Exercise intensities modulate ACE2/MasR/eNOS pathway in male Wistar rat's lung.
Yani Medina LestariVita Murniati TarawanAchadiyani AchadiyaniPutri Teesa Radhiyanti SantosoHamidie Ronald Daniel RayRonny LesmanaHanna GoenawanPublished in: Physiological reports (2023)
Specific exercise intensities could improve lung vascular function by increasing nitric oxide (NO). The ACE2/MasR/eNOS axis is one of the pathways facilitating NO synthesis. This study examines the effect of different intensities of aerobic training on the ACE2/MasR/eNOS axis and histology of lung muscular arteries. Male Wistar rats were used in this study and randomized into control and exercise groups receiving low-, moderate-, and high-intensity training. The training was conducted for 30 min daily, five times a week, for 8 weeks. We observed that different exercise intensities affect the ACE2/MasR/eNOS pathway differently. Compared to control, high-intensity aerobic exercise significantly increased ACE2, Mas receptor (MasR), and eNOS mRNA expressions (p < 0.01). Moderate-intensity exercise significantly increased MasR and eNOS mRNA expressions compared to the control (p < 0.05), and this intensity also increased ACE2 mRNA but not significantly. Low-intensity exercise increased ACE2, MasR, and eNOS mRNA expressions but not significantly. Low-, moderate-, or high-intensity exercises reduced the medial wall thickness of the lung muscular arteries but not significantly. In conclusion, high-intensity exercise may induce NO synthesis in the lung by increasing mRNA expression of ACE2, MasR, and eNOS without decreasing the medial wall thickness of the muscular artery. Thus, high-intensity exercise may be the optimal intensity to improve NO synthesis and vascular function in the lung.
Keyphrases
- high intensity
- resistance training
- nitric oxide synthase
- angiotensin converting enzyme
- pi k akt
- nitric oxide
- angiotensin ii
- endothelial cells
- randomized controlled trial
- signaling pathway
- physical activity
- optical coherence tomography
- cell proliferation
- oxidative stress
- open label
- double blind
- body composition
- placebo controlled
- phase iii
- preterm birth
- gestational age