Heat shock proteins and endogenous antioxidants in skeletal muscle: acute responses to exercise and adaptations to training
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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.
Avhandling (doktorgrad) - Norges idrettshøgskole, 2014