Exercise-induced increase in maximal in vitro Na-K-ATPase activity in human skeletal muscle

Juel, Carsten; Nordsborg, Nikolai Baastrup; Bangsbo, Jens

doi:10.1152/ajpregu.00591.2012

Cited by 26 publications

(37 citation statements)

References 24 publications

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“…The Na + concentration was either 0, 5 or 40 mM (the ionic strength was kept constant by substituting NaCl with choline chloride). 40 mM Na + has previously been shown to fully activate the Na + dependent Na,K-ATPase activity [4], [13]. Graphs demonstrating the Na + -dependency of the ATPase activity have been published previously [13].…”

Section: Methodsmentioning

confidence: 98%

“…The human study was approved by the regional ethics committee for the capital region of Denmark (H-A-2009-016). These samples have been used in another study [13]. All subjects gave written informed consent to participate.…”

Section: Methodsmentioning

confidence: 99%

“…40 mM Na + has previously been shown to fully activate the Na + dependent Na,K-ATPase activity [4], [13]. Graphs demonstrating the Na + -dependency of the ATPase activity have been published previously [13]. After 5 min preincubation at 37°C, the reaction was started by adding Mg-ATP to a final concentration of 0.5 mM, and after 30 min, the reaction was terminated by adding 1 mL Biomol Green reagent.…”

Section: Methodsmentioning

confidence: 99%

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Purinergic Effects on Na,K-ATPase Activity Differ in Rat and Human Skeletal Muscle

2014

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BackgroundP2Y receptor activation may link the effect of purines to increased maximal in vitro activity of the Na,K-ATPase in rat muscle. The hypothesis that a similar mechanism is present in human skeletal muscle was investigated with membranes from rat and human skeletal muscle.ResultsMembranes purified from rat and human muscles were used in the Na,K-ATPase assay. Incubation with ADP, the stable ADP analogue MeS-ADP and UDP increased the Na+ dependent Na,K-ATPase activity in rat muscle membranes, whereas similar treatments of human muscle membranes lowered the Na,K-ATPase activity. UTP incubation resulted in unchanged Na,K-ATPase activity in humans, but pre-incubation with the antagonist suramin resulted in inhibition with UTP, suggesting that P2Y receptors are involved. The Na,K-ATPase in membranes from both rat and human could be stimulated by protein kinase A and C activation. Thus, protein kinase A and C activation can increase Na,K-ATPase activity in human muscle but not via P2Y receptor stimulation.ConclusionThe inhibitory effects of most purines (with the exception of UTP) in human muscle membranes are probably due to mass law inhibition of ATP hydrolysis. This inhibition could be blurred in rat due to receptor mediated activation of the Na,K-ATPase. The different effects could be related to a high density of ADP sensitive P2Y1 and P2Y13 receptors in rat, whereas the UTP sensitive P2Y11 could be more abundant in human. Alternatively, rat could possesses a mechanism for protein-protein interaction between P2Y receptors and the Na,K-ATPase, and this mechanism could be absent in human skeletal muscle (perhaps with the exception of the UTP sensitive P2Y11 receptor).PerspectiveRat muscle is not a reliable model for purinergic effects on Na,K-ATPase in human skeletal muscle.

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Section: Methodsmentioning

confidence: 98%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Purinergic Effects on Na,K-ATPase Activity Differ in Rat and Human Skeletal Muscle

2014

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“…During intense muscle contractions resulting from cardiac stress, ion gradients across the muscle membrane undergo substantive perturbations, which may lead to disturbances in its excitability and muscle exhaustion. The Na, K‐ATPase partially counteracts these changes through the regulation of the Na + and K + ions, thus playing an important role in establishing muscle function during increased workload . Notably, τ i has been proposed as a measure of Na, K‐ATPase activity, whereas decreases in τ i shown in our study reflect the upregulation of Na, K‐ATPase activity during pharmacological stress.…”

Section: Discussionmentioning

confidence: 63%

Quantification of regional myocardial mean intracellular water lifetime: A nonhuman primate study in myocardial stress

Sampath¹,

Parimal²,

Huang

et al. 2020

NMR in Biomedicine

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Heart failure with preserved ejection fraction (HFpEF) is typically associated with early metabolic remodeling. Noninvasive imaging biomarkers that reflect these changes will be crucial in determining responses to early drug interventions in these patients. Mean intracellular water lifetime (τi) has been shown to be partially inversely related to Na, K‐ATPase transporter activity and may thus provide insight into the metabolic status in HFpEF patients. Here, we aim to perform regional quantification of τi using dynamic contrast‐enhanced (DCE) magnetic resonance imaging (MRI) in the nonhuman primate (NHP) heart and evaluate its region‐specific variations under conditions of myocardial stress in the context of perturbed myocardial function. Cardiac stress was induced in seven naïve cynomolgus macaques using a dobutamine stepwise infusion protocol. All animals underwent 3 T cardiac dual‐bolus DCE and tagging MRI experiments. The shutter‐speed model was employed to quantify regional τi from the DCE‐MR images. Additionally, τi values were correlated with myocardial strains. During cardiac stress, there was a significant decrease in global τi (192.9 ± 76.3 ms vs 321.6 ± 70 ms at rest, P < 0.05) in the left ventricle, together with an increase in global peak circumferential strain (−15.4% ± 2.7% vs −10.1% ± 2.9% at rest, P < 0.05). Specifically, slice‐level analysis further revealed that a greater significant decrease in mean τi was observed in the apical region (ΔτI = 182.4 ms) compared with the basal (Δτi = 113.2 ms) and midventricular regions (Δτi = 108.4 ms). Regional analysis revealed that there was a greater significant decrease in mean τi in the anterior (Δτi = 243.9 ms) and antero‐lateral (Δτi = 177.2 ms) regions. In the inferior and infero‐septal regions, although a decrease in τi was observed, it was not significant. Whole heart regional quantification of τi is feasible using DCE‐MRI. τi is sensitive to regional changes in metabolic state during cardiac stress, and its value correlates with strain.

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“…This method has recently been criticised as being an inadequate measure of NKA activity during exercise, when intracellular sodium concentration is expected to be elevated and which activates the NKA [33]. Although the method is Na + -insensitive, it remains valid as a marker of NKA activity in resting muscle, when intracellular Na + is not raised.…”

Section: Methodsmentioning

confidence: 99%

Unaccustomed Eccentric Contractions Impair Plasma K+ Regulation in the Absence of Changes in Muscle Na+,K+-ATPase Content

et al. 2014

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The Na+,K+-ATPase (NKA) plays a fundamental role in the regulation of skeletal muscle membrane Na+ and K+ gradients, excitability and fatigue during repeated intense contractions. Many studies have investigated the effects of acute concentric exercise on K+ regulation and skeletal muscle NKA, but almost nothing is known about the effects of repeated eccentric contractions. We therefore investigated the effects of unaccustomed maximal eccentric knee extensor contractions on K+ regulation during exercise, peak knee extensor muscle torque, and vastus lateralis muscle NKA content and 3-O-MFPase activity. Torque measurements, muscle biopsies, and venous blood samples were taken before, during and up to 7 days following the contractions in six healthy adults. Eccentric contractions reduced peak isometric muscle torque immediately post-exercise by 26±11% and serum creatine kinase concentration peaked 24 h post-exercise at 339±90 IU/L. During eccentric contractions, plasma [K+] rose during Set 1 and remained elevated at ∼4.9 mM during sets 4–10; this was despite a decline in work output by Set 4, which fell by 18.9% at set 10. The rise in plasma [K+].work−1 ratio was elevated over Set 2 from Set 4– Set 10. Eccentric contractions had no effect on muscle NKA content or maximal in-vitro 3-O-MFPase activity immediately post- or up to 7 d post-exercise. The sustained elevation in plasma [K+] despite a decrease in work performed by the knee extensor muscles suggests an impairment in K+ regulation during maximal eccentric contractions, possibly due to increased plasma membrane permeability or to excitation-contraction uncoupling.

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Exercise-induced increase in maximal in vitro Na-K-ATPase activity in human skeletal muscle

Cited by 26 publications

References 24 publications

Purinergic Effects on Na,K-ATPase Activity Differ in Rat and Human Skeletal Muscle

Purinergic Effects on Na,K-ATPase Activity Differ in Rat and Human Skeletal Muscle

Quantification of regional myocardial mean intracellular water lifetime: A nonhuman primate study in myocardial stress

Unaccustomed Eccentric Contractions Impair Plasma K+ Regulation in the Absence of Changes in Muscle Na+,K+-ATPase Content

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