title: During hypoxic exercise some vasoconstriction is needed to match O2 delivery with O2 demand at the microcirculatory level.
abstract: To test the hypothesis that the increased sympathetic tonus elicited by chronic hypoxia is needed to match O(2) delivery with O(2) demand at the microvascular level eight male subjects were investigated at 4559 m altitude during maximal exercise with and without infusion of ATP (80 mug (kg body mass)(-1) min(-1)) into the right femoral artery. Compared to sea level peak leg vascular conductance was reduced by 39% at altitude. However, the infusion of ATP at altitude did not alter femoral vein blood flow (7.6 +/- 1.0 versus 7.9 +/- 1.0 l min(-1)) and femoral arterial oxygen delivery (1.2 +/- 0.2 versus 1.3 +/- 0.2 l min(-1); control and ATP, respectively). Despite the fact that with ATP mean arterial blood pressure decreased (106.9 +/- 14.2 versus 83.3 +/- 16.0 mmHg, P < 0.05), peak cardiac output remained unchanged. Arterial oxygen extraction fraction was reduced from 85.9 +/- 5.3 to 72.0 +/- 10.2% (P < 0.05), and the corresponding venous O(2) content was increased from 25.5 +/- 10.0 to 46.3 +/- 18.5 ml l(-1) (control and ATP, respectively, P < 0.05). With ATP, leg arterial-venous O(2) difference was decreased (P < 0.05) from 139.3 +/- 9.0 to 116.9 +/- 8.4(-1) and leg .VO(2max) was 20% lower compared to the control trial (1.1 +/- 0.2 versus 0.9 +/- 0.1 l min(-1)) (P = 0.069). In summary, at altitude, some degree of vasoconstriction is needed to match O(2) delivery with O(2) demand. Peak cardiac output at altitude is not limited by excessive mean arterial pressure. Exercising leg .VO(2peak) is not limited by restricted vasodilatation in the altitude-acclimatized human.
authors.affiliation: Copenhagen Muscle Research Center, Rigshospitalet, Blegdamsvej 9, 2100 Copenhagen Ø, Denmark. lundby@idraet.au.dk
authors.forename: Carsten
authors.initials: C
authors.lastname: Lundby
authors.forename: Robert
authors.initials: R
authors.lastname: Boushel
authors.forename: Paul
authors.initials: P
authors.lastname: Robach
authors.forename: Kirsten
authors.initials: K
authors.lastname: Møller
authors.forename: Bengt
authors.initials: B
authors.lastname: Saltin
authors.forename: José A L
authors.initials: JA
authors.lastname: Calbet
mesh_terms: D000255:Adenosine Triphosphate / Q000494:pharmacology; D000328:Adult; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002302:Cardiac Output / Q000187:drug effects / Q000502:physiology; D002320:Cardiovascular Physiological Phenomena / Q000187:drug effects; D015444:Exercise / Q000502:physiology*; D005263:Femoral Artery / Q000502:physiology; D006801:Humans; D000860:Hypoxia / Q000378:metabolism* / Q000503:physiopathology*; D008297:Male; D008833:Microcirculation / Q000502:physiology; D010100:Oxygen / Q000378:metabolism*; D010101:Oxygen Consumption / Q000187:drug effects / Q000502:physiology; D011659:Pulmonary Gas Exchange / Q000187:drug effects / Q000502:physiology; D012123:Pulmonary Ventilation / Q000187:drug effects / Q000502:physiology; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014665:Vasodilator Agents; D000255:Adenosine Triphosphate; D010100:Oxygen