title: Effects of normoxic and hypoxic exercise regimens on cardiac, muscular, and cerebral hemodynamics suppressed by severe hypoxia in humans.
abstract: 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% O(2)) resting control, 2) hypoxic (15% O(2)) resting control, 3) normoxic exercise (50% maximum work rate under 21% O(2); N-E group), 4) hypoxic-relative exercise (50% maximal heart rate reserve under 15% O(2); H-RE group), or 5) hypoxic-absolute exercise (50% maximum work rate under 15% O(2); 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 (Delta total Hb/min) and reoxygenation rate by acute 12% O(2) exposure. Simultaneously, the two hypoxic interventions enhanced perfusion (Delta total Hb) and O(2) extraction [Delta deoxyHb] of the VL muscle during the 12% O(2) exercise. Although acute 12% O(2) exercise decreased oxygenation (Delta O(2)Hb) 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 O(2) delivery/utilization in skeletal muscles but not cerebral tissues.
authors.affiliation: Graduate Institute of Rehabilitation Science, Chang Gung University, 259 Wen-Hwa 1st Rd., Kwei-Shan, Tao-Yuan 333, Taiwan. s5492@mail.cgu.edu.tw
authors.forename: Jong-Shyan
authors.initials: JS
authors.lastname: Wang
authors.forename: Min-Huan
authors.initials: MH
authors.lastname: Wu
authors.forename: Tso-Yen
authors.initials: TY
authors.lastname: Mao
authors.forename: Tieh-cheng
authors.initials: TC
authors.lastname: Fu
authors.forename: Chih-Chin
authors.initials: CC
authors.lastname: Hsu
mesh_terms: D000328:Adult; D054022:Cerebrum / Q000098:blood supply* / Q000502:physiology*; D015444:Exercise / Q000502:physiology*; D006321:Heart / Q000502:physiology*; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D000860:Hypoxia; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000502:physiology*; D010100:Oxygen / Q000097:blood; D012123:Pulmonary Ventilation / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology; D055815:Young Adult
chemical_list: D010100:Oxygen