Cardiac Hypoxic Resistance And Decreasing Lactate During Maximum Apnea In Elite Breath Hold Divers
Authors: Thomas Kjeld, Jakob Møller, Kristian Fogh, Egon Godthaab Hansen, Henrik Christian Arendrup, Anders Brenøe Isbrand, Bo Zerahn, Jens Højberg, Ellen Ostenfeld, Henrik Thomsen, Lars Christian Gormsen & Marcus Carlsson
DOI / Source: https://doi.org/10.1038/s41598-021-81797-1
Date: 28 January 2021
Reading level: Advanced
Why This Matters for Freedivers
This paper suggests that elite divers can tolerate very low oxygen during long apneas without obvious “heart ischemia” signals, likely helped by a strong diving response and increased blood flow to the heart. But it also underlines how extreme maximum apneas really are (SpO₂ ~52% is no joke): these are elite-only conditions, and the safety lesson is to respect recovery, avoid pushing max efforts casually, and remember that “adaptation” has limits—even if the heart is surprisingly resilient in this group.
Synopsis
If you hold your breath long enough, your whole body becomes a controlled emergency — but the big question is: what happens to the heart when oxygen gets extremely low? This study looked at elite breath-hold divers who can do 5–6 minute apneas and asked something very specific: do their hearts show signs of oxygen starvation (ischemia) during a maximum breath-hold, or do they have special protection like diving mammals? 
The researchers used an impressive “multi-tool” setup. In different parts of the study they measured: (1) myocardial blood flow using PET/CT (in 6 divers), (2) heart structure/function and oxygenation signals using cardiac MRI including BOLD (in 8 divers), and (3) arterial blood gases during a maximum pool apnea. The divers did a warm-up of several apneas first to trigger the diving response, then performed maximal efforts. 
Here’s the striking result: even though the divers reached extreme whole-body hypoxia (at the end of a max pool apnea, arterial oxygen saturation dropped to about 52%, and arterial oxygen pressure fell to roughly 4.3 kPa), the heart did not show clear signs of ischemia on MRI oxygenation measures, and PET/CT actually showed increased blood flow to the heart during apnea (especially in the 4-minute window). At the same time, heart rate fell strongly (classic diving response), blood pressure rose, and—oddly but importantly—blood lactate went down, not up. The authors interpret that as a hint that these elite divers may shift the heart’s fuel use in a way that resembles diving mammals: using different energy pathways and handling lactate differently under hypoxia.
Abstract
Breath-hold divers (BHD) enduring apnea for more than 4 min are characterized by resistance to release of reactive oxygen species, reduced sensitivity to hypoxia, and low mitochondrial oxygen consumption in their skeletal muscles similar to northern elephant seals. The muscles and myocardium of harbor seals also exhibit metabolic adaptations including increased cardiac lactate-dehydrogenase- activity, exceeding their hypoxic limit. We hypothesized that the myocardium of BHD possesses similar adaptive mechanisms. During maximum apnea 15O-H2O-PET/CT (n=6) revealed no myocardial perfusion deficits but increased myocardial blood flow (MBF). Cardiac MRI determined blood oxygen level dependence oxygenation (n=8) after 4 min of apnea was unaltered compared to rest, whereas cine-MRI demonstrated increased left ventricular wall thickness (LVWT). Arterial blood gases were collected after warm-up and maximum apnea in a pool. At the end of the maximum pool apnea (5 min), arterial saturation decreased to 52%, and lactate decreased 20%. Our findings contrast with previous MR studies of BHD, that reported elevated cardiac troponins and decreased myocardial perfusion after 4 min of apnea. In conclusion, we demonstrated for the first time with 15O-H2O-PET/CT and MRI in elite BHD during maximum apnea, that MBF and LVWT increases while lactate decreases, indicating anaerobic/fat-based cardiac-metabolism similar to diving mammals.