Skip to main content

Quantitative Biology of Exercise-Induced Signal Transduction Pathways

  • Chapter
  • First Online:
Oxygen Transport to Tissue XXXIX

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 977))

Abstract

Exercise is essential in regulating energy metabolism. Exercise activates cellular, molecular, and biochemical pathways with regulatory roles in training response adaptation. Among them, endurance/strength training of an individual has been shown to activate its respective signal transduction pathways in skeletal muscle. This was further studied from the viewpoint of quantitative difference (QD). For the mean values, \( \overline{x} and\ \overline{y} \), of two sets of data, their QD is defined as \( l=\left|{ \log}_{\tau}\left(\overline{x}/\overline{y}\right)\right| \) (\( \tau =\left(\sqrt{5}-1\right)/2\approx 0.618 \)). The function-specific homeostasis (FSH) of a function of a biosystem is a negative-feedback response of the biosystem to maintain the function-specific conditions inside the biosystem so that the function is perfectly performed. A function in/far from its FSH is called a normal/dysfunctional function. A cellular normal function can resist the activation of other signal transduction pathways so that there are normal function-specific signal transduction pathways which full activation maintains the normal function. Results: An acute endurance/strength training may be dysfunctional, but its regular training may be normal. The normal endurance/strength training of an individual may resist the activation of other signal transduction pathways in skeletal muscle so that there may be normal endurance/strength training-specific signal transduction pathways (NEPs/NSPs) in skeletal muscle. The endurance/strength training may activate NSPs/NEPs, but the QD from the control is smaller than 0.80. The simultaneous activation of both NSPs and NEPs may enhance their respective activation, and the QD from the control is larger than 0.80. The low level laser irradiation pretreatment of rats may promote the activation of NSPs in endurance training skeletal muscle. Conclusion: There may be NEPs/NSPs in skeletal muscle trained by normal endurance/strength training.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 149.00
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 199.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 199.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

References

  1. Rodbell M (1980) The role of hormone receptors and GTP-regulatory proteins in membrane transduction. Nature 284(5751):17–22

    Article  CAS  PubMed  Google Scholar 

  2. Levy ED, Landry CR, Michnick SW (2010) Cell signaling: signaling through cooperation. Science 328(5981):983–984

    Article  CAS  PubMed  Google Scholar 

  3. Hawley JA, Hargreaves M, Joyner MJ et al (2014) Integrative biology of exercise. Cell 159(4):738–749

    Article  CAS  PubMed  Google Scholar 

  4. Nuzzo R (2014) Scientific method: statistical errors. Nature 506(7487):150–152

    Article  CAS  PubMed  Google Scholar 

  5. Liu CY, Wu CY, Li FH et al (2017) Self-similarity constant and quantitative difference and their applications in sports science. J Phys Educ 24 (to be published in Chinese)

    Google Scholar 

  6. Whitlook MC, Schluter D (2015) The analysis of biological data, 2nd edn. Roberts and Company Publishers, Colorado, pp 176–177

    Google Scholar 

  7. West BJ (2010) Fractal physiology and the fractional calculus: a perspective. Front Physiol 1:12

    PubMed  PubMed Central  Google Scholar 

  8. Liu TCY, Wu DF, Zhu L et al (2014) Micro-environment dependent photobiomodulation on function-specific signal transduction pathways. Int J Photoenergy 2014: Article ID 904304, 8 p

    Google Scholar 

  9. Cheung K, Hume P, Maxwell L (2003) Delayed onset muscle soreness: treatment strategies and performance factors. Sports Med 33(2):145–164

    Article  PubMed  Google Scholar 

  10. Bartlett JD, Close GL, Drust B et al (2014) The emerging role of p53 in exercise metabolism. Sports Med 44(3):303–309

    Article  PubMed  Google Scholar 

  11. Philp A, Chen A, Lan D et al (2011) Sirtuin 1 (SIRT1) deacetylase activity is not required for mitochondrial biogenesis or peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) deacetylation following endurance exercise. J Biol Chem 286(35):30561–30570

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  12. Geng T, Li P, Okutsu M et al (2010) PGC-1alpha plays a functional role in exercise-induced mitochondrial biogenesis and angiogenesis but not fiber-type transformation in mouse skeletal muscle. Am J Physiol Cell Physiol 298(3):C572–C579

    Article  CAS  PubMed  Google Scholar 

  13. Drummond MJ, Fry CS, Glynn EL et al (2009) Rapamycin administration in humans blocks the contraction-induced increase in skeletal muscle protein synthesis. J Physiol 587(Pt 7):1535–1546

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  14. Wang L, Mascher H, Psilander N et al (2011) Resistance exercise enhances the molecular signaling of mitochondrial biogenesis induced by endurance exercise in human skeletal muscle. J Appl Physiol (1985) 111(5):1335–1344

    Article  CAS  Google Scholar 

  15. Liu YY (2015) Effects of low level laser pre-irradiation and exercise on skeletal muscle mitochondrial apoptosis pathways of aging rats and its mechanism. PhD thesis, South China Normal University

    Google Scholar 

  16. White JP, Wrann CD, Rao RR et al (2014) G protein-coupled receptor 56 regulates mechanical overload-induced muscle hypertrophy. Proc Natl Acad Sci U S A 11(44):15756–15761

    Article  Google Scholar 

  17. Ma X, Fu Y, Xiao H et al (2015) Cardiac fibrosis alleviated by exercise training is AMPK-dependent. PLoS One 10(6):e0129971

    Article  PubMed  PubMed Central  Google Scholar 

  18. Silva JA Jr, Santana ET, Manchini MT et al (2014) Exercise training can prevent cardiac hypertrophy induced by sympathetic hyperactivity with modulation of kallikrein-kinin pathway and angiogenesis. PLoS One 9(3):e91017

    Article  PubMed  PubMed Central  Google Scholar 

  19. Schweitzer GG, Cartee GD (2011) Postexercise skeletal muscle glucose transport is normal in kininogen-deficient rats. Med Sci Sports Exerc 43(7):1148–1153

    Article  CAS  PubMed  PubMed Central  Google Scholar 

Download references

Acknowledgments

This work was supported by National Science Foundation of China (61575065, 11604104), Doctoral Fund of Ministry of Education of China (20124407110013), Guangdong Scientific Project (2012B031600004) and The Sports Scientific Project of Guangdong (GDSS2014103).

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Timon Cheng-Yi Liu .

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 2017 Springer International Publishing AG

About this chapter

Cite this chapter

Liu, T.CY., Liu, G., Hu, SJ., Zhu, L., Yang, XB., Zhang, QG. (2017). Quantitative Biology of Exercise-Induced Signal Transduction Pathways. In: Halpern, H., LaManna, J., Harrison, D., Epel, B. (eds) Oxygen Transport to Tissue XXXIX. Advances in Experimental Medicine and Biology, vol 977. Springer, Cham. https://doi.org/10.1007/978-3-319-55231-6_54

Download citation

Publish with us

Policies and ethics