Peripheral blood mononuclear cells’ (PBMCs) mitochondrial respiration is impaired and likely involved in myocardial injury and heart failure pathophysiology, but its response to acute and severe hypoxia, often associated with such diseases, is largely unknown in humans. We therefore determined the effects of acute hypoxia on PBMC mitochondrial respiration and ROS production in healthy volunteers exposed to controlled oxygen reduction, achieving an inspired oxygen fraction of 10.5%. We also investigated potential relationships with gene expression of key biomarkers of hypoxia, succinate and inflammation, as hypoxia and inflammation share common mechanisms involved in cardiovascular disease. Unlike global mitochondrial respiration, hypoxemia with a spO₂ ≤ 80% significantly reduced PBMC complex II respiration (from 6.5 ± 1.2 to 3.1 ± 0.5 pmol/s/10⁶ cell, p = 0.04). Complex II activity correlated positively with spO₂ (r = 0.63, p = 0.02) and inversely correlated with the succinate receptor SUCNR1 (r = −0.68), the alpha-subunit of the hypoxia-inducible factor (HIF-1α, r = −0.61), the chemokine ligand-9 (r = −0.68) and interferon-stimulated gene 15 (r = −0.75). In conclusion, severe hypoxia specifically impairs complex II respiration in association with succinate, inflammation and HIF-1α pathway interactions in human PBMCs. These results support further studies investigating whether modulation of complex II activity might modify the inflammatory and metabolic alterations observed in heart failure.

The continuous monitoring of oxygen saturation (SpO₂) and respiratory rates (RRs) are major clinical issues in many cardio-respiratory diseases and have been of tremendous importance during the COVID-19 pandemic. The early detection of hypoxemia was crucial since it precedes significant complications, and SpO₂ follow-up allowed early hospital discharge in patients needing oxygen therapy. Nevertheless, fingertip devices showed some practical limitations. In this study, we investigated the reliability of the new Multisense^® pulse oximetry system compared to a reference pulse oximeter (Vyntus CPX Pulse Oximeter) during hypoxia. In a population of sixteen healthy male subjects (mean age: 31.5 ± 7.0 years, BMI: 24.9 ± 3.6 kg/m², and 35% with darker skin tones), simultaneous SpO₂ and RR measurements were collected over 12.4 h, during which FiO₂ was progressively reduced from 21% to 10.5%. The average root mean square error (ARMS) of SpO₂ for Multisense^® placed on the back and chest was 2.94% and 2.98%, respectively, with permutation testing confirming a significant ARMS below 3.5% for both positions and no statistically significant difference in the ARMS between patch placements. Positive correlations and acceptable accuracy between devices were observed at both locations (r = 0.92, p < 0.001 and r = 0.90, p < 0.001 for back and chest placements, respectively). Bland–Altman analysis further indicated limits of agreement that support consistency across placements, with similar agreement levels noted across skin tones. Similar findings were obtained with the RR measurements. In conclusion, Multisense^® demonstrated robust accuracy in measuring SpO₂ and RRs during hypoxia in humans comparable to standard hospital-grade equipment. The effectiveness of the findings suggests that this wearable device is a valuable tool for the continuous monitoring of SpO₂ and RRs, potentially enhancing patient safety and optimizing hospital resource allocation. Nevertheless, to overcome study limitations and allow generalized use, further work on a larger population sample, including more subjects with a high phototype and desaturation below 80%, would be useful.