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Longer Bouts of Intermittent Hypoxia Coupled with Increased Levels of Sustained Hypercapnia Lead to Increases in the Magnitude of Ventilatory Long‐Term Facilitation in African Americans Compared to Caucasians
Author(s) -
Kissane Dylan,
Panza Gino,
Puri Shipra,
Lin HoSheng,
Mateika Jason
Publication year - 2022
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2022.36.s1.r5189
Subject(s) - hypercapnia , medicine , hypoxic ventilatory response , hypoxia (environmental) , anesthesia , ventilation (architecture) , respiratory minute volume , facilitation , cardiology , respiratory system , chemistry , biology , oxygen , acidosis , mechanical engineering , organic chemistry , neuroscience , engineering
Ventilatory long term facilitation (vLTF) is a form of neural plasticity that results in a sustained increase in minute ventilation following exposure to MIH. A number of studies have shown that mild intermittent hypoxia (MIH) when accompanied by slight hypercapnia elicits vLTF in humans. However, the impact of race on the magnitude of vLTF remains unknown. Therefore, we examined the impact of race on the magnitude of vLTF. Methods Data was collected from 47 participants that identified as either African American or Caucasian. These individuals completed one of two MIH protocols. Both protocols began with a ten‐minute normoxic baseline followed by a ten‐minute period characterized by sustained hypercapnia. One protocol (P1) was characterized by 12 two‐minute bouts of hypoxia interspersed with 2 minutes of normoxia. During P1, the partial pressure of end‐tidal carbon dioxide (P ET CO 2 ) was maintained 2 mmHg above baseline. The other protocol (P2) was characterized by 12 four‐minute bouts of hypoxia interspersed with 4 minutes of normoxia. During P2, P ET CO 2 was maintained 4 mmHg above baseline. Exposure to intermittent hypoxia was followed by a 30‐minute recovery period in both protocols. The magnitude of vLTF was calculated by dividing minute ventilation during recovery by baseline values (i.e. 10 minute period of sustained hypercapnia). Results Resting minute ventilation was similar between groups (11.6 ± 2.6 vs 11.4 ± 2.1 L/min, P ≥ 0.9). By design, P ET CO 2 was significantly higher in P2 compared to P1 during the baseline period characterized by sustained hypercapnia (41.2 ± 2.9 vs 42.2 ± 1.6 mmHg, P ≤ 0.05). The chemoreflex sensitivity to CO 2 was similar between groups (1.6 ± 2.3 vs 1.5 ± 1.5, P ≥ 0.9). In both protocols, minute ventilation during recovery was significantly higher than baseline (P1: 17.8 ± 3.9 vs. 11.6 ± 2.6, P2: 20.7 ± 4.2 vs. 11.4 ± 2.1, P ≤ 0.01). Moreover, minute ventilation was significantly greater during recovery in P2 compared to P1 (P ≤ 0.01). When standardized to baseline, vLTF was significantly greater in P2 compared to P1 (1.3 ± 0.2 vs 1.2 ± 0.2, P ≤ 0.01). No difference in the magnitude of vLTF was evident in the Caucasian group compared to the African American group when both absolute (17.3 ± 3.7 vs 18.5 ± 4.3, P ≥ 0.3) and standardized measures (1.2 ± 0.1 vs 1.3 ± 0.2, P ≥ 0.8) of minute ventilation were compared following P1. However, the magnitude of LTF (i.e. standardized to baseline) was reduced in the Caucasian group compared to the African American group following the completion of P2 (1.3 ± 0.2 vs. 1.4 ± 0.1, P ≤ 0.04). Conclusions vLTF was evident following the completion of both protocols. However, the magnitude of vLTF was greater after P2. Likewise, the magnitude of vLTF was greater in African Americans compared to Caucasians following P2. Our data indicate that the magnitude of LTF may be impacted by race, particularly if longer bouts of intermittent hypoxia coupled to a higher sustained level of carbon dioxide is employed.