The Impact of 5-Aminolevulinic Acid Supplementation on Redox Balance and Aerobic Capacity.
Norio SagaAiling HuTakuji YamaguchiYuna NaraokaHiroyuki KobayashiPublished in: International journal of molecular sciences (2024)
We examined the impact of 5-aminolevulinic acid (5-ALA) and sodium-ferrous-citrate supplementation on aerobic capacity and redox balance through a placebo-controlled, double-blind trial. Fourteen healthy volunteers were randomly assigned to Pla + ALA (4-week placebo followed by 4-week 5-ALA supplementation) or ALA + Pla (4-week 5-ALA supplement followed by a 4-week placebo) group and administered 5-ALA (25 mg/day) or placebo once daily. The participants underwent submaximal incremental cycling tests at weeks 0, 2, 4, 6, and 8. In the cycling test at week 0, individual load-intensity stages required for blood lactate levels >2 mmol/L (lactate threshold, LT) and 4 mmol/L (onset of blood lactate accumulation, OBLA) were determined. The heart rate (HR), blood lactate (La), and oxidative stress markers (diacron reactive oxygen metabolite, d-ROMs; biological antioxidant potential, BAP) were measured at resting, LT, and OBLA states in each cycling test. Marker values were not significantly different between the groups. HR, La, and d-ROMs at resting, LT, and OBLA states were not significantly different among the conditions. BAP and BAP/d-ROMs ratios were significantly different in the OBLA state at week 4 of the 5-ALA group compared with that of the placebo group ( p < 0.05). In conclusion, 5-ALA supplementation might improve redox balance during high-intensity aerobic exercise.
Keyphrases
- placebo controlled
- high intensity
- double blind
- heart rate
- phase iii
- phase ii
- study protocol
- clinical trial
- heart rate variability
- oxidative stress
- resistance training
- phase ii study
- blood pressure
- randomized controlled trial
- physical activity
- dna damage
- radiation therapy
- signaling pathway
- endoplasmic reticulum stress
- anti inflammatory
- ischemia reperfusion injury
- open label
- induced apoptosis