Heat shock proteins and endogenous antioxidants in skeletal muscle: acute responses to exercise and adaptations to training
Doctoral thesis
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http://hdl.handle.net/11250/276629Utgivelsesdato
2014Metadata
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Sammendrag
Muscular training adaptations do not only involve the normally investigated increases in muscle size
(strength training) or mitochondrial capacity (endurance training), because several homeostatic
systems need to follow. As discussed above, these systems react to different types of exerciseinduced
stress. For instance, the HSPs can be induced by different types of stress which can be
prompted by different types of exercise. Several HSPs increase in content after periods of both
endurance and strength training, but changes in HSP levels seem to be more pronounced after
exercise with high intensity – which logically induces higher stress than low intensity.
Correspondingly, the acute responses after a single bout of exercise are also affected by intensity,
where higher intensity induces larger increases in protein content. Some studies have investigated
the translocation of the HSP after bouts of high-force eccentric exercise. These studies show that the
HSPs rapidly translocate to structures that are highly stressed after this form of exercise which
mostly includes proteins in cytoskeletal structures. Translocation of the HSP after lower intensity
exercise is, however, still unknown. Importantly, ischemia per se can result in similar translocation to
cytoskeletal structures as observed after high-force exercise. It is therefore likely that HSPs also
translocate to these structures after exercises not associated with large grade of muscle damage, e.g.
“normal” strength training or low load occlusion training (low load blood flow restricted strength
exercise).
The formation of RONS during exercise, can, together with the other types of stress from exercise,
induce damage to proteins, nucleotides and lipids, and cause improper cell functions. The
neutralization of the damaging properties of these reactive species is caused by the interaction of a
network of several antioxidants. Most of these antioxidants are produced in the cell (endogenous
antioxidants), but several important antioxidants must come from the diet (exogenous antioxidants).
The endogenous antioxidants seem to increase as an adaptation to both endurance and strength
training, and exercise intensity and duration – which most likely reflects levels of oxidative stress in
the muscle cell. To help fight oxidative stress and reduce high concentration of RONS, many athletes
take antioxidant supplements (Sobal & Marquart, 1994). As this might seem logical and beneficial
when doing hard and frequent training, it might interfere with important cellular processes related to
training adaptations. Several studies have reported negative effects of high doses of antioxidants on
training adaptations like in the HSPs and the endogenous antioxidants. However, conflicting results
exists, which might come from the studied population, tissues examined, doses and timing of the
antioxidant supplements. Paper I: Cumming, K. T., G. Paulsen, M. Wernbom, I. Ugelstad, and T. Raastad. 2014. Acute response and
subcellular movement of HSP27, aB-crystallin and HSP70 in human skeletal muscle after blood flow
restricted low-load resistance exercise. Acta. Physiol. (Oxf.) 211:634–646. Paper II: Tatt ut av filen i Brage p.g.a. copyright-restriksjoner. / Not in the file in Brage because of copyright issues. Paper III: Cumming, K. T., T. Raastad, G. Holden, N. E. Bastani, D. Schneeberger, M. P. Paronetto, N. Mercatelli,
H. N. Østgaard, I. Ugelstad, D. Caporossi, R. Blomhoff, and G. Paulsen. (2014). Effects of vitamin C and
E supplementation on endogenous antioxidant systems and heat shock proteins in response to
endurance training. Physiol Rep 2(9):e12142. Paper IV: Tatt ut av filen i Brage p.g.a. copyright-restriksjoner. / Not in the file in Brage because of copyright issues.
Beskrivelse
Avhandling (doktorgrad) - Norges idrettshøgskole, 2014