Effects of normoxic and hypoxic exercise regimens on cardiac, muscular, and cerebral hemodynamics suppressed by severe hypoxia in humans

2010 
Hypoxic preconditioning prevents cerebrovascular/cardiovascular disorders by increasing resistance to acute ischemic stress, but severe hypoxic exposure disturbs vascular hemodynamics. This study compared how various exercise regimens with/without hypoxia affect hemodynamics and oxygenation in cardiac, muscle, and cerebral tissues during severe hypoxic exposure. Sixty sedentary males were randomly divided into five groups. Each group ( n = 12) received one of five interventions: 1 ) normoxic (21% O2) resting control, 2 ) hypoxic (15% O2) resting control, 3 ) normoxic exercise (50% maximum work rate under 21% O2; N-E group), 4 ) hypoxic-relative exercise (50% maximal heart rate reserve under 15% O2; H-RE group), or 5 ) hypoxic-absolute exercise (50% maximum work rate under 15% O2; H-AE group) for 30 min/day, 5 days/wk, for 4 wk. A recently developed noninvasive bioreactance device was used to measure cardiac hemodynamics, and near-infrared spectroscopy was used to assess perfusion and oxygenation in the vastus lateralis (VL)/gastrocnemius (GN) muscles and frontal cerebral lobe (FC). Our results demonstrated that the H-AE group had a larger improvement in aerobic capacity compared with the N-E group. Both H-RE and H-AE ameliorated the suppression of cardiac stroke volume and the GN hyperemic response (Δtotal Hb/min) and reoxygenation rate by acute 12% O2 exposure. Simultaneously, the two hypoxic interventions enhanced perfusion (Δtotal Hb) and O2 extraction [ΔdeoxyHb] of the VL muscle during the 12% O2 exercise. Although acute 12% O2 exercise decreased oxygenation (ΔO2Hb) of the FC, none of the 4-wk interventions influenced the cerebral perfusion and oxygenation during normoxic/hypoxic exercise tests. Therefore, we conclude that moderate hypoxic exercise training improves cardiopulmonary fitness and increases resistance to disturbance of cardiac hemodynamics by severe hypoxia, concurrence with enhancing O2 delivery/utilization in skeletal muscles but not cerebral tissues.
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