Speckle-tracking echocardiography was performed in 21 healthy volunteers in normoxia and after 30 min of hypoxic breathing (fraction of inspired oxygen, 0.12). Measurements were also obtained after the administration of atropine in normoxia (n?= 21) and after bisoprolol intake in normoxia (n?= 6) and in hypoxia (n?= 10).
Hypoxia increased heart rate (from 68 ¡À 11 to 74 ¡À 9 beats/min, P?= .001), without changing mean blood pressure (P?= NS), and decreased total peripheral resistance (P?= .003). Myocardial deformation magnitude increased (circumferential strain, ?19.6 ¡À 1.9 % vs ?21.2 ¡À 2.5 % ; radial strain, 19.2 ¡À 3.7 % vs 22.6 ¡À 4.1 % , P < .05; longitudinal and circumferential strain rate, ?0.88 ¡À 0.11 vs ?0.99 ¡À 0.15 sec?1 and ?1.03 ¡À 0.16 vs ?1.18 ¡À 0.18 sec?1, respectively, P < .05 for both; peak twist, 8.98 ¡À 3.2¡ã vs 11.1 ¡À 2.9¡ã, P < .05). Except for peak twist, these deformation parameters were correlated with total peripheral resistance (P < .05). Atropine increased only longitudinal strain rate magnitude (?0.88 ¡À 0.11 vs ?0.97 ¡À 0.14 sec?1, P < .05). The increased magnitude of myocardial deformation persisted in hypoxia under bisoprolol (P < .05). In normoxia, bisoprolol decreased heart rate (73 ¡À 10 vs 54 ¡À 7 beats/min, P?= .0005), mean blood pressure (88 ¡À 7 vs 81 ¡À 4 mm Hg, P?= .0027), without altering deformation.
Hypoxic breathing increases left ventricular deformation magnitude in normal subjects, and this effect may not be attributed to hypoxia-induced tachycardia or ¦Â1-adrenergic pathway changes but to hypoxia-induced systemic vasodilation.