Introduction Improved myocardial contractility is a critical circulatory adaptation to exercise training. However, the types of exercise that enhance left ventricular (LV) contractile and diastolic functions have not yet been established. This study investigated how high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) influence LV mechanics during exercise. Methods Fifty-four healthy sedentary men were randomized to engage in either HIIT (3-min intervals at 40% and 80% of V˙O2max, n = 18) or MICT (sustained 60% of V˙O2max, n = 18) for 30 min·d−1, 5 d·wk−1 for 6 wk or to a control group (n = 18) that did not engage in exercise intervention. LV mechanics during semiupright bicycle exercise tests were measured by two-dimensional speckle-tracking echocardiography. Results Before the interventions, acute bicycle exercise increased (i) peak basal/apical radial and circumferential and peak longitudinal strains and strain rates, (ii) peak basal/apical rotations and torsion, and (iii) peak systolic twisting and early diastolic untwisting velocities in the LV. After the interventions, the HIIT group exhibited greater LV mass and diastolic internal diameter as well as higher ratio of E wave to A wave and early diastolic propagation velocity than did the MICT group. Despite decreased peak apical rotation and torsion, HIIT enhanced peak apical radial strain and strain rate as well as shortened the time to reach peak untwisting velocity in the LV during exercise. However, the LV mechanics during exercise were unchanged in the control group. Conclusion HIIT but not MICT induces eccentric myocardial hypertrophy. Moreover, HIIT effectively improves the LV mechanics during exercise by increasing contractile and diastolic functions.

Introduction Physical exercise or hypoxic exposure influences erythrocyte susceptibility to osmotic stress, and the aquaporin 1 (AQP1) facilitates the transport of water in erythrocytes. This study investigated whether high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) affect erythrocyte osmotic deformability by modulating AQP1 function under hypoxic stress. Methods Forty-five healthy sedentary males were randomized to engage in either HIIT (3-min intervals at 40% and 80% V˙O2 reserve, n = 15) or MICT (sustained 60% V˙O2 reserve, n = 15) on a bicycle ergometer for 30 min·d−1, 5 d·wk−1 for 6 wk, or to a control group that did not perform any exercise (n = 15). All subjects were analyzed with osmotic gradient ektacytometry for assessing erythrocyte membrane stability and osmotic deformability after hypoxic exercise (HE) (100 W under 12%O2 for 30 min). Results Before the intervention, HE increased the shear stress at 50% of maximal elongation (SS1/2) and the ratio of SS1/2 to maximal elongation index (SS1/2/EImax) on erythrocytes pretreated with 50 Pa of shear stress for 30 min and diminished HgCl2-depressed osmolality at 50%EImax (Ohyper). However, both HIIT and MICT for 6 wk diminished the elevations of erythrocyte SS1/2 and SS1/2/EImax caused by HE. Moreover, HIIT also increased contents of erythrocyte AQP1 proteins while enhancing HgCl2-depressed Ohyper and area under elongation index–osmolarity curve after HE. Additionally, changes in erythrocyte AQP1 contents were associated with changes in HgCl2-depressed erythrocyte Ohyper and area under elongation index–osmolarity curve. Conclusions Acute HE reduces erythrocyte membrane stability, whereas either HIIT or MICT attenuates the depression of erythrocyte membrane stability by HE. Moreover, HIIT increases the AQP1 content and facilitates the HgCl2-mediated osmotic deformability of erythrocytes after HE.

The antioxidant capacity of erythrocytes protects individuals against the harmful effects of oxidative stress. Despite improved hemodynamic efficiency, the effect of eccentric cycling training (ECT) on erythrocyte antioxidative capacity remains unclear. This study investigates how ECT affects erythrocyte antioxidative capacity and metabolism in sedentary males. Thirty-six sedentary healthy males were randomly assigned to either concentric cycling training (CCT, n = 12) or ECT (n = 12) at 60% of the maximal workload for 30 min/day, 5 days/week for 6 weeks or to a control group (n = 12) that did not receive an exercise intervention. A graded exercise test (GXT) was performed before and after the intervention. Erythrocyte metabolic characteristics and O2 release capacity were determined by UPLC-MS and high-resolution respirometry, respectively. An acute GXT depleted Glutathione (GSH), accumulated Glutathione disulfide (GSSG), and elevated the GSSG/GSH ratio, whereas both CCT and ECT attenuated the extent of the elevated GSSG/GSH ratio caused by a GXT. Moreover, the two exercise regimens upregulated glycolysis and increased glucose consumption and lactate production, leading to intracellular acidosis and facilitation of O2 release from erythrocytes. Both CCT and ECT enhance antioxidative capacity against severe exercise-evoked circulatory oxidative stress. Moreover, the two exercise regimens activate erythrocyte glycolysis, resulting in lowered intracellular pH and enhanced O2 released from erythrocytes.

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.

Cycling AIT is superior to cycling MCT in enhancing aerobic capacity. Moreover, either cycling AIT or MCT effectively alleviates HE-evoked impairments of erythrocyte rheological characteristics and band 3 function.