Table 2. Literature compiled on oxidative stress imposed through various exercise modalities.
| Publication information (Ref#) | Research model | Age at start (weeks) | Stress intensity | Length of stress | p53 expression (residue modification) | p53 cellular localization | Regulation of signaling pathways with stress | Signaling pathway(s) activated | Path model | |
|---|---|---|---|---|---|---|---|---|---|---|
| mRNA | Protein | |||||||||
| Acute exercise programs | ||||||||||
| Saleem, Hood, J Physiol, 2013 [24] |
(C57Bl/6J p53 KO and WT mice n = 6 |
12 | 15 m/min for 90 min (±3 h recovery) | 90 min | ↓ p53 mRNA (w/acute and acute + recovery) | ↑ p-p53 @ ser15 in SS and IMF mito ↓ p53 in nucleus |
↑ PGC-1α, ↑Tfam, ↑NRF-1 ↑COX-IV, ↑CS, ↑COX-I greater with 3 h recovery | n/a | Mitochondrial biogenesis, mtDNA integrity (tfam-p53) | n/a |
| Saleem et al., Am J Physiol Cell Physiol, 2014 [12] | C57BL/6J p53 KO and WT mice n = 6 |
8 | 15 m/min for 90 min (±3 h recovery) | 90 min | n/a | n/a | ↑ PGC-1α, ↑Tfam, ↑NRF-1, ↑COX-IV greater with 3 h recovery | ↑ p-p38 MAPK@ tyr180, ↑p-AMPK @ tyr172, ↑p-CaMKII @ tyr286, ↑LC3-II (mito) | Mitochondrial biogenesis, autophagy | n/a |
| Chronic exercise programs | ||||||||||
| Qi et al., Free Radic Biol Med, 2011 [18] | Goto-Kakizaki rats n = 7 |
10–12 | Progressive: 20 m/min @ 30 min → 1 h | 8 weeks (6 days/week) | ↓ p53 protein | n/a | ↓TIGAR, ↑ mtDNA (ATPase + CytB) | ↓ TIGAR, ↑ COX II, ↑ GSH, ↑ GSH:GSSG | Insulin resistance, glycolysis, mitochondrial biogenesis | Non-obese type II diabetes |
| Safdar et al., Skelet Muscle, 2016 [32] | C57Bl/6J PolG WT and KO, p53 MSKO, and PolG-p53 MSKO mice n = 4–6 |
12 | 15 m/min @ 45 min | 26 weeks (3 days/week) | No change | ↓ Nuclear p53 ↑mito p53 (↑ p53-polG-tfam @ Cox II + cytob) |
↑ mtDNA copy number | ↑ SOD2, ↑ catalase, ↑ Tfam, ↑ ERRα | Antioxidant, mitochondrial biogenesis | n/a |
| Park et al., Circ Res, 2009 [26] | C57BL/6J p53 KO and WT and HT mice n = 5 |
8–12 | Progressive: 10 m/min @ 40 min → 14 m/min @ 90 min) | 5 weeks (5 days/week) | n/a | n/a | ↑ Tfam, ↑ mtDNA copy number | ↑ SDH | Mitochondrial biogenesis, glycolytic vs. oxidative respiration | n/a |
| Saleem et al., Physiol Genomics, 2009 [11] | C57BI/6J p53 KO and WT mice n = 7–8 |
9–12 | Voluntary wheel running program; acute in situ stimulation (1 and 3 TPS) | 6–8 weeks | ↑ p-p53 @ ser15 (acute) | n/a | n/a | ↑ COX (chronic), ↑ p-AMPK @ tyr172 + ↑ p-p38 @ tyr180 (acute) | Mitochondrial biogenesis | n/a |
| Siu, Always, J Appl Physiol, 2005 [33] | (Japanese Coturnix quails n = 8 |
8 and 208 | Stretch-overload model (12% body weight over the left humeral-ulnar joint for joint extension) | 7 and 21 days | n/a | ↑ Nuclear p53 | n/a | ↑ Id2 (nuclear) (7 days in PAT; 7 and 21 days in ALD) | Hypertrophy | n/a |
Notes: Literature (seven studies) was grouped by acute (two studies) or chronic (five studies) exercise. Arrows indicate whether markers regulated by this form of stress increased (↑) or decreased (↓) in expression and/or activation. If a WT vs. KO model is employed, only the results from the WT group are indicated. A caveat to this is the study published by Safdar et al., Skelet Muscle, 2016 which examines exercise in Polg1 MSKO models only. Various time measurements are indicated for the length of imposed stress. WT: wildtype; KO: knockout; HT: heterozygous; MSKO: muscle-specific KO; mito: mitochondria; SS: subsarcolemmal; IMF: intermyofibrillar; PAT: patagialis; ADL: anterior latissimus dorsi.