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.

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.

Human muscle sarcoplasmic reticulum function during submaximal exercise in normoxia and hypoxia

2004 ◽  
Vol 97 (1) ◽  
pp. 180-187 ◽  
Author(s):  
T. A. Duhamel ◽  
H. J. Green ◽  
J. G. Perco ◽  
S. D. Sandiford ◽  
J. Ouyang
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Atpase Activity ◽  
Vastus Lateralis ◽  
Maximal Activity ◽  
Human Muscle ◽  
Hill Coefficient ◽  
Moderate Intensity ◽  
Vastus Lateralis Muscle ◽  
Moderate Intensity Exercise ◽  
Dependent Atpase

In this study, the response of the sarcoplasmic reticulum (SR) to prolonged exercise, performed in normoxia (inspired O2 fraction = 0.21) and hypoxia (inspired O2 fraction = 0.14) was studied in homogenates prepared from the vastus lateralis muscle in 10 untrained men (peak O2 consumption = 3.09 ± 0.25 l/min). In normoxia, performed at 48 ± 2.2% peak O2 consumption, maximal Ca2+-dependent ATPase activity was reduced by ∼25% at 30 min of exercise compared with rest (168 ± 10 vs. 126 ± 8 μmol·g protein−1·min−1), with no further reductions observed at 90 min (129 ± 6 μmol·g protein−1·min−1). No changes were observed in the Hill coefficient or in the Ca2+ concentration at half-maximal activity. The reduction in maximal Ca2+-dependent ATPase activity at 30 min of exercise was accompanied by oxalate-dependent reductions ( P < 0.05) in Ca2+ uptake by ∼20% (370 ± 22 vs. 298 ± 25 μmol·g protein−1·min−1). Ca2+ release, induced by 4-chloro- m-cresol and assessed into fast and slow phases, was decreased ( P < 0.05) by ∼16 and ∼32%, respectively, by 90 min of exercise. No differences were found between normoxia and hypoxia for any of the SR properties examined. It is concluded that the disturbances induced in SR Ca2+ cycling with prolonged moderate-intensity exercise in human muscle during normoxia are not modified when the exercise is performed in hypoxia.

Effects of 4-h ischemia and 1-h reperfusion on rat muscle sarcoplasmic reticulum function

2001 ◽  
Vol 281 (4) ◽  
pp. E867-E877 ◽  
Author(s):  
R. Tupling ◽  
H. Green ◽  
G. Senisterra ◽  
J. Lepock ◽  
N. McKee
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Phase 1 ◽  
Late Phase ◽  
Maximal Activity ◽  
Hill Coefficient ◽  
Sprague Dawley ◽  
Rapid Phase ◽  
Sprague Dawley Rats ◽  
The Hill

To investigate the hypothesis that ischemia and reperfusion would impair sarcoplasmic reticulum (SR) Ca2+ regulation in skeletal muscle, Sprague-Dawley rats ( n = 20) weighing 290 ± 3.5 g were randomly assigned to either a control control (CC) group, in which only the effects of anesthetization were studied, or to a group in which the muscles in one hindlimb were made ischemic for 4 h and allowed to recover for 1 h (I). The nonischemic, contralateral muscles served as control (C). Measurements of Ca2+-ATPase properties in homogenates and SR vesicles, in mixed gastrocnemius and tibialis anterior muscles, indicated no differences between groups on maximal activity, the Hill coefficient, and Ca50, defined as the Ca2+concentration needed to elicit 50% of maximal activity. In homogenates, Ca2+ uptake was lower ( P < 0.05) by 20–25%, measured at 0.5 and 1.0 μM of free Ca2+ ([Ca2+]f) in C compared with CC. In SR vesicles, Ca2+ uptake was lower ( P < 0.05) by 30–38% in I compared with CC at [Ca2+]f between 0.5 and 1.5 μM. Silver nitrate induced Ca2+ release, assessed during both the initial, early rapid ( phase 1), and slower, prolonged late ( phase 2) phases, in homogenates and SR vesicles, indicated a higher ( P < 0.05) release only in phase 1in SR vesicles in I compared with CC. These results indicate that the alterations in SR Ca2+ regulation, previously observed after prolonged ischemia by our group, are reversed within 1 h of reperfusion. However, the lower Ca2+ uptake observed in long-term, nonischemic homogenates suggests that altered regulation may occur in the absence of ischemia.

Comparative effects of a low-carbohydrate diet and exercise plus a low-carbohydrate diet on muscle sarcoplasmic reticulum responses in males

2006 ◽  
Vol 291 (4) ◽  
pp. C607-C617 ◽  
Author(s):  
T. A. Duhamel ◽  
H. J. Green ◽  
J. G. Perco ◽  
J. Ouyang
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Atpase Activity ◽  
Phase 1 ◽  
Hill Coefficient ◽  
Carbohydrate Diet ◽  
Low Carbohydrate Diet ◽  
Diet And Exercise ◽  
Low Carbohydrate ◽  
The Hill ◽  
The Relationship

We employed a glycogen-depleting session of exercise followed by a low-carbohydrate (CHO) diet to investigate modifications that occur in muscle sarcoplasmic reticulum (SR) Ca2+-cycling properties compared with low-CHO diet alone. SR properties were assessed in nine untrained males [peak aerobic power (V̇o2 peak) = 43.6 ± 2.6 (SE) ml·kg−1·min−1] during prolonged cycle exercise to fatigue performed at ∼58% V̇o2 peak after 4 days of low-CHO diet (Lo CHO) and after glycogen-depleting exercise plus 4 days of low-CHO (Ex+Lo CHO). Compared with Lo CHO, Ex+Lo CHO resulted in 12% lower ( P < 0.05) resting maximal Ca2+-ATPase activity ( Vmax = 174 ± 12 vs. 153 ± 10 μmol·g protein−1·min−1) and smaller reduction in Vmax induced during exercise. A similar effect was observed for Ca2+ uptake. The Hill coefficient, defined as slope of the relationship between cytosolic free Ca2+ concentration and Ca2+-ATPase activity, was higher ( P < 0.05) at rest (2.07 ± 0.15 vs. 1.90 ± 0.10) with Ex+Lo CHO, an effect that persisted throughout the exercise. The coupling ratio, defined as the ratio of Ca2+ uptake to Vmax, was 23–30% elevated ( P < 0.05) at rest and during the first 60 min of exercise with Ex+Lo CHO. The ∼27 and 34% reductions ( P < 0.05) in phase 1 and phase 2 Ca2+ release, respectively, observed during exercise with Lo CHO were not altered by Ex+Lo CHO. These results indicate that when prolonged exercise precedes a short-term Lo CHO diet, Ca2+ sequestration properties and efficiency are improved compared with those during Lo CHO alone.

Ischemia-induced structural change in SR Ca2+-ATPase is associated with reduced enzyme activity in rat muscle

2001 ◽  
Vol 281 (5) ◽  
pp. R1681-R1688 ◽  
Author(s):  
R. Tupling ◽  
H. Green ◽  
G. Senisterra ◽  
J. Lepock ◽  
N. McKee
Keyword(s):  
Atpase Activity ◽  
Binding Capacity ◽  
Maximal Activity ◽  
Hill Coefficient ◽  
In Vivo Model ◽  
Sprague Dawley ◽  
Atp Binding Site ◽  
Structural Modifications ◽  
The Hill

In this study, we employed an in vivo model of prolonged ischemia in rat skeletal muscle to investigate the hypothesis that structural modifications to the sarcoplasmic reticulum (SR) Ca2+-ATPase can explain the alterations in Ca2+-ATPase activity that occur with ischemia. To induce total ischemia, a tourniquet was placed around the upper hindlimb in 27 female Sprague-Dawley rats weighing 256 ± 6.7 g (mean ± SE) and was inflated to 350 mmHg for 4 h. The contralateral limb served as control (C) to the ischemic limb (I), and the limbs of animals killed immediately after anesthetization served as a double control (CC). Mixed gastrocnemius and tibialis anterior muscles were sampled and used for SR vesicle preparation. Maximal Ca2+-ATPase activity (μmol · g protein−1 · min−1) of C (15,802 ± 1,246) and I (11,609 ± 1,029) was 90 and 73% ( P < 0.05) of CC (17,562 ± 1,682), respectively. No differences were found between groups in either the Hill coefficient or the free Ca2+ at half-maximal activity. The fluorescent probes, FITC and N-cyclohexyl- N′-(dimethylamino-α-naphthyl) carbodiimide, used to assess structural alterations in the regions of the ATP binding site and the Ca2+ binding sites of the Ca2+-ATPase, respectively, indicated a 26% reduction ( P < 0.05) in FITC binding capacity (absolute units) in I (0.22 ± 0.01) compared with CC (0.29 ± 0.02) and C (0.29 ± 0.03). Our results suggest that the reduction in maximal SR Ca2+-ATPase activity in SR vesicles with ischemia is related to structural modification in the region of the nucleotide binding domain by mechanisms that are as yet unclear.

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.

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 Induced overexpression of phospholemman S68E mutant improves cardiac contractility and mortality after ischemia-reperfusion

2014 ◽  
Vol 306 (7) ◽  
pp. H1066-H1077 ◽  
Author(s):  
JuFang Wang ◽  
Jianliang Song ◽  
Erhe Gao ◽  
Xue-Qian Zhang ◽  
Tongda Gu ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Ischemia Reperfusion ◽  
Cardiac Contractility ◽  
Left Ventricular ◽  
Wild Type ◽  
Protein Levels ◽  
Plasmic Reticulum ◽  
Intracellular Ca ◽  
Similar Survival

Phospholemman (PLM), when phosphorylated at Ser68, inhibits cardiac Na+/Ca2+ exchanger 1 (NCX1) and relieves its inhibition on Na+-K+-ATPase. We have engineered mice in which expression of the phosphomimetic PLM S68E mutant was induced when dietary doxycycline was removed at 5 wk. At 8–10 wk, compared with noninduced or wild-type hearts, S68E expression in induced hearts was ∼35–75% that of endogenous PLM, but protein levels of sarco(endo)plasmic reticulum Ca2+-ATPase, α1- and α2-subunits of Na+-K+-ATPase, α1c-subunit of L-type Ca2+ channel, and phosphorylated ryanodine receptor were unchanged. The NCX1 protein level was increased by ∼47% but the NCX1 current was depressed by ∼34% in induced hearts. Isoproterenol had no effect on NCX1 currents but stimulated Na+-K+-ATPase currents equally in induced and noninduced myocytes. At baseline, systolic intracellular Ca2+ concentrations ([Ca2+]i), sarcoplasmic reticulum Ca2+ contents, and [Ca2+]i transient and contraction amplitudes were similar between induced and noninduced myocytes. Isoproterenol stimulation resulted in much higher systolic [Ca2+]i, sarcoplasmic reticulum Ca2+ content, and [Ca2+]i transient and contraction amplitudes in induced myocytes. Echocardiography and in vivo close-chest catheterization demonstrated similar baseline myocardial function, but isoproterenol induced a significantly higher +dP/d t in induced compared with noninduced hearts. In contrast to the 50% mortality observed in mice constitutively overexpressing the S68E mutant, induced mice had similar survival as wild-type and noninduced mice. After ischemia-reperfusion, despite similar areas at risk and left ventricular infarct sizes, induced mice had significantly higher +dP/d t and −dP/d t and lower perioperative mortality compared with noninduced mice. We propose that phosphorylated PLM may be a novel therapeutic target in ischemic heart disease.

Effects of progressive exercise and hypoxia on human muscle sarcoplasmic reticulum function

2004 ◽  
Vol 97 (1) ◽  
pp. 188-196 ◽  
Author(s):  
T. A. Duhamel ◽  
H. J. Green ◽  
S. D. Sandiford ◽  
J. G. Perco ◽  
J. Ouyang
Keyword(s):  
Sarcoplasmic Reticulum ◽  
G Protein ◽  
Power Output ◽  
Maximal Activity ◽  
Peak Oxygen Consumption ◽  
Hill Coefficient ◽  
Oxygen Fraction ◽  
Mechanical Power Output ◽  
Progressive Exercise ◽  
Inspired Oxygen

This study examined the effects of progressive exercise to fatigue in normoxia (N) on muscle sarcoplasmic reticulum (SR) Ca2+ cycling and whether alterations in SR Ca2+ cycling are related to the blunted peak mechanical power output (POpeak) and peak oxygen consumption (V̇o2 peak) observed during progressive exercise in hypoxia (H). Nine untrained men (20.7 ± 0.42 yr) performed progressive cycle exercise to fatigue on two occasions, namely during N (inspired oxygen fraction = 0.21) and during H (inspired oxygen fraction = 0.14). Tissue extracted from the vastus lateralis before exercise and at power output corresponding to 50 and 70% of V̇o2 peak (as determined during N) and at fatigue was used to investigate changes in homogenate SR Ca2+-cycling properties. Exercise in H compared with N resulted in a 19 and 21% lower ( P < 0.05) POpeak and V̇o2 peak, respectively. During progressive exercise in N, Ca2+-ATPase kinetics, as determined by maximal activity, the Hill coefficient, and the Ca2+ concentration at one-half maximal activity were not altered. However, reductions with exercise in N were noted in Ca2+ uptake (before exercise = 357 ± 29 μmol·min−1·g protein−1; at fatigue = 306 ± 26 μmol·min−1·g protein−1; P < 0.05) when measured at free Ca2+ concentration of 2 μM and in phase 2 Ca2+ release (before exercise = 716 ± 33 μmol·min−1·g protein−1; at fatigue = 500 ± 53 μmol·min−1·g protein−1; P < 0.05) when measured in vitro in whole muscle homogenates. No differences were noted between N and H conditions at comparable power output or at fatigue. It is concluded that, although structural changes in SR Ca2+-cycling proteins may explain fatigue during progressive exercise in N, they cannot explain the lower POpeak and V̇o2 peak observed during H.

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