06/12/2025
🧠 𝙀𝙭𝙚𝙧𝙘𝙞𝙨𝙚 𝙄𝙣𝙩𝙚𝙣𝙨𝙞𝙩𝙮 𝙈𝙖𝙩𝙩𝙚𝙧𝙨: 𝙁𝙞𝙣𝙙𝙞𝙣𝙜 𝙩𝙝𝙚 𝙊𝙥𝙩𝙞𝙢𝙖𝙡 𝘿𝙤𝙨𝙚 𝙛𝙤𝙧 𝘽𝙧𝙖𝙞𝙣 𝙃𝙚𝙖𝙡𝙩𝙝
▪️ Aerobic exercise is a recognized medical intervention effective in preventing and managing chronic conditions, including dementia, by protecting against age-related brain atrophy and cognitive decline.
▪️ The key molecular link mediating this neuroprotective effect is muscle–brain crosstalk, facilitated by factors released from skeletal muscle during contraction, known as myokines.
💬 𝗠𝘆𝗼𝗸𝗶𝗻𝗲𝘀: 𝗠𝗼𝗹𝗲𝗰𝘂𝗹𝗮𝗿 𝗠𝗲𝘀𝘀𝗲𝗻𝗴𝗲𝗿𝘀
▪️ Neuroprotective myokines—including FNDC5/Irisin, Cathepsin B (CTSB), and Vascular Endothelial Growth Factor (VEGF), along with metabolites in the kynurenine pathway—are upregulated during exercise.
▪️ These factors ultimately enhance the expression of Brain-Derived Neurotrophic Factor (BDNF), a pivotal neurotrophin crucial for neurogenesis, synaptic plasticity, learning, and memory, predominantly expressed in the hippocampus.
⚡𝗧𝗵𝗲 𝗖𝗲𝗻𝘁𝗿𝗮𝗹 𝗤𝘂𝗲𝘀𝘁𝗶𝗼𝗻 𝗼𝗳 𝗜𝗻𝘁𝗲𝗻𝘀𝗶𝘁𝘆
▪️ While the neuroprotective effects of exercise are clear, the most effective “dose” of aerobic exercise to promote beneficial changes in these myokine pathways is currently unknown.
▪️ Most existing evidence stems from moderate-intensity exercise studies, and research on high-intensity exercise (like High-Intensity Interval Training or HIIT) is scarce.
▪️ The review emphasizes that intensity matters, highlighting the need for standardized intensity classifications (e.g., Low, Moderate, High, based on metabolic thresholds) to effectively compare research findings.
🔬 𝗜𝗻𝘁𝗲𝗻𝘀𝗶𝘁𝘆 𝗮𝗻𝗱 𝗞𝗲𝘆 𝗣𝗮𝘁𝗵𝘄𝗮𝘆𝘀: 𝗪𝗵𝗮𝘁 𝘁𝗵𝗲 𝗘𝘃𝗶𝗱𝗲𝗻𝗰𝗲 𝗦𝗵𝗼𝘄𝘀
▪️ FNDC5/Irisin: There is emerging evidence suggesting that high-intensity exercise may have a superior impact on circulating Irisin levels compared to lower intensities.
▪️ Moderate- to high-intensity training has also been shown to be superior (≈ 2-fold) to low-intensity training in increasing FNDC5 protein levels in rodent skeletal muscle.
▪️ CTSB: This protease promotes adult hippocampal neurogenesis (AHN) and neural debris clearance.
▪️ Moderate-intensity exercise increases CTSB in muscle and plasma, but research on high-intensity exercise effects is lacking.
▪️ Kynurenine Metabolites: The balance between neuroprotective Kynurenic Acid (KA) and neurotoxic Quinolinic Acid (QA) is critical.
▪️ High-intensity training is hypothesized to be superior in promoting neuroprotective metabolites (via PGC-1α activation), but current human studies show no difference in key metabolite levels between low- and high-intensity exercise.
▪️ Adult Hippocampal Neurogenesis (AHN): In contrast to myokine upregulation, low- to moderate-intensity training appears to be the strongest stimulus to enhance AHN (cell proliferation and maturation) in rodents, often improving AHN to a greater extent than high-intensity training.
🎯 𝘾𝙤𝙣𝙘𝙡𝙪𝙨𝙞𝙤𝙣 𝙖𝙣𝙙 𝙁𝙪𝙩𝙪𝙧𝙚 𝘿𝙞𝙧𝙚𝙘𝙩𝙞𝙤𝙣
▪️ The current evidence is insufficient to draw definitive conclusions on the optimal intensity for maximizing neuroprotective myokine benefits.
▪️ Future research must utilize well-controlled studies, such as work-matched training interventions, and standardize intensity definitions to accurately determine the optimal exercise dose.
▪️ Understanding how exercise intensity regulates myokines holds significant promise in offering therapeutic avenues to alleviate the burden of neurodegenerative conditions like dementia.
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