Prolonged submaximal exercise induces isoform-specific Na+-K+-ATPase mRNA and protein responses in human skeletal muscle.

@article{Murphy2006ProlongedSE,
  title={Prolonged submaximal exercise induces isoform-specific Na+-K+-ATPase mRNA and protein responses in human skeletal muscle.},
  author={Kate T. Murphy and Aaron C. Petersen and Craig A. Goodman and Xiaofei Gong and James A Leppik and Andrew P. Garnham and David Cameron-Smith and Rodney J. Snow and Michael J. McKenna},
  journal={American journal of physiology. Regulatory, integrative and comparative physiology},
  year={2006},
  volume={290 2},
  pages={
          R414-24
        }
}
  • K. Murphy, A. Petersen, +6 authors M. McKenna
  • Published 1 February 2006
  • Biology
  • American journal of physiology. Regulatory, integrative and comparative physiology
This study investigated effects of prolonged submaximal exercise on Na+-K+-ATPase mRNA and protein expression, maximal activity, and content in human skeletal muscle. We also investigated the effects on mRNA expression of the transcription initiator gene, RNA polymerase II (RNAP II), and key genes involved in protein translation, eukaryotic initiation factor-4E (eIF-4E) and 4E-binding protein 1 (4E-BP1). Eleven subjects (6 men, 5 women) cycled at 75.5% (SD 4.8%) peak O2 uptake and continued… 

Figures and Tables from this paper

Muscle Na+-K+-ATPase activity and isoform adaptations to intense interval exercise and training in well-trained athletes.
TLDR
The Na+ -K+ -ATPase mRNA response to interval exercise of increased alpha- but not beta-mRNA was largely preserved posttrain, suggesting a functional role of alpha mRNA upregulation.
Effects of acute exercise and long-term exercise on total Na+,K+ -ATPase content and Na+,K+ -ATPase isoform expression profile in equine muscle.
TLDR
Determination of Na(+),K(+)-ATPase gene expression may be relevant for understanding alterations in excitability during neuromuscular diseases, and Expression of these isoforms changed as a result of strenuous exercise and long-term training, representing an adaptive response.
Post-exercise cold-water immersion increases Na+,K+-ATPase α2-isoform mRNA content in parallel with elevated Sp1 expression in human skeletal muscle
TLDR
These human findings highlight 1) sprint-interval exercise increases the mRNA content of NKA α1 and β3, and decreases that of Nka β2, which may relate, in part, to exercise-induced muscle hypoxia, and 2) post-exercise CWI augments NKAα2 mRNA, which might be associated with promoted Sp1 activation.
Exercise-induced regulation of muscular Na+-K+ pump, FXYD1, and NHE1 mRNA and protein expression: importance of training status, intensity, and muscle type.
TLDR
Increased expression of Na(+)-K(+) pump subunits, FXYD1 and NHE1 after 3 days exercise training does not appear to be an effect of increased constitutive mRNA levels, and sprint exercise can reduce mRNA expression concomitant with increased protein expression.
Digoxin and exercise effects on Na+,K+-ATPase isoform gene and protein expression in human skeletal muscle
TLDR
This thesis investigated whether in-vivo inhibition of Na+,K+-ATPase by digoxin adversely effected muscle performance and Na+, K+- ATPase isoform expression and protein abundance in skeletal muscle of healthy individuals.
Dissociation between changes in muscle Na+-K+-ATPase isoform abundance and activity with consecutive days of exercise and recovery.
TLDR
It is concluded that 3 days of prolonged exercise is a powerful stimulus for the rapid upregulation of the Na(+)-K(+-ATPase subunit isoforms and is not accompanied by increases in the maximal catalytic activity.
Muscle Na+-K+-ATPase response during 16 h of heavy intermittent cycle exercise.
TLDR
It is concluded that repeated sessions of heavy exercise, although resulting in increases in the alpha(2)- and alpha(3)-isoforms and decreases in beta(3-isoform, also result in depression in maximal catalytic activity.
Dissociation between short-term unloading and resistance training effects on skeletal muscle Na+,K+-ATPase, muscle function, and fatigue in humans.
TLDR
Despite considerably impaired muscle function and earlier fatigue onset, muscle NKA content and homogenate α1 and α2 abundances were unchanged, thus being resilient to inactivity induced by ULLS, and fiber type-specific downregulation with inactivity and upregulation with RT of several NKA isoforms indicate complex regulation of muscle Nka expression in humans.
Influence of chronic and acute spinal cord injury on skeletal muscle Na+-K+-ATPase and phospholemman expression in humans.
TLDR
The severity of the spinal cord lesion and the level of postinjury physical activity in patients with SCI are important factors controlling the expression of Na(+)-K(+)+)-ATPase and its regulatory proteins PLM and FXYD5.
Effect of exercise and training on phospholemman phosphorylation in human skeletal muscle.
TLDR
It is shown that only acute exercise, and not short-term training, increases phosphorylation of PLM on Ser(63) and Ser(68), and data from one-legged cycling indicate that this effect of exercise on PLM phosphorylated is not due to systemic factors.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 52 REFERENCES
Contraction-induced increases in Na+-K+-ATPase mRNA levels in human skeletal muscle are not amplified by activation of additional muscle mass.
TLDR
Activation of additional muscle mass does not result in a higher exercise-induced increase in Na(+)-K( +)-ATPase subunit-specific mRNA, and no reliable detection of alpha(3) and alpha(4) was possible.
Intense exercise up‐regulates Na+,K+‐ATPase isoform mRNA, but not protein expression in human skeletal muscle
TLDR
Human skeletal muscle expresses each of the Na+,K+‐ATPase α1, α2, α3, β1, β2 and β3 isoforms, evidenced at both transcription and protein levels.
Prolonged exercise to fatigue in humans impairs skeletal muscle Na+-K+-ATPase activity, sarcoplasmic reticulum Ca2+ release, and Ca2+ uptake.
TLDR
Prolonged exhaustive submaximal exercise in humans induces marked metabolic changes, but little is known about effects on muscle Na+-K+-ATPase activity and sarcoplasmic reticulum Ca2+ regulation, which suggests that acutely downregulated muscle Na+, K+, and Ca2- transport processes may be important factors in fatigue during prolonged exercise in human.
Depressed Na+-K+-ATPase activity in skeletal muscle at fatigue is correlated with increased Na+-K+-ATPase mRNA expression following intense exercise.
We investigated whether depressed muscle Na(+)-K(+)-ATPase activity with exercise reflected a loss of Na(+)-K(+)-ATPase units, the time course of its recovery postexercise, and whether this depressed
Malleability of human skeletal muscle Na(+)-K(+)-ATPase pump with short-term training.
TLDR
It is indicated that prolonged aerobic exercise represents a potent stimulus for the rapid adaptation of Na(+)-K( +)-ATPase content, isoform, and activity characteristics.
Sprint training increases human skeletal muscle Na(+)-K(+)-ATPase concentration and improves K+ regulation.
TLDR
The increased muscle [3H]ouabain binding site concentration and the reduced ratio of rise in [K+] relative to work output with exercise are both consistent with improved plasma and skeletal muscle K+ regulation after sprint training.
Inactivation of human muscle Na+-K+-ATPase in vitro during prolonged exercise is increased with hypoxia.
TLDR
It is concluded that, although exercise in H resulted in a greater inactivation of Na+-K+-ATPase activity compared with N, neuromuscular fatigue and membrane excitability are not differentially altered.
Availability of eIF4E regulates skeletal muscle protein synthesis during recovery from exercise.
TLDR
It is demonstrated that recovery of muscle protein synthesis after exercise is related to the availability of eIF4E for 48S ribosomal complex formation, and postexercise meal composition influences recovery via modulation of translation initiation.
Exercise increases the plasma membrane content of the Na+ -K+ pump and its mRNA in rat skeletal muscles.
TLDR
Examination of the effect of 1 h of treadmill running on the subcellular distribution and expression of Na+-K+ pump subunits in rat skeletal muscles concludes that increased presence of alpha1- and alpha2-polypeptides at the plasma membrane and subsequent elevation of the alpha1 and beta2-subunit mRNAs may be mechanisms by which acute exercise regulates the Na-k+ pump of skeletal muscle.
Effect of high-intensity training on exercise-induced gene expression specific to ion homeostasis and metabolism.
TLDR
Cellular adaptations to high-intensity exercise training may, in part, be induced by transcriptional regulation after training, when the transcriptional response to an exercise bout at a given workload is diminished.
...
1
2
3
4
5
...