The neurogenic potential of the brain decreases during ageing, whereas the risk of neurodegenerative diseases and stroke rises. This creates a mismatch between the rate of neuron loss and the brain's capacity for replacement. Adult neurogenesis primarily occurs in the subgranular zone (SGZ) and the ventricular‐subventricular zone (V‐SVZ). Exercise enhances SGZ neurogenesis, and we previously showed that V‐SVZ neurogenesis is induced by exercise via activation of the lactate receptor HCA1. Here, we investigated how high‐intensity interval training (HIIT) and medium‐intensity interval training (MIIT) affect neurogenesis in these niches. Wild‐type (WT) and HCA1 knockout (KO) mice were randomized to sedentary, HIIT or MIIT (n = 5–8 per group) for 3 weeks. In the SGZ, HIIT increased the density of doublecortin (DCX)‐positive cells in WT mice by 85% (5.77±1.76 vs. 3.12±1.54 cells/100 µm, P = 0.013) and KO mice (67% increase; 7.91±2.92 vs. 4.73±1.63 cells/100 µm, P = 0.004). MIIT did not alter the density of DCX‐positive cells in either genotype. HIIT increased the density of Ki‐67‐positive cells only in KO mice (P = 0.038), whereas no differences in nestin‐positive cells were observed. In the V‐SVZ, HIIT increased the density of DCX‐positive cells in WT mice by 155% (117.79±39.72 vs. 46.25±19.96 cells/100 µm, P < 0.001) and MIIT increased the density of DCX‐positive cells by 80% (83.26±39.48 vs. 46.25±19.96 cells/100µm, P = 0.027). No exercise‐induced changes were observed in KO mice. Similar patterns were noted for Ki‐67 positive and DCX/Ki‐67 double‐positive cells in the V‐SVZ. These findings suggest that HIIT enhances neurogenesis more robustly than MIIT in both niches, with HCA1 playing a crucial role in V‐SVZ neurogenesis.
High‐intensity interval exercise is more efficient than medium intensity exercise at inducing neurogenesis
Marvin Lambertus,S. Geiseler,Cecilie Morland
Published 2024 in Journal of Physiology
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- Publication year
2024
- Venue
Journal of Physiology
- Publication date
2024-11-23
- Fields of study
Medicine
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- Source metadata
Semantic Scholar, PubMed
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