Effetti dell’ipobarismo sulla funzionalità mitocondriale e sullo stress ossidativo negli atleti.

Intermittent hypoxic training (IHT) simulates high-altitude hypoxic environments and involves discontinuous exposure to normobaric or hypobaric hypoxia to replicate key aspects of altitude acclimatization and improve athletic performance at sea level. IHT generally includes two strategies: inducing hypoxia at rest to primarily stimulate altitude acclimatization or inducing hypoxia during exercise to primarily increase the training stimulus. Hypoxia conditioning is based on the principle of hormesis: a mild but potentially damaging stressor can increase the resilience of target cells/tissues (1, 2), whereas severe and/or prolonged hypoxia can inflict permanent damage. This "trains" adaptive flexibility in response to stress (3). Cellular and systemic responses to hypoxia include vascular and metabolic remodeling and respiratory and cardiovascular mechanisms to maintain oxygen supply (4). Crucial aspects include the dose of hypoxia (intensity, duration, frequency, mode of administration), the combination of hypoxia with physical activity or drug treatments, the mode and timing of application, and the impact of environmental factors and individual physiological factors (4). IH stimulates the synthesis of serum erythropoietin (sEPO), which allows increased erythrocyte numbers and improved oxygen delivery to working muscles (5) triggering several biochemical and structural changes in skeletal muscle that promote oxidative processes (6, 7). In addition, some authors suggest that IH may improve performance in anaerobic exercise (8, 9), perhaps through increasing the buffering capacity of muscle and increasing the activity of glycolytic enzymes (10). Hypoxia also induces numerous mitochondrial responses and adaptations (11). Mitochondria respond acutely to hypoxia by increasing the efficiency of electron transport to maintain ATP production (4). It is believed that among the main benefits of hypoxic treatment are reduction of inflammation and enhancement of antioxidant capacity, mitochondrial efficiency, and neurological resilience (4). Inflammation is triggered and regulated by innate cells such as monocytes, a heterogeneous population with the capacity to produce pro-inflammatory cytokines. In recent years, a bioenergetic approach has been used to better understand monocyte regulation and activation because under conditions that diverge from normal physiology, including inflammation or hypoxia, monocytes activate transcriptional responses that modulate or change cellular metabolism. Recent studies have shown that monocyte bioenergetics and inflammatory phenotype can change in response to different infections or pathological stimuli such as hypoxia. The purpose of the present study is to evaluate IHT effects on athletes' health and mitochondrial metabolism. Thirty nonprofessional athletes will be selected, a group of 10 athletes will constitute the control group and will not undergo hypobaric treatment, a group of 10 will enter the hypobaric tent during sports activity while a final group of 10 will exercise and subsequently undergo hypobaric treatment at rest. Participants will undergo assessment of vital parameters and blood sampling before and after the first session, at the end of the planned three weeks and one month after the end of the sessions. Vitals will be assessed using a certified device, the ButterfLife ®, which measures the 5 vital parameters determined by WHO (heart rate, max and min blood pressure, respiratory rate, oxygen saturation and temperature). A panel of hematochemical analysis, analysis of pro-inflammatory cytokines, and a marker of neuronal damage (neurofilament light chain - NfL) will be performed at each of these times. Monocyte subpopulations will also be analyzed and their mitochondrial activity characterized (analysis of mitochondrial morphology and metabolism).