Document Type : Original Article
Authors
- Beydolah Shahouzehi 1, 2
- Banafsheh Daneshmand 3
- Mahdieh Nazari-Robati 4
- Soheil Aminizadeh 5
- Yaser Masoumi-Ardakani 6
1 Student Research Committee, Kerman University of Medical Science, Kerman, Iran
2 Gastroenterology and Hepatology Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Sciences, Kerman, Iran
3 Department of Physiology (Sport Science), Central Tehran Branch, Islamic Azad University, Tehran, Iran
4 Department of Clinical Biochemistry, Faculty of Medicine, Kerman University of Medical Sciences, Kerman, Iran
5 Department of Physiology and Pharmacology, Afzalipour School of Medicine, and Physiology Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran
6 Physiology Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Sciences, Kerman, Iran
Abstract
Background: Apoptosis is a defensive measure that removes dysfunctional cells. Exercise training has a broad spectrum of benefits that influence apoptosis and cell viability. L-carnitine (LCAR), a supplement nowadays, has shown beneficial effects against cell death. We investigated the simultaneous effect of exercise training (acute exercise [AE] and high-intensity interval training [HIIT]) and LCAR supplementation on the proteins involved in apoptosis. The animals were anesthetized twenty-four hours after the conclusion of the final training session.
Methods: Forty-eight male Wistar rats (210±10 g) were assigned to six groups (n=8) as follows: Control, LCAR (200 mg/kg/d LCAR, IP), AE, HIIT, LCAR+AE, and LCAR+HIIT. The animals were anesthetized and sacrificed twenty-four hours after the last training session; the rats’ blood sample was collected, and the serum was separated. The serum Bcl-2 levels, as an anti-apoptotic factor, and caspase-3 and BAX, as proapoptotic factors, were measured using specific ELISA kits.
Results: AE increased apoptosis, but HIIT’s effects were almost neutral. LCAR administration in groups that performed either AE or HIIT significantly attenuated apoptosis. However, in group 6 (LCAR+HIIT), the anti-apoptotic effects were noteworthy because LCAR+HIIT significantly increased Bcl-2 and reduced caspase-3 levels compared to the control group.
Conclusion: HIIT improved cell viability through increasing Bcl-2 levels, and LCAR strengthened HIIT’s anti-apoptotic properties. AE increased proapoptotic proteins, and LCAR modified the elevated proapoptotic markers in the AE group. Therefore, LCAR may be considered a promising supplement against exercise-mediated injury. This study can be extended to humans to evaluate the beneficial effects of LCAR+HIIT and LCAR+AE.
Keywords
Main Subjects
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