EFFECTS OF ACUTE NORMOBARIC HYPOXIA DURING EXERCISE AND CONCURRENT MENTAL STRESS ON THE CARDIOVASCULAR SYSTEM IN HEALTHY ATHLETES

BACKGROUND: Exercise and hypoxia are individually recognized as physiological stressors that challenge cardiovascular homeostasis through mechanisms orchestrated by medullary cardiovascular control centers. During physical exertion, the activation of the “exercise pressor reflex” facilitates systemic adjustments to preserve perfusion of vital organs such as the heart and brain while maintaining systemic blood pressure. The intersection of acute hypoxia (AH) and physical exercise imposes considerable cardiovascular strain. Moreover, cognitive load—another potent physiological stressor—has been shown to stimulate cardiovascular activity, potentially via overlapping central pathways with the exercise pressor reflex. Activities combining AH, EXE, and MT, such as military aviation or high-altitude sports, present complex stress environments. Despite this, there is limited evidence on how simultaneous exposure to these stressors impacts systemic hemodynamics, cerebral oxygenation, and autonomic regulation, especially in healthy trained individuals. AIM: This research aims to evaluate the integrative cardiovascular responses to exercise under normobaric hypoxia with concurrent cognitive engagement in healthy athletes. Specifically, the study assesses key hemodynamic parameters including stroke volume (SV), cardiac output (CO), mean arterial pressure (MBP), and systemic vascular resistance (SVR), alongside cerebral oxygenation and cognitive performance outcomes. METHODS: Two experimental protocols were developed. In Experiment 1, fifteen healthy, physically active males (mean age 29.0 ± 5.9 years) performed submaximal cycling (80% of GET) under NORMO and HYPO (13.5% O₂) conditions. A cognitive task was administered during the final three minutes of each six-minute session. Experiment 2 involved sixteen athletes (eight female; mean age: men 29.63 ± 6.41; women 27.25 ± 4.33), who underwent cardiopulmonary exercise testing (CPT) in both NORMO and HYPO (simulated altitude: ~3500 m) to determine VO₂ peak and Wmax. They subsequently completed 23-minute steady-state cycling sessions (at 40% of CPT-derived max workload) during which cognitive tasks were interspersed. In both studies, cardiovascular and oxygenation metrics were recorded via impedance cardiometry and near-infrared spectroscopy (NIRS), respectively. Two-way repeated measures ANOVA was used for statistical analysis (significance set at p < 0.05). RESULTS: In Experiment 1, MT execution during exercise induced significant increases in HR and VFR under both NORMO and HYPO conditions. Cerebral oxygenation (COX) decreased significantly during hypoxia and reaction time was prolonged, although accuracy remained unchanged. In Experiment 2, peak workload (Wmax) and VO₂ peak were significantly lower in HYPO than NORMO. However, no significant differences in SV, CO, SVR, or other cardiovascular variables were observed across EXE phases or conditions, aside from expected SpO₂ reductions during HYPO. No interaction effects were detected between variables. DISCUSSION: These findings indicate that cardiovascular responses to EXE under hypoxic conditions are primarily governed by relative rather than absolute workload. Although AH increases physiological strain at constant mechanical loads (as in Exp 1), adjusting effort relative to individual capacity (as in Exp 2) appears to mitigate hemodynamic alterations. This suggests the presence of effective compensatory mechanisms, potentially involving heightened chemoreceptor and metaboreceptor activity in AH. The results carry significant implications for both athletic training and clinical rehabilitation. Hypoxic exercise may offer a viable strategy to elicit cardiovascular benefits at reduced workloads, enhancing exercise tolerance in populations with cardiopulmonary limitations. Further research is warranted to elucidate underlying regulatory mechanisms and explore translational applications in therapeutic settings.