Paradoxical effects of prior activity on human sarcoplasmic reticulum Ca2+-ATPase response to exercise

2003 ◽  
Vol 95 (1) ◽  
pp. 138-144 ◽  
Author(s):  
A. R. Tupling ◽  
H. J. Green ◽  
B. D. Roy ◽  
S. Grant ◽  
J. Ouyang
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Atpase Activity ◽  
Standardized Test ◽  
Intermittent Exercise ◽  
Vastus Lateralis ◽  
Plasmic Reticulum ◽  
Paradoxical Effects ◽  
Before And After ◽  
Response To Exercise ◽  
Serca 2A

To investigate the effects of intermittent heavy exercise (HE) on sarcoplasmic reticulum (SR) maximal Ca2+-ATPase activity ( Vmax) and Ca2+ uptake, a continuous two-stage standardized cycling test was performed before and after HE by untrained men [peak aerobic power (V̇o2 peak) = 42.9 ± 2.7 ml · kg-1 · min-1]. The HE consisted of 16 bouts of cycling performed for 6 min each hour at 90% V̇o2 peak. Tissue was obtained from the vastus lateralis by needle biopsy before and during each cycle test. Before HE, reductions ( P < 0.05; μmol · g protein-1 · min-1) of 16 and 31% were observed in Vmax and Ca2+ uptake, respectively, after 40 min of the standardized test. Resting Vmax and Ca2+ uptake were depressed ( P < 0.05) by 19 and 30%, respectively, when measured 36–48 h after HE. During the standardized test, after HE, Vmax increased ( P < 0.05) by 20%, whereas no change was observed in Ca2+ uptake. The HE protocol resulted in small increases ( P < 0.05) and decreases ( P < 0.05) in sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) 2a and SERCA1 expression, respectively, as determined by Western blotting techniques. These results indicate that SR Ca2+-sequestering function in response to a prolonged exercise test depends on prior activity status, such that rested muscles exhibit a decrease and prior exercised muscles, an increase in Ca2+-ATPase activity. Moreover, it appears that changes in SERCA content can occur in response to a sustained session of intermittent exercise.

scholarly journals Adaptations in human muscle sarcoplasmic reticulum to prolonged submaximal training

2003 ◽  
Vol 94 (5) ◽  
pp. 2034-2042 ◽  
Author(s):  
H. J. Green ◽  
C. S. Ballantyne ◽  
J. D. MacDougall ◽  
M. A. Tarnopolsky ◽  
J. D. Schertzer
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Atpase Activity ◽  
Vastus Lateralis ◽  
Training Session ◽  
Maximal Activity ◽  
Hill Coefficient ◽  
Protein Levels ◽  
Plasmic Reticulum ◽  
Cycle Training ◽  
The Hill

In this study, we employed single-leg submaximal cycle training, conducted over a 10-wk period, to investigate adaptations in sarcoplasmic reticulum (SR) Ca2+-regulatory proteins and processes of the vastus lateralis. During the final weeks, the untrained volunteers (age 21.4 ± 0.3 yr; means ± SE, n = 10) were exercising 5 times/wk and for 60 min/session. Analyses were performed on tissue extracted by needle biopsy ∼4 days after the last training session. Compared with the control leg, the trained leg displayed a 19% reduction ( P < 0.05) in homogenate maximal Ca2+-ATPase activity (192 ± 11 vs. 156 ± 18 μmol · g protein−1 · min−1), a 4.3% increase ( P < 0.05) in pCa50, defined as the Ca2+ concentration at half-maximal activity (6.01 ± 0.05 vs. 6.26 ± 0.07), and no change in the Hill coefficient (1.75 ± 0.15 vs. 1.76 ± 0.21). Western blot analysis using monoclonal antibodies (7E6 and A52) revealed a 13% lower ( P < 0.05) sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) 1 in trained vs. control in the absence of differences in SERCA2a. Training also resulted in an 18% lower ( P < 0.05) SR Ca2+ uptake and a 26% lower ( P < 0.05) Ca2+ release. It is concluded that a downregulation in SR Ca2+ cycling in vastus lateralis occurs with aerobic-based training, which at least in the case of Ca2+ uptake can be explained by reduction in Ca2+-ATPase activity and SERCA1 protein levels.

Enhanced sarcoplasmic reticulum Ca2+ release following intermittent sprint training

2000 ◽  
Vol 279 (1) ◽  
pp. R152-R160 ◽  
Author(s):  
Niels Ørtenblad ◽  
Per K. Lunde ◽  
Klaus Levin ◽  
Jesper L. Andersen ◽  
Preben K. Pedersen
Keyword(s):  
Sarcoplasmic Reticulum ◽  
High Intensity ◽  
Vastus Lateralis ◽  
Ryanodine Receptors ◽  
Vastus Lateralis Muscle ◽  
Sprint Training ◽  
High Intensity Training ◽  
Before And After ◽  
Muscle Biopsies ◽  
Intensity Training

To evaluate the effect of intermittent sprint training on sarcoplasmic reticulum (SR) function, nine young men performed a 5 wk high-intensity intermittent bicycle training, and six served as controls. SR function was evaluated from resting vastus lateralis muscle biopsies, before and after the training period. Intermittent sprint performance (ten 8-s all-out periods alternating with 32-s recovery) was enhanced 12% ( P < 0.01) after training. The 5-wk sprint training induced a significantly higher ( P < 0.05) peak rate of AgNO3-stimulated Ca2+ release from 709 (range 560–877; before) to 774 (596–977) arbitrary units Ca2+ ⋅ g protein− 1 ⋅ min− 1(after). The relative SR density of functional ryanodine receptors (RyR) remained unchanged after training; there was, however, a 48% ( P < 0.05) increase in total number of RyR. No significant differences in Ca2+ uptake rate and Ca2+-ATPase capacity were observed following the training, despite that the relative density of Ca2+-ATPase isoforms SERCA1 and SERCA2 had increased 41% and 55%, respectively ( P < 0.05). These data suggest that high-intensity training induces an enhanced peak SR Ca2+ release, due to an enhanced total volume of SR, whereas SR Ca2+ sequestration function is not altered.

Effects of prior exercise and a low-carbohydrate diet on muscle sarcoplasmic reticulum function during cycling in women

2006 ◽  
Vol 101 (3) ◽  
pp. 695-706 ◽  
Author(s):  
T. A. Duhamel ◽  
H. J. Green ◽  
J. G. Perco ◽  
J. Ouyang
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Atpase Activity ◽  
Vastus Lateralis ◽  
Phase 1 ◽  
Vastus Lateralis Muscle ◽  
Low Carbohydrate Diet ◽  
Hill Slope ◽  
Low Carbohydrate ◽  
Exercise Induced

The effects of exercise and diet on sarcoplasmic reticulum Ca2+-cycling properties in female vastus lateralis muscle were investigated in two groups of women following four different conditions. The conditions were 4 days of a low-carbohydrate (Lo CHO) and glycogen-depleting exercise plus a Lo CHO diet (Ex + Lo CHO) ( experiment 2) and 4 days of normal CHO (Norm CHO) and glycogen-depleting exercise plus Norm CHO (Ex + Norm CHO) ( experiment 1). Peak aerobic power (V̇o2peak) was 38.1 ± 1.4 (SE); n = 9 and 35.6 ± 1.4 ml·kg−1·min−1; n = 9, respectively. Sarcoplasmic reticulum properties measured in vitro in homogenates (μmol·g protein−1·min−1) indicated exercise-induced reductions ( P < 0.05) in maximal Ca2+-ATPase activity (0 > 30, 60 min > fatigue), Ca2+ uptake (0 > 30 > 60 min, fatigue), and Ca2+ release, both phase 1 (0, 30 > 60 min, fatigue) and phase 2 (0 > 30, 60 min, fatigue; 30 min > fatigue) in Norm CHO. Exercise was without effect in altering the Hill slope ( nH), defined as the slope of relationship between Ca2+-ATPase activity and Ca2+ concentration. No differences were observed between Norm CHO and Ex+Norm CHO. Compared with Norm CHO, Lo CHO resulted in a lower ( P < 0.05) Ca2+ uptake, phase 1 Ca2+ release (30 min), and nH. Ex + Lo CHO resulted in a greater ( P < 0.05) Ca2+ uptake and nH compared with Lo CHO. The results demonstrate that Lo CHO alone can disrupt SR Ca2+ cycling and that, with the exception of Ca2+ release, a glycogen-depleting session of exercise before Lo CHO can reverse the effects.

scholarly journals Phospholamban Knockout Breaks Arrhythmogenic Ca 2+ Waves and Suppresses Catecholaminergic Polymorphic Ventricular Tachycardia in Mice

2013 ◽  
Vol 113 (5) ◽  
pp. 517-526 ◽  
Author(s):  
Yunlong Bai ◽  
Peter P. Jones ◽  
Jiqing Guo ◽  
Xiaowei Zhong ◽  
Robert B. Clark ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Mouse Model ◽  
Ventricular Myocytes ◽  
Mutant Mice ◽  
Polymorphic Ventricular Tachycardia ◽  
Patch Clamp Recording ◽  
Plasmic Reticulum ◽  
Paradoxical Effects ◽  
Triggered Arrhythmias ◽  
The Impact

Rationale : Phospholamban (PLN) is an inhibitor of cardiac sarco(endo)plasmic reticulum Ca 2+ ATPase. PLN knockout (PLN-KO) enhances sarcoplasmic reticulum Ca 2+ load and Ca 2+ leak. Conversely, PLN-KO accelerates Ca 2+ sequestration and aborts arrhythmogenic spontaneous Ca 2+ waves (SCWs). An important question is whether these seemingly paradoxical effects of PLN-KO exacerbate or protect against Ca 2+ -triggered arrhythmias. Objective : We investigate the impact of PLN-KO on SCWs, triggered activities, and stress-induced ventricular tachyarrhythmias (VTs) in a mouse model of cardiac ryanodine-receptor (RyR2)-linked catecholaminergic polymorphic VT. Methods and Results : We generated a PLN-deficient, RyR2-mutant mouse model (PLN −/− /RyR2-R4496C +/− ) by crossbreeding PLN-KO mice with catecholaminergic polymorphic VT–associated RyR2-R4496C mutant mice. Ca 2+ imaging and patch-clamp recording revealed cell-wide propagating SCWs and triggered activities in RyR2-R4496C +/− ventricular myocytes during sarcoplasmic reticulum Ca 2+ overload. PLN-KO fragmented these cell-wide SCWs into mini-waves and Ca 2+ sparks and suppressed the triggered activities evoked by sarcoplasmic reticulum Ca 2+ overload. Importantly, these effects of PLN-KO were reverted by partially inhibiting sarco(endo)plasmic reticulum Ca 2+ ATPase with 2,5-di-tert-butylhydroquinone. However, Bay K, caffeine, or Li + failed to convert mini-waves to cell-wide SCWs in PLN −/− /RyR2-R4496C +/− ventricular myocytes. Furthermore, ECG analysis showed that PLN-KO mice are not susceptible to stress-induced VTs. On the contrary, PLN-KO protected RyR2-R4496C mutant mice from stress-induced VTs. Conclusions : Our results demonstrate that despite severe sarcoplasmic reticulum Ca 2+ leak, PLN-KO suppresses triggered activities and stress-induced VTs in a mouse model of catecholaminergic polymorphic VT. These data suggest that breaking up cell-wide propagating SCWs by enhancing Ca 2+ sequestration represents an effective approach for suppressing Ca 2+ -triggered arrhythmias.

Muscle sarcoplasmic reticulum Ca2+ cycling adaptations during 16 h of heavy intermittent cycle exercise

2005 ◽  
Vol 99 (3) ◽  
pp. 836-843 ◽  
Author(s):  
G. P. Holloway ◽  
H. J. Green ◽  
T. A. Duhamel ◽  
S. Ferth ◽  
J. W. Moule ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Atpase Activity ◽  
Vastus Lateralis ◽  
Phase 1 ◽  
Hill Coefficient ◽  
Kinetic Properties ◽  
Cycle Exercise ◽  
Tissue Samples ◽  
The Hill

The repetition-dependent effects of a repetitive heavy exercise protocol previously shown to alter muscle mechanic behavior (Green HJ, Duhamel TA, Ferth S, Holloway GP, Thomas MM, Tupling AR, Rich SM, and Yau JE. J Appl Physiol 97: 2166–2175, 2004) on muscle sarcoplasmic reticulum (SR) Ca2+-transport properties, measured in vitro, were examined in 12 untrained volunteers [peak aerobic power (V̇o2 peak) = 44.3 ± 0.66 ml·kg−1·min−1]. The protocol involved 6 min of cycle exercise performed at ∼91% V̇o2 peak once per hour for 16 h. Tissue samples were obtained from the vastus lateralis before (B) and after (A) exercise at repetitions 1 (R1), 2 (R2), 9 (R9), and 16 (R16). Reductions ( P < 0.05) in maximal Ca2+-ATPase activity ( Vmax) of 26 and 12% with exercise were only observed at R1 and R16, respectively. Vmax remained depressed ( P < 0.05) at R2 (B) but not at R9 (B) and R16 (B). No changes were observed in two other kinetic properties of the enzyme, namely the Hill coefficient (defined as the slope of the relationship between Ca2+-ATPase activity and free Ca2+ concentration) and the Ca50 (defined as the free Ca2+ concentration needed to elicit 50% Vmax). Changes in Ca2+ uptake (measured at 2,000 nM) with exercise and recovery generally paralleled Vmax. The apparent coupling ratio, defined as the ratio between Ca2+ uptake and Vmax, was unaffected by the intermittent protocol. Reductions ( P < 0.05) in phase 1 Ca2+ release (32%) were only observed at R1. No differences were observed between B and A for R2, R9, and R16 or between B and B for R1, R2, R9, and R16. The changes in phase 2 Ca2+ release were as observed for phase 1 Ca2+ release. It is concluded that the SR Ca2+-handling properties, in general, display rapid adaptations to repetitive exercise.

scholarly journals Effects of fatigue and training on sarcoplasmic reticulum Ca2+ regulation in human skeletal muscle

2002 ◽  
Vol 92 (3) ◽  
pp. 912-922 ◽  
Author(s):  
Jia L. Li ◽  
Xiao N. Wang ◽  
Steve F. Fraser ◽  
Michael F. Carey ◽  
Tim V. Wrigley ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Atpase Activity ◽  
Human Skeletal Muscle ◽  
Fiber Type ◽  
Vastus Lateralis ◽  
Human Muscle ◽  
Training Status ◽  
Type Ii ◽  
Muscle Biopsies ◽  
And Training

Little is known about fatigue and training effects on sarcoplasmic reticulum (SR) function in human muscle, and we therefore investigated this in eight untrained controls (UT), eight endurance-trained (ET), and eight resistance-trained athletes (RT). Muscle biopsies (vastus lateralis) taken at rest and after 50 maximal quadriceps contractions (180°/s, 0.5 Hz) were analyzed for fiber composition, metabolites and maximal SR Ca2+ release, Ca2+ uptake, and Ca2+-ATPase activity. Fatigue reduced ( P < 0.05) Ca2+ release (42.1 ± 3.8%, 43.4 ± 3.9%, 31.3 ± 6.1%), Ca2+ uptake (43.0 ± 5.2%, 34.1 ± 4.6%, 28.4 ± 2.8%), and Ca2+-ATPase activity (38.6 ± 4.2%, 48.5 ± 5.7%, 29.6 ± 5.0%), in UT, RT, and ET, respectively. These decreases were correlated with fatigability and with type II fiber proportion ( P < 0.05). Resting SR measures were correlated with type II proportion ( r ≥ 0.51, P < 0.05). ET had lower resting Ca2+ release, Ca2+ uptake, and Ca2+-ATPase ( P < 0.05) than UT and RT ( P < 0.05), probably because of their lower type II proportion; only minor effects were found in RT. Thus SR function is markedly depressed with fatigue in controls and in athletes, is dependent on fiber type, and appears to be minimally affected by chronic training status.

Chronic intermittent hypoxia and incremental cycling exercise independently depress muscle in vitro maximal Na+-K+-ATPase activity in well-trained athletes

2005 ◽  
Vol 98 (1) ◽  
pp. 186-192 ◽  
Author(s):  
R. J. Aughey ◽  
C. J. Gore ◽  
A. G. Hahn ◽  
A. P. Garnham ◽  
S. A. Clark ◽  
...  
Keyword(s):  
Atpase Activity ◽  
Vastus Lateralis ◽  
Incremental Exercise ◽  
Peak Oxygen Consumption ◽  
Vastus Lateralis Muscle ◽  
Minor Effect ◽  
Moderate Altitude ◽  
Ouabain Binding ◽  
Before And After

Athletes commonly attempt to enhance performance by training in normoxia but sleeping in hypoxia [live high and train low (LHTL)]. However, chronic hypoxia reduces muscle Na+-K+-ATPase content, whereas fatiguing contractions reduce Na+-K+-ATPase activity, which each may impair performance. We examined whether LHTL and intense exercise would decrease muscle Na+-K+-ATPase activity and whether these effects would be additive and sufficient to impair performance or plasma K+ regulation. Thirteen subjects were randomly assigned to two fitness-matched groups, LHTL ( n = 6) or control (Con, n = 7). LHTL slept at simulated moderate altitude (3,000 m, inspired O2 fraction = 15.48%) for 23 nights and lived and trained by day under normoxic conditions in Canberra (altitude ∼600 m). Con lived, trained, and slept in normoxia. A standardized incremental exercise test was conducted before and after LHTL. A vastus lateralis muscle biopsy was taken at rest and after exercise, before and after LHTL or Con, and analyzed for maximal Na+-K+-ATPase activity [K+-stimulated 3- O-methylfluorescein phosphatase (3- O-MFPase)] and Na+-K+-ATPase content ([3H]ouabain binding sites). 3- O-MFPase activity was decreased by −2.9 ± 2.6% in LHTL ( P < 0.05) and was depressed immediately after exercise ( P < 0.05) similarly in Con and LHTL (−13.0 ± 3.2 and −11.8 ± 1.5%, respectively). Plasma K+ concentration during exercise was unchanged by LHTL; [3H]ouabain binding was unchanged with LHTL or exercise. Peak oxygen consumption was reduced in LHTL ( P < 0.05) but not in Con, whereas exercise work was unchanged in either group. Thus LHTL had a minor effect on, and incremental exercise reduced, Na+-K+-ATPase activity. However, the small LHTL-induced depression of 3- O-MFPase activity was insufficient to adversely affect either K+ regulation or total work performed.

scholarly journals AIF4-induced inhibition of the ATPase activity, the Ca2+-transport activity and the phosphoprotein-intermediate formation of plasma-membrane and endo(sarco)plasmic-reticulum Ca2+-transport ATPases in different tissues. Evidence for a tissue-dependent functional difference

1989 ◽  
Vol 261 (2) ◽  
pp. 655-660 ◽  
Author(s):  
L Missiaen ◽  
F Wuytack ◽  
H De Smedt ◽  
F Amant ◽  
R Casteels
Keyword(s):  
Smooth Muscle ◽  
Plasma Membrane ◽  
Sarcoplasmic Reticulum ◽  
Atpase Activity ◽  
Intermediate Formation ◽  
Functional Difference ◽  
Transport Activity ◽  
Fast Skeletal Muscle ◽  
Transport Atpase ◽  
Plasmic Reticulum

AIF4- inhibits the (Ca2+ + Mg2+)-ATPase activity of the plasma-membrane and the sarcoplasmic-reticulum Ca2+-transport ATPase [Missiaen, Wuytack, De Smedt, Vrolix & Casteels (1988) Biochem. J. 253, 827-833]. The aim of the present work was to investigate this inhibition further. We now report that AIF4- inhibits not only the (Ca2+ + Mg2+)-ATPase activity, but also the ATP-dependent 45Ca2+ transport, and the formation of the phosphoprotein intermediate by these pumps. Mg2+ potentiated the effect of AIF4-, whereas K+ had no such effect. The plasma-membrane Ca2+-transport ATPase from erythrocytes was 20 times less sensitive to inhibition by AIF4- as compared with the Ca2+-transport ATPase from smooth muscle. The endoplasmic-reticulum Ca2+-transport ATPase from smooth muscle was inhibited to a greater extent than the sarcoplasmic-reticulum Ca2+-transport ATPase of slow and fast skeletal muscle.

Effect of disuse on sarcoplasmic reticulum in fast and slow skeletal muscle

1982 ◽  
Vol 243 (3) ◽  
pp. C156-C160 ◽  
Author(s):  
D. H. Kim ◽  
F. A. Witzmann ◽  
R. H. Fitts
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Atpase Activity ◽  
Time Course ◽  
Vastus Lateralis ◽  
Control Level ◽  
Type I ◽  
Uptake Capacity ◽  
Three Samples ◽  
Fast Twitch

The effect of 6 wk of hindlimb immobilization on rat skeletal muscle sarcoplasmic reticulum (SR) was determined in the slow-twitch, type I soleus (SOL), the fast-twitch, type IIA deep region of the vastus lateralis (DVL), and the fast-twitch, type IIB superficial region of the vastus lateralis (SVL). Immobilization produced a significant decline in the Ca2+ uptake rate (Vmax) of SR vesicles from the slow SOL (0.930 +/- 0.116 to 0.365 +/- 0.071 mumol Ca2+ . mg-1 . min-1), while the SR Vmax increased in the fast SVL (2.763 +/- 0.133 to 5.209 +/- 0.687) and was unaltered in the DVL. Vesicles from the fast SVL and DVL also exhibited a higher total Ca2+ uptake capacity following immobilization. An evaluation of the time course of the immobilization-mediated effect revealed an increased Ca2+ uptake capacity in all three samples after 1 wk. In the SOL total Ca2+ uptake returned to control level after 2 wk, while in the fast-twitch muscles the higher capacities were maintained. The Ca2+-stimulated SR ATPase activity was not altered in any of the muscles studies, although the total SR ATPase activity increased twofold in the slow SOL.

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