Ischaemia-modified albumin during experimental apnoea

Abstract

Ischaemia-modified albumin (IMA) is a marker of the release of reactive oxygen species (ROS) during hypoxaemia. In elite divers, breath-hold induces ROS production. Our aim was to evaluate the kinetics of IMA serum levels during apnea. Twenty breath-hold divers were instructed to perform a submaximal static breath-hold. Twenty non-diver subjects served as controls. Blood samples were collected at rest, every minute, at the end of breath-hold, and 10 min after recovery. The IMA level increased after 1 min of breath-hold (p < 0.003) and remained high until recovery. Divers were separated into 2 groups: subjects who held their breath for less than 4 min (G-4) and those who held it for more than 4 min (G+4). After 3 min of apnoea, the increase of IMA was higher in the G-4 group than in the G+4 group (p < 0.008). However, at the end of apnoea, the IMA level did not differ between groups. If IMA level was globally correlated with the apnoea duration, it is interesting to note that the higher IMA level was not found in the best divers. Similarly, if arterial blood oxygen saturation (SpO2) was globally inversely correlated with apnoea duration, the lowest SpO2 at the end of breath-hold was not found in the divers that performed the best apnoea. We concluded that these divers save their oxygen. The IMA level provides a useful measure of resistance to hypoxaemia.

Cardiac hypoxic resistance and decreasing lactate during maximum apnea in elite breath hold divers

“…The question is, why the otherwise highly adapted BHD, possessing extreme tolerance for hypoxia [1][2][3][4][5]7 including a mitochondrial adaption to hypoxia in their skeletal muscles similar to the northern elephant seal 7 , should display or suffer from cardiac injury after only 4 min of apnea 9,10 ? However, high altitude permanent residents, chronically exposed to hypoxia, suffer more often from acute coronary syndromes than comparable low altitude populations, probably due to hyperlipidemia 32 and hence arteriosclerotic coronary disease, and it may be, that the BHD studied by Kyhl et al and by Eichhorn et al, were not as cardiac healthy as the subjects with normal lipids 33 and low resting MBF 34 in our study (Tables 1 and 4) or as well adapted as discussed below 12 . Diving seals are exposed to repetitive cycles of ischemia and following reperfusion.…”

“…Similarly sleeping seals experience sleep apnea, but do not increase production of ROS nor suffer systemic or local oxidative damage 15 in contrast to terrestrial animals with sleep apnea. Joulia et al demonstrated in BHD that ischemia-modified albumin (IMA), a marker of the release of ROS during hypoxemia, increases less in the BHD who endured apnea for more than 4 min, than compared to those who endure less than 4 min of apnea 12 . Our study included only BHD who endured apnea for more than 5 min, and our results indicated that they have a similar resistance to cardiac hypoxia as observed in adult diving mammals 8 .…”

Physiological stress markers during breath‐hold diving and SCUBA diving

“…This protocol has been previously used on elite apnea divers (Joulia et al. , ). Briefly, subjects rested supine and breathed normally in ambient room conditions (25± 2°C) for 10 min.…”

Physiology, pathophysiology and (mal)adaptations to chronic apnoeic training: a state-of-the-art review

“…Moreover, a cross-sectional study that investigated the arterial stiffness of 115 female lifelong Ama BHDs (i.e., 38 ± 8 years practicing apnoea) with age-matched physically active adults demonstrating similar arterial stiffness, cardio-ankle vascular index and β-stiffness index (Tanaka et al 2016). Therefore, in totality, despite some findings that indicate acute cardiac disturbances (Joulia et al 2015;Marlinge et al 2019), the current evidence suggests that long-term participation in apnoea-related activities does not affect cardiac health nor vascular integrity (Fig. 2).…”