نوع مقاله : مقاله پژوهشی
نویسندگان
گروه فیزیولوژی ورزشی، دانشکده علوم ورزشی، دانشگاه شهید چمران اهواز، اهواز، ایران.
چکیده
کلیدواژهها
موضوعات
عنوان مقاله [English]
نویسندگان [English]
Background and Purpose: The increasing aging population and the process of aging itself are associated with impairments in memory, learning, neuroplasticity, and cognitive function of the central nervous system. Given the potential of high-intensity interval training (HIIT) to alter systemic lactate levels, this study aimed to investigate the effects of HIIT and lactate as a non-pharmacological and therapeutic strategy on the levels of transporters associated with age-related markers such as cognition, memory, learning, and neural plasticity in young adult and aging-induced male rats.
Materials and Methods: In this study, 40 male Wistar rats with an average age of 12 weeks and a weight range of 200–220 grams were purchased and randomly divided into four groups: young adult control, aging induction control, young adult with interval training, and aging induction with interval training. To induce the aging model, for 8 weeks, two groups of rats received intraperitoneal injections of D-galactose daily, while the other two groups received normal saline. After aging induction, the high-intensity interval training protocol was conducted for 8 weeks. Each week included 3 training sessions, with each session consisting of 6 repetitions of 4 minutes of exercise at an intensity equivalent to 85–95% of maximal exercise capacity, followed by 3 minutes of recovery at an intensity equivalent to 40–50% of maximal exercise capacity. Forty-eight hours after the last training session, the hippocampal tissue was extracted from the rats' brains, and the levels of lactate transporters MCT2 and MCT4 were measured using the Western blot method. Data were analyzed using one-way ANOVA followed by Tukey’s post hoc test. Statistical significance was considered at P≤0.05.
Results: In young adult rats, HIIT did not significantly alter MCT2 levels (P ≥ 0.05), whereas in aging-induced rats, MCT2 expression was significantly reduced (P < 0.0001). HIIT in aging-induced rats significantly increased MCT2 levels (P < 0.001). HIIT significantly upregulated MCT4 in young adult rats (P < 0.01). Aging induction significantly decreased MCT4 levels (P < 0.0001), but HIIT reversed this decline in aging-induced rats (P < 0.001).
Conclusion: Aging leads to reduced hippocampal MCT2 and MCT4 levels; however, exercise-particularly HIIT-can mitigate this decline. While the responsiveness of these transporters to exercise differed between young and aging-induced rats, HIIT proved to be an effective method to enhance MCT2 and MCT4 expression in aged animals. This training modality may serve as a non-pharmacological approach to improving cognitive function in the elderly through lactate metabolism regulation and age-related neural adaptations in the hippocampus.
Keywords: Aging, Hippocampus, HIIT, Lactate, MCT2, MCT4
کلیدواژهها [English]
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