Article Title



T. Kelly1, K. DiMarco1, Courtney Brown2, Mohini Bryant-Ekstrand1, Rachel Lord3, Tony Dawkins3, Aimee Drane3, Joel E. Futral1, Otto Barak4, Tanja Dragun5, Michael Stembridge3, Boris Spajić6, Ivan Drviš6, Joseph W. Duke7, Philip N. Ainslie2, Glen E. Foster2, Zeljko Dujic5, & A.T. Lovering1

1University of Oregon, Department of Human Physiology, Eugene OR, USA; 2University of British Columbia, Centre for Heart, Lung, and Vascular Health, School of Health and Exercise Sciences, Kelowna, BC, Canada; 3Cardiff Metropolitan University, School of Sport and Health Sciences, Cardiff, Wales, UK; 4University of Novi Sad, Department of Physiology, Novi Sad, Serbia; 5University of Split School of Medicine, Department of Integrative Physiology, Split, Croatia; 6University of Zagreb, Faculty of Kinesiology, Zagreb, Croatia; 7Northern Arizona University, Department of Biological Sciences, Flagstaff, AZ, USA

PURPOSE: Our lab has previously reported blunted hypoxic pulmonary vasoconstriction in apnea divers (Kelly et al, Exp Physiol 2022). Why this occurs remains speculative but may relate to interactions between inflammatory cytokines and nitric oxide availability. We hypothesized that in apnea divers there would be a positive correlation between levels of inflammatory cytokines and degree of hypoxic pulmonary vasoconstriction. METHODS: 16 (4 women) apnea divers and 16 (4 women) non-diving age and sex-matched controls were recruited from diving camps in and around Split, Croatia and Eugene, Oregon. Serum was collected from each participant, then transthoracic ultrasound measures were made to calculate cardiac output (QT) and pulmonary artery systolic pressure (PASP). Total pulmonary resistance (TPR) was calculated as PASP/QT and converted to dynes/sec/cm-5. After baseline ultrasound measures, participants breathed on a dynamic end-tidal forcing machine targeting an end-tidal O2 ~50mmHg (corresponding to O2 saturation of ~80%) while clamping end-tidal CO2 at baseline value (~40mmHg). Ultrasound measures were repeated after 20 to 30-minutes of hypoxic breathing. ΔTPR was calculated as the change in TPR from baseline to the end of the hypoxic challenge. Serum was analyzed for cytokines using a flow cytometry bead-based multiplex assay. RESULTS: Data were analyzed by Pearson correlation. In apnea divers there were significant correlations between ΔTPR and levels of IL-8 (r = -.8151, r2 = .6644, p = .0481), IFN-a2 (r = -.8344, r2 = .6962, p = .0052), and IL-12p70 (r = -.9209, r2 = .8481, p = .0264). There were no significant correlations in Controls. CONCLUSION: We report strong negative correlations between ΔTPR in response to a 20 to 30-minute hypoxic challenge and several inflammatory cytokines. Our results suggest that apnea divers may have an altered inflammatory cytokine profile which is related to reduced hypoxic pulmonary vasoconstriction.

US Fulbright Scholar’s Program # PS00273429, Burroughs Wellcome Fund # 1018799

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