2+ -ATPase (SERCA) 1 in trained vs. control in the absenceof differences in SERCA2a. Training also resulted in an 18% lower( P SR Ca 2+ uptake and a 26% lower( P 2+ release. It is concludedthat a downregulation in SR Ca 2+ cycling in vastuslateralis occurs with aerobic-based training, which at least in thecase of Ca 2+ uptake can be explained by reduction inCa 2+ -ATPase activity and SERCA1 protein levels.
calcium homeostasis Ca + ATPase Ca + uptake Ca + release exercise

INTRODUCTION

REGULAR CONTRACTILE ACTIVITY is a potentially potent stimulus foraltering the composition, structure, and function of the muscle cell.Nowhere is this more evident than with the chronic low-frequencyelectrical stimulation (CLFS) model in which contractile activity ischaracteristically induced for 12-24 h/day over several weeks.Induced patterns of submaximal contractions of this nature typicallyapplied to muscles composed of a predominance of fast-twitch (type II)fibers result in extensive reorganization of both the excitation andcontraction processes and the energy metabolic pathways involved inenergy supply. Although the magnitude of the adaptations vary,qualitatively similar adaptations appear to occur between species (dog,rat, mouse, rabbit) ( 29 ).


Despite the fact that the CLFS model has proved invaluable for studyingthe limits of phenotypic plasticity in skeletal muscle and the factorsregulating the expression of a large number of proteins involved infiber-type transformation, it is nonphysiological ( 30 ). Inphysiological models, voluntary activity is used to elicit trainingadaptations. Voluntary training typically involves a relatively briefsession of exercise followed by a prolonged recovery period, whichcould last for 2-3 days depending on the training frequency.Moreover, it is not clear how the intracellular signals mediatingaltered protein expression in CLFS translate into different programs ofvoluntary training. Unlike CLFS, the properties that have been exploredwith voluntary training have been much more limited. To a large extent,the focus has been directed toward the energy metabolic pathways andmore recently the contractile protein myosin. The processes involved inexcitation-contraction coupling, namely those involved in thetransmission of the neural signal to the interior of the fiber, andwhich result in an increase in the free cytosolic Ca 2+ ([Ca 2+ ] f ) in signal involved inmyofibrillar activation and muscle contraction, has received scant attention.


One vital organelle that is the primary regulator of[Ca 2+ ] f levels in the skeletal muscle cell isthe sarcoplasmic reticulum (SR). The SR is a membranous network thatenvelops the myofibrils and acts as a storage depot forCa 2+. Also embedded in the SR is a collection of specialproteins that regulate the release of Ca 2+ into the cytosoland the sequestration of Ca 2+ back into the lumen of theSR. The ryanodine receptor (RyR) or Ca 2+ -release channeland the SR Ca 2+ -ATPase (SERCA) are the principalproteins involved in Ca 2+ release and Ca 2+ uptake, respectively. Both RyR and SERCA exist as several isoforms inmammalian tissue ( 1, 8 ).


As with a variety of other cellular proteins, the proteins involved inSR Ca 2+ cycling can also undergo extensive replacement whenCLFS is administered to fast-twitch (type II)-based muscles. Providedthat CLFS is of sufficient daily volume and duration, RyRprotein content decreases dramatically ( 9, 14, 26 ) withoutchanges in RyR1 to RyR2, the isoform that predominates in heart muscles( 8 ). Although not measured, the downregulation in RyRwould be expected to be accompanied by a pronounced decrease inCa 2+ -release kinetics ( 8 ). The CLFS model canalso induce large reductions in SERCA content. However, unlike RyR, ashift from SERCA1, the predominant isoform observed in type II musclefibers, to SERCA2a, the major isoform that exits in slow-twitch (type I) fibers, occurs ( 3, 14, 26, 27 ). Because the alteration in SERCA isoform content with CLFS might be expected to change, theCa 2+ affinity as measured by the Hill coefficient andCa 2+ concentration at half-maximal activity(pCa 50 ), it is surprising that no study has apparentlyaddressed this issue ( 29 ). Similarly, the coupling ratio,defined as the ratio between Ca 2+ uptake andCa 2+ -ATPase activity, appears unexplored with CLFS( 3 ). On the basis of the adaptations that occur with CLFS,it is reasonable to suggest that the functional alterations in SRCa 2+ cycling occur, in large part, as a result of areduction in protein content both to the RyR and SERCA.


In contrast to CLFS, SR adaptations to voluntary training remain poorlycharacterized, particularly with regard to the relationship between thenature of the contractile stimulus and the resulting alterations inprotein expression and function. At least in terms of the contractileintensity and the strain put on the excitation-contraction processesand metabolic flux, low-intensity aerobic running would appear to havea close parallel to CLFS. As a consequence, the adaptations that occurwith a training program of this nature would be expected to resemble,at least qualitatively, those occurring with CLFS. There is someevidence that this occurs. In one of the earliest studies usingtreadmill running in rats, Kim et al. ( 17 ) reporteddecreases in maximal SR Ca 2+ uptake( V max ) and in Ca 2+ affinity but onlyin tissue composed of a predominance of fast-twitch, low-oxidativefibers and not in tissue of predominant fast-twitch, high-oxidativefibers or slow-twitch-based muscle. That the reduction in V max is due at least in part to areduction in SR Ca 2+ -ATPase protein is supported by thefindings of Green et al. ( 12 ), who reported reductions inCa 2+ -ATPase protein content after a similar but moreextreme running program also using rats.


Additional evidence that the adaptations in the SR may be specific tothe nature of the training has been recently published using sprinttraining in humans ( 28 ). In this study, large increases inboth SERCA1 and SERCA2 protein content were observed in tissue obtainedfrom the vastus lateralis. Surprisingly, however, the increases in theCa 2+ -ATPase protein were not accompanied by increases inmaximal Ca 2+ -ATPase activity or inCa 2+ -uptake kinetics. These investigators also reportedincreases in SR Ca 2+ -release rates that were accompanied byincreases in RyR protein content as measured by Western blot but not by[ 3 H]ryanodine binding ( 28 ). These resultssuggest that modification of the protein levels of the SR may occurindependently of changes in the functional properties of the SR. Atpresent it is unclear whether this effect is species specific or due tothe nature of the exercise used for training.


The purpose of this study was to investigate the alterations in theCa 2+ -exchange properties of the SR in human muscle inresponse to a training program involving prolonged aerobic-basedexercise. We have hypothesized that, similar to CLFS, reductions inCa 2+ uptake and Ca 2+ -ATPase would occur inconjunction with a shift toward SERCA2a, the predominant isoform oftype 1 fibers, and that these adaptations would occur independently ofchanges in Ca 2+ sensitivity or coupling ratios. Moreover,we have also postulated that the adaptations in Ca 2+ sequestration would be accompanied by reductions inCa 2+ -release kinetics.

METHODS

Subjects. Ten healthy men (age 21.4 ± 0.3 yr; body mass 76.8 ± 2.2 kg; means ± SE) volunteered for the study. All participants were active but not engaged in exercise, either high resistance or endurance, on a regular basis for at least 6 mo before the beginning ofthe study. Written consent was obtained from all volunteers as requiredafter approval of the study by the Office of Human Research.


Experimental design. The training program consisted of 10 wk of single-leg submaximal cycleperformed in the recumbent position. Participants cycled at 60 revolutions/min at a power output that initially corresponded to 75%of the pretraining peak power output. Training initially consisted of3 × 30 min sessions/wk, gradually progressing to 5 × 60 minsessions/wk. The power output was adjusted throughout the training tomaintain individual target heart rates in the range of 140 and 160 beats/min. The leg assigned for training, dominant vs. nondominant, wasrandomly assigned. The dominant leg was selected on the basis of theleg preferred in a vertical pump with a single foot takeoff. For eachparticipant, the other leg served as the untrained control.


Before the beginning of training, each volunteer performed single-legprogressive cycle tests for measurement of peak aerobic power( O 2 peak ). Individual tests, separatedby at least 24 h, were performed on each leg in randomized order.In the progressive cycle protocol, a brief warm-up was provided beforeapplication of square increases in power output every 2 min. The O 2 peak, measured with open-circuitspirometry ( 23 ), was defined as the highest value averagedover 60 s that was attained before fatigue. The O 2 peak protocols were again measured 2 days after the training period.

[masoud_cmp]

we employed single-leg submaximal cycle training, conducted overa 10-wk period, to investigate adaptations in sarcoplasmic reticulum(SR) Ca 2+ -regulatory proteins and processes of the vastuslateralis. During the final weeks, the untrained volunteers (age21.4 ± 0.3 yr; means ± SE, n = 10) wereexercising 5 times/wk and for 60 min/session. Analyses were performedon tissue extracted by needle biopsy ~4 days after the last trainingsession. Compared with the control leg, the trained leg displayed a19% reduction ( P maximalCa 2+ -ATPase activity (192 ± 11 vs. 156 ± 18 µmol · gprotein 1 · min 1 ), a4.3% increase ( P 50,defined as the Ca 2+ concentration at half-maximal activity(6.01 ± 0.05 vs. 6.26 ± 0.07), and no change in the Hillcoefficient (1.75 ± 0.15 vs. 1.76 ± 0.21). Western blotanalysis using monoclonal antibodies (7E6 and A52) revealed a 13%lower ( P reticulumCa 2+ -ATPase (SERCA) 1 in trained vs. control in the absenceof differences in SERCA2a. Training also resulted in an 18% lower( P SR Ca 2+ uptake and a 26% lower( P 2+ release. It is concludedthat a downregulation in SR Ca 2+ cycling in vastuslateralis occurs with aerobic-based training, which at least in thecase of Ca 2+ uptake can be explained by reduction inCa 2+ -ATPase activity and SERCA1 protein levels.
【关键词】 calcium homeostasis Ca + ATPase Ca + uptake Ca + release exercise


INTRODUCTION


REGULAR CONTRACTILE ACTIVITY is a potentially potent stimulus foraltering the composition, structure, and function of the muscle cell.Nowhere is this more evident than with the chronic low-frequencyelectrical stimulation (CLFS) model in which contractile activity ischaracteristically induced for 12-24 h/day over several weeks.Induced patterns of submaximal contractions of this nature typicallyapplied to muscles composed of a predominance of fast-twitch (type II)fibers result in extensive reorganization of both the excitation andcontraction processes and the energy metabolic pathways involved inenergy supply. Although the magnitude of the adaptations vary,qualitatively similar adaptations appear to occur between species (dog,rat, mouse, rabbit) ( 29 ).


Despite the fact that the CLFS model has proved invaluable for studyingthe limits of phenotypic plasticity in skeletal muscle and the factorsregulating the expression of a large number of proteins involved infiber-type transformation, it is nonphysiological ( 30 ). Inphysiological models, voluntary activity is used to elicit trainingadaptations. Voluntary training typically involves a relatively briefsession of exercise followed by a prolonged recovery period, whichcould last for 2-3 days depending on the training frequency.Moreover, it is not clear how the intracellular signals mediatingaltered protein expression in CLFS translate into different programs ofvoluntary training. Unlike CLFS, the properties that have been exploredwith voluntary training have been much more limited. To a large extent,the focus has been directed toward the energy metabolic pathways andmore recently the contractile protein myosin. The processes involved inexcitation-contraction coupling, namely those involved in thetransmission of the neural signal to the interior of the fiber, andwhich result in an increase in the free cytosolic Ca 2+ ([Ca 2+ ] f ) in signal involved inmyofibrillar activation and muscle contraction, has received scant attention.


One vital organelle that is the primary regulator of[Ca 2+ ] f levels in the skeletal muscle cell isthe sarcoplasmic reticulum (SR). The SR is a membranous network thatenvelops the myofibrils and acts as a storage depot forCa 2+. Also embedded in the SR is a collection of specialproteins that regulate the release of Ca 2+ into the cytosoland the sequestration of Ca 2+ back into the lumen of theSR. The ryanodine receptor (RyR) or Ca 2+ -release channeland the SR Ca 2+ -ATPase (SERCA) are the principalproteins involved in Ca 2+ release and Ca 2+ uptake, respectively. Both RyR and SERCA exist as several isoforms inmammalian tissue ( 1, 8 ).


As with a variety of other cellular proteins, the proteins involved inSR Ca 2+ cycling can also undergo extensive replacement whenCLFS is administered to fast-twitch (type II)-based muscles. Providedthat CLFS is of sufficient daily volume and duration, RyRprotein content decreases dramatically ( 9, 14, 26 ) withoutchanges in RyR1 to RyR2, the isoform that predominates in heart muscles( 8 ). Although not measured, the downregulation in RyRwould be expected to be accompanied by a pronounced decrease inCa 2+ -release kinetics ( 8 ). The CLFS model canalso induce large reductions in SERCA content. However, unlike RyR, ashift from SERCA1, the predominant isoform observed in type II musclefibers, to SERCA2a, the major isoform that exits in slow-twitch (type I) fibers, occurs ( 3, 14, 26, 27 ). Because the alteration in SERCA isoform content with CLFS might be expected to change, theCa 2+ affinity as measured by the Hill coefficient andCa 2+ concentration at half-maximal activity(pCa 50 ), it is surprising that no study has apparentlyaddressed this issue ( 29 ). Similarly, the coupling ratio,defined as the ratio between Ca 2+ uptake andCa 2+ -ATPase activity, appears unexplored with CLFS( 3 ). On the basis of the adaptations that occur with CLFS,it is reasonable to suggest that the functional alterations in SRCa 2+ cycling occur, in large part, as a result of areduction in protein content both to the RyR and SERCA.


In contrast to CLFS, SR adaptations to voluntary training remain poorlycharacterized, particularly with regard to the relationship between thenature of the contractile stimulus and the resulting alterations inprotein expression and function. At least in terms of the contractileintensity and the strain put on the excitation-contraction processesand metabolic flux, low-intensity aerobic running would appear to havea close parallel to CLFS. As a consequence, the adaptations that occurwith a training program of this nature would be expected to resemble,at least qualitatively, those occurring with CLFS. There is someevidence that this occurs. In one of the earliest studies usingtreadmill running in rats, Kim et al. ( 17 ) reporteddecreases in maximal SR Ca 2+ uptake( V max ) and in Ca 2+ affinity but onlyin tissue composed of a predominance of fast-twitch, low-oxidativefibers and not in tissue of predominant fast-twitch, high-oxidativefibers or slow-twitch-based muscle. That the reduction in V max is due at least in part to areduction in SR Ca 2+ -ATPase protein is supported by thefindings of Green et al. ( 12 ), who reported reductions inCa 2+ -ATPase protein content after a similar but moreextreme running program also using rats.


Additional evidence that the adaptations in the SR may be specific tothe nature of the training has been recently published using sprinttraining in humans ( 28 ). In this study, large increases inboth SERCA1 and SERCA2 protein content were observed in tissue obtainedfrom the vastus lateralis. Surprisingly, however, the increases in theCa 2+ -ATPase protein were not accompanied by increases inmaximal Ca 2+ -ATPase activity or inCa 2+ -uptake kinetics. These investigators also reportedincreases in SR Ca 2+ -release rates that were accompanied byincreases in RyR protein content as measured by Western blot but not by[ 3 H]ryanodine binding ( 28 ). These resultssuggest that modification of the protein levels of the SR may occurindependently of changes in the functional properties of the SR. Atpresent it is unclear whether this effect is species specific or due tothe nature of the exercise used for training.


The purpose of this study was to investigate the alterations in theCa 2+ -exchange properties of the SR in human muscle inresponse to a training program involving prolonged aerobic-basedexercise. We have hypothesized that, similar to CLFS, reductions inCa 2+ uptake and Ca 2+ -ATPase would occur inconjunction with a shift toward SERCA2a, the predominant isoform oftype 1 fibers, and that these adaptations would occur independently ofchanges in Ca 2+ sensitivity or coupling ratios. Moreover,we have also postulated that the adaptations in Ca 2+ sequestration would be accompanied by reductions inCa 2+ -release kinetics.


METHODS


Subjects. Ten healthy men (age 21.4 ± 0.3 yr; body mass 76.8 ± 2.2 kg; means ± SE) volunteered for the study. All participants were active but not engaged in exercise, either high resistance or endurance, on a regular basis for at least 6 mo before the beginning ofthe study. Written consent was obtained from all volunteers as requiredafter approval of the study by the Office of Human Research.


Experimental design. The training program consisted of 10 wk of single-leg submaximal cycleperformed in the recumbent position. Participants cycled at 60 revolutions/min at a power output that initially corresponded to 75%of the pretraining peak power output. Training initially consisted of3 × 30 min sessions/wk, gradually progressing to 5 × 60 minsessions/wk. The power output was adjusted throughout the training tomaintain individual target heart rates in the range of 140 and 160 beats/min. The leg assigned for training, dominant vs. nondominant, wasrandomly assigned. The dominant leg was selected on the basis of theleg preferred in a vertical pump with a single foot takeoff. For eachparticipant, the other leg served as the untrained control.


Before the beginning of training, each volunteer performed single-legprogressive cycle tests for measurement of peak aerobic power( O 2 peak ). Individual tests, separatedby at least 24 h, were performed on each leg in randomized order.In the progressive cycle protocol, a brief warm-up was provided beforeapplication of square increases in power output every 2 min. The O 2 peak, measured with open-circuitspirometry ( 23 ), was defined as the highest value averagedover 60 s that was attained before fatigue. The O 2 peak protocols were again measured 2 days after the training period.

[Rishter]

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