Responses and Adaptation to Altitude Exposure and Training

Altitude Exposure O 2 % is same as sea level, but P O 2 is  Hypoxia drives cardiorespiratory system to maintain O 2 delivery Exercise VO 2 remains the same, but % of VO 2max  Acute effects differ from chronic adaptations

Oxygen transport cascade

Responses to acute altitude exposure   O 2 driving force  length of time required to saturate Hb  SaO 2sat   fluid loss   catecholamine release  TPR, BP   VE diminishes  PO 2  PCO 2 & H + leftward shift of HbO 2 curve   La response   Q submax,   VO 2max

Chronic pulmonary adaptations to altitude exposure   pulmonary capillarization   VE  CO 2 release leftward shift of HbO 2   HCO 3 - secretion rightward shift of HbO 2 curve   La response (from acute exposure) La paradox

Chronic CV adaptations to altitude exposure  RBC 2,3-DPG  HbO 2 binding strength rightward shift of HbO 2 curve  PV  SV, Q  EPO ( at >10,000 ft)  Hb, RBC, Hct  mitochondria/enzymes

Catecholamine release changes with chronic altitude exposure

Altitude training adaptations  training volume at altitude  O 2 transport, but  buffering capacities n/c in VO 2max at sea level

Altitude training adaptations  training volume at altitude  O 2 transport, but  buffering capacities n/c in VO 2max at sea level Live (moderately) high, train low theory Responders/non-responders maintained training volume,  EPO release,  VO 2max, running endurance