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Hypoxia-Induced Adaptations Across Athletic Populations: Insights From Hematology, Muscle Physiology, and Stress Pathways | ||
| New Approaches in Exercise Physiology | ||
| مقاله 8، دوره 7، شماره 14، اسفند 2025 | ||
| نوع مقاله: Research Paper | ||
| شناسه دیجیتال (DOI): 10.22054/nass.2025.90067.1211 | ||
| نویسندگان | ||
| Leila Fasihi* 1؛ Zahra Soukhteh2 | ||
| 1MSc Student of Exercise Physiology Department of Physical Education and sport science, Faculty of Physical Education and sport science, University of Allameh Tabatabai, Tehran, Iran | ||
| 2MSc. student of Exercise Physiology, Department of Physical Education and Sport Sciences, Faculty of Humanities, Tarbiat Modares University, Tehran, Iran. | ||
| چکیده | ||
| Hypoxia is a powerful environmental stimulus that elicits multi-system adaptations in athletes, yet the relative contributions of hematological, muscular, and stress-related mechanisms remain incompletely understood. This narrative review aims to synthesize current evidence on hypoxia-induced adaptations across athletic populations, with a particular focus on hematological changes, skeletal muscle physiology, and oxidative and neuroendocrine stress pathways. Eligible studies examined hematological variables, muscle adaptations, oxidative stress and redox signaling, autonomic and hormonal responses, and/or performance outcomes. Findings indicate that sustained hypoxic exposure can increase erythropoietin production and, when sufficient hypoxic dose and iron availability are present, elevate total hemoglobin mass and red blood cell volume. However, inter-individual variability and iron metabolism tightly modulate these responses. At the muscular level, hypoxia promotes mitochondrial biogenesis, angiogenesis, improved buffering capacity, and enhanced peripheral oxygen extraction, often contributing to performance gains even in so-called “non-responders” with minimal hematological change. Concurrently, hypoxia activates stress pathways—including reactive oxygen species signaling, HIF-1α–mediated transcription, sympathetic activation, and transient inflammation—which act as both challenges and drivers of adaptation, depending on dose and recovery. In conclusion, hypoxic training exerts its ergogenic effects through an integrated network of hematological, muscular, and stress-related mechanisms. Optimizing altitude and hypoxic interventions requires individualized programming that considers hypoxic dose, iron status, training load, and recovery to harness adaptive stress while avoiding maladaptation. | ||
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