Abstract
Pathological erythrocyte aggregation reduces capillary perfusion and oxygen transfer to tissue, which is determined by the negative surface charge on the erythrocyte membrane (intrinsic aggregability) and fibrinogen–erythrocyte interaction (extrinsic factor). Exercise-induced oxidative stress is important for rheological adaptation to training but may also cause erythrocyte senescence. This study clarifies the effects of hypoxic exercise training on intrinsic/extrinsic factors of aggregation. In total, 60 healthy sedentary males were randomly assigned to either hypoxic (HE; FIO2 = 0.15) or normoxic exercise training (NE; FIO2 = 0.21) groups for 30 min·d−1, 5 d·wk−1 for 6 weeks at 60 % of the maximum work rate or to a control group (CTL). A hypoxia exercise test (HET, FIO2 = 0.12) was performed before and after the intervention. Erythrocyte aggregation was assessed by ektacytometry, and fibrinogen binding affinity and senescence biomarkers were assessed by flow cytometry. An acute 12% oxygen HET significantly enhanced erythrocyte global aggregation through intrinsic aggregability. Resting aggregation is promoted by both intrinsic aggregability and fibrinogen binding probability and force after HE, whereas NE is mainly associated with ameliorated fibrinogen–erythrocyte interactions. The HET still facilitated global aggregation after HE because of the augmented fibrinogen-related factors, even though the intrinsic factor was suppressed. Additionally, HE further increased reticulocyte counts while reducing the expression of CD47 and CD147. Resting aggregability is promoted by both intrinsic and extrinsic factors after HE, whereas NE is mainly associated with an ameliorated affinity for fibrinogen. Although an accelerated turnover rate was observed, HE further led to erythrocyte senescence.
Highlights
Erythrocyte aggregation is a critical hemorheological property that contributes to dynamically regulating blood flow and influencing oxygen delivery
Erythrocyte aggregation occurs at low shear rates and depends on both cellular and plasma fibrinogen-related erythrocyte adhesion factors [4], as well as the disaggregating shear force generated by blood flow [3]
Following six weeks of interventions, both normoxic exercise training (NE) and hypoxic exercise training (HE) significantly increased the work rate, VE, and VO2 at the ventilatory threshold and peak exercise performance; HE was superior to NE in improving the peak performance (Table 1, p < 0.05)
Summary
Erythrocyte aggregation is a critical hemorheological property that contributes to dynamically regulating blood flow and influencing oxygen delivery. A great amount of evidence indicates that the aggregation tendency can be modified by several properties, such as erythrocyte aging in vivo [5], reactive oxygen species (ROS) [6], inflammatory status [7], or the blood hematocrit [8]. Endurance exercise is an efficient and safe strategy to improve cardiopulmonary capacity. A number of studies have well established the effects of endurance training on hemorheological properties [9]. In patients with marked obesity or insulin resistance who receive therapeutic exercise training, plasma viscosity and hemorheology are mostly improved and reflect a change in plasma fibrinogen [10]. Altitude/hypoxic training appears to be more effective than sea-level/normoxic training for improving cardiopulmonary capacity [11]. Inappropriate hypoxia, such as severe sleep apnea, impairs rheological properties as well [12]
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