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Metabolic stress and high intensity exercise

Julien S Baker

Institute of Clinical Exercise and Health Science, Applied Physiology Research Laboratory, School of Science and Sport, University of the West of Scotland, UK

E-mail : bhuvaneswari.bibleraaj@uhsm.nhs.uk

Duncan Buchan

Institute of Clinical Exercise and Health Science, Applied Physiology Research Laboratory, School of Science and Sport, University of the West of Scotland, UK

DOI: 10.15761/PMRR.1000136

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Exercise-induced catecholamine responses are related to exercise intensity and are affected by the preceding training regimen. Although most investigations of catecholamine responses to training have utilized aerobic exercise models, it is likely that anaerobic training regimens will produce a considerably different physiological profile. Furthermore, depending on the acute resistance exercise variables (i.e., choice of exercise, order of exercise, rest intervals, load, volume of exercise), considerable physiological variation exists between different exercise protocols. To date, few studies have investigated catecholamine responses to an anaerobic overtraining models.

Total stress response to exercise is reflected by the adrenal medulla response. This may be measured by the accumulation of adrenaline (A) and noradrenaline (NA). This increase may be markedly influenced by the effect of physical exertion, cold and emotional factors. Plasma catecholamine levels also increase as a result of both increases in the duration of exercise and the severity of exercise [1]. The plasma concentrations of catecholamines have been shown to increase during different types of aerobic and anaerobic exercises [2]. However, it has been found that plasma adrenaline increase in heavy high intensity exercise may be higher than in aerobic exercise [3].

Different high intensity activities such as sprinting [4] and cycle ergometry [5,6] as well as heavy resistance exercise training [7] have all been found to elevate plasma catecholamine levels.

At identical submaximal exercise levels several authors observed [8] a lesser increase in free plasma adrenaline (A) and noradrenaline (NA) in endurance trained athletes than in sedentary subjects. Conversely, Kjaer et al. [9,10] found that endurance trained athletes compared to untrained ones  exhibited not only similar plasma NA but also higher plasma A concentrations. Brief high intensity exhaustive exercise has been shown to increase plasma catecholamine levels to values higher than those observed during aerobic activity [8]. Therefore it may be possible that sprinters exhibit a higher adrenal response to sympathetic activity. It has often been emphasised that feedback mechanisms are important for the hormonal response to exercise [11]. A reduction in plasma glucose levels during exercise gives rise to an increase in the plasma concentration of adrenaline, and it has been postulated that increasing adrenaline secretion may function as a safety backup mechanism, preventing hypoglycaemia and lack of substrate in the working muscle [12]. It seems, however, that rapid changes in endocrine and metabolic responses found at the onset and the cessation of exercise, occur too quickly to be explained by feedback mechanisms only. This may be partly explained by the direct stimulation from the motor centres of the brain, the feed - forward or central command mechanisms which are also involved with respiratory and circulatory regulation [13]. These mechanisms will also be active in substrate mobilisation during exercise. Physical training may alter the hormonal response of several hormones to a given exercise work load. The release and rate of release of hormones are controlled in response to specific needs.

The rates of secretion should be related to their metabolic functions and needs of a particular circumstance ie whether high or low intensity [14].

Previous experiments have demonstrated the importance of anaerobic glycolysis in the resynthesis of adenosine triphosphate (ATP) during high intensity performance.

Exercise of this intensity although predominantly anaerobic, provides a severe challenge to the control of the cardiovascular system and elevates sympathetic activity.

The stimulation of glycogenolysis by adrenaline has been demonstrated, and significant correlations have been observed between ATP resynthesis and plasma adrenaline concentration [4]. These studies have also found that during maximal exercise large concentrations in circulating adrenaline and noradrenaline occur. Therefore, catecholamine consentration has a significant role to play in metabolic function during high intensitiy anaerobic metabolism.

References

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  2. Galbo H (1986) Autonomic neuroendocrine responses to exercise. Scandinavian Journal of Sports Science 8: 3-17.
  3. Kindermann, W, Schnabel A, Schmitt WM, Biro G, Cassens J, et al. (1982), Catecholamines, growth hormone, cortisol, insulin and sex hormones in anaerobic and aerobic exercise. Eur J Appl Physiol Occup Physiol 49: 389-399. [Crossref]
  4. Cheetham M, Boobis L, Brooks S, Williams C (1986) Human muscle metabolism during sprint running. J Appl Physiol (1985) 61: 54-60.
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  6. Gratas-Delamarche A, Le Cam R, Delamarche P, Monnier M, Koubi H (1994) Lactate and catecholamine responses in male and female sprinters during a Wingate test. Eur J Appl Physiol Occup Physiol 68: 362-366. [Crossref]
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  9. Kjaer M, Christensen NJ, Sonne B, Richter EA, Galbo H (1985) Effect of exercise on epinephrine turnover in trained and untrained male subjects. J Appl Physiol (1985) 59: 1061-1067. [Crossref]
  10. Kjaer M, Galbo H (1988) Effect of physical training on the capacity to secrete epinephrine. J Appl Physiol (1985) 64: 11-16. [Crossref]
  11. Newsholme EA, Leech AR (1983) Biochemistry for the Medical Sciences. Chichester: John Wiley and Sons.
  12. Kjaer M (1989) Epinephrine and some other hormonal responses to exercise in man: with special reference to physical training. Int J Sports Med 10: 2-15. [Crossref]
  13. Rowell LB, Blackmon JR (1986) Lack of sympathetic vasoconstriction in hypoxemic humans at rest. Am J Physiol 251: H562-570. [Crossref]
  14. Brooks S, Burrin J, Cheetham ME, Hall GM, Yeo T, et al. (1988) The responses of the catecholamines and beta-endorphin to brief maximal exercise in man. Eur J Appl Physiol Occup Physiol 57: 230-234. [Crossref]

Editorial Information

Editor-in-Chief

Martin Grabois
Baylor College of Medicine

Article Type

Editorial article

Publication history

Received date: February 14, 2017
Accepted date: February 25, 2017
Published date: February 28, 2017

Copyright

© 2017 Baker JS. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Citation

Baker JS (2017) Metabolic stress and high intensity exercise. Phys Med Rehabil Res 2: DOI: 10.15761/PMRR.1000136

Corresponding author

Julien S Baker

Institute of Clinical Exercise and Health Science, Applied Physiology Research Laboratory, School of Science and Sport, University of the West of Scotland, Hamilton, Lanarkshire, Scotland, ML3 OJB, Tel: 01698 283100 ext: 8271; Fax: 01698 894404;

E-mail : bhuvaneswari.bibleraaj@uhsm.nhs.uk

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