Altering cell signalling pathways regulating mitochondrial biogenesis within human skeletal muscle by manipulatingmuscle glycogen content with acute endurance exercise:Examining glycogen threshold hypothesis
Başlık çevirisi mevcut değil.
- Tez No: 796083
- Danışmanlar: Belirtilmemiş.
- Tez Türü: Yüksek Lisans
- Konular: Spor, Sports
- Anahtar Kelimeler: PGC-1α, p53, PPAR, GLYCOGEN, TRAIN-LOW
- Yıl: 2018
- Dil: İngilizce
- Üniversite: Lıverpool John Moores Unıversıty
- Enstitü: Yurtdışı Enstitü
- Ana Bilim Dalı: Belirtilmemiş.
- Bilim Dalı: Belirtilmemiş.
- Sayfa Sayısı: Belirtilmemiş.
Özet
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Özet (Çeviri)
It is currently unknown that there is a `so-called glycogen threshold` to enhance mitochondrial biogenesis in human skeletal muscle. This study aimed to examine effects of carbohydrate (CHO) availability on cellular level adaptations in human skeletal muscle, moreover elucidate the `so-called glycogen threshold` that deemed superior to induce the pathways that have putative roles in regulation of mitochondrial biogenesis with acute exercise. In a randomised, crossover, repeated measures design, 8 physically active males participated in a sleep-low exercise model (14 h between glycogen depletion and main exercise) that comprising a late afternoon glycogen depleting session, then completing morning high-intensity interval training (8x5 min bouts at 85% PPO). Participants exercised HIIT under three different conditions that high CHO availability (HIGH) (7.2 g.kg-1.bm-1 CHO via 1.2 g.kg-1.bm-1 CHO for six hours post-exercise), medium CHO availability (MED) (3.6 g.kg-1.bm-1 CHO via 1.2 g.kg-1.bm-1 CHO for three hours post-exercise), or low CHO availability (LOW) (no food consumed). Pre-exercise muscle glycogen content was correlated (P<0.001) to CHO availability (208 mmol.kg-1 d.w., 332 mmol.kg-1 d.w., and 531 mmol.kg-1 d.w., respectively). Muscle glycogen utilization was correlated (P<0.001) to CHO availability as well, but with no difference (P=0.31) between MED and LOW groups (107 mmol.kg-1 d.w., 159 mmol.kg-1 d.w., and 277 mmol.kg-1 d.w., respectively). PGC-1α and p53 mRNA increased (P≤0.05 for both) at 3 h postexercise; however PPAR did not show any difference (P=0.10) compared to preexercise in all conditions. Despite the fat oxidation rates had correlated (P<0.001) inversely to CHO availability, PGC-1α (P=0.32), p53 (P=0.65), and PPAR (P=0.45) mRNA did not show any difference between conditions at 3 h post-exercise. We conclude that sleep-low exercise protocol does not enhance the mRNA expression of genes associated with regulatory roles in mitochondrial biogenesis, although it does increase fat oxidation rates in acute exercise. We did not manage to elucidate `socalled glycogen threshold` therefore, future studies are warranted to questioning and clarifying glycogen threshold hypothesis.
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