L30 Exercise And High Altitude Flashcards
Cardio respiration and exercise
O2 consumption, CO2 production ventilation rate and CO all increase and are well matched
Exercising muscle demands
O2 and steady supply of fuel
Causes disruption homeostasis seen in exercise
Must increase total blood flow
Metabolic vasodilation must occur in muscle
Shunting of blood from gut to working muscle must be achieved
Relationship btw work load and arteriovenous (a-v) O2 difference
At rest a-v diff ~ 5.6 vol %
During exercise may rise to 16 vol%
V gets lower, difference gets bigger
(Vol% = [mlO2/100ml blood] x 100)
Exercise and TPR
Skeletal muscle vasodilation causes a significant drops in TPR
As metabolic rate increases, TPR decreases
Exercise and BP
Diastolic P changes little while systolic and MAP increases
MAP increases w/ decreasing TPR because increased CO (MAP=CO x TPR)
Effects of endurance training on HR?
Maximal HR does not change with training
Trained and untrained reach similar max HR
Resting HR is altered with training
Resting HR lower in trained
Greater vagal tone, reduced SNS tone
CO maintained by increased SV
Maximal HR determined by age
Effects of endurance training on SV
Increases SV via
Increased heart size / ventricular V
Decreased HR , greater filling
Increased contractility from enhanced release of Ca from SR
Effects of endurance training on blood V
Total volume increases with training
Increase in plasma volume
Minor increases in cell volume
Provides cardiovascular stability during exercise
Reduces cardiovascular drift
Fluid volume lost through sweating causes a decrease in venous return which reduces SV ; increases HR ( CV drift to maintain CO)
Sedentary versus trained
Differences occur:
At same workload:
CO remains same
But at lower HR and higher SV in the trained
At same VO2:
Trained outworks the sedentary
Uses energy more efficiently
Maximal VO2:
Trained has a great VO2max and CO
Adaption got high altitude
Barometric pressure decreases exponentially with altitude
PIO2 at top mt Everest only 43mmHg (normal = 150mmHg)
Adaptation to high altitude
Resolute the hypoxia association w high altitude ~15 million people live above 10,000ft and some live about 16k feet (Andes)
Acclimatization to high altitude possible bu combo of respiratory and circulatory changes:
Respiratory: hyperventilation
Circulatory: polycythemia (increase RBCs) and increase conc of 2,3DPG in RBCs
2,3DPG levels
Individuals adapted to high altitude (>3000m) showed increased synthesis of 2,3DPG (AKA 2,3BPG) in RBCs
Causes O2 hemoglobin dissociation curve to shift right (oxygen saturation curve = sigmoid)
Decreases affinity of Hb for O2- enhances transferring of O2 to tissues
Mildly impairs loading in the lungs
Polycythemia
Increase in RBC conc.
Caused by increase erythropoietin release from kidney
Increased RBC increases O2 carrying compactly (O2 conc) of blood at any given PO2
Blood viscosity also increase w polycythemia. Increases the afterload experiences by the heart
Other features of high altitude exposure
Increased capillary density in peripheral tissues
Pulmonary hypertension:
Occurs globally in lung and related to increased pulmonary vascular resistance
Can cause right heart hypertrophy if high altitude exposure is chronic
Due to hypoxia vasoconstriction of pulmonary vasculature
Pulmonary vascular resistance:
Hypoxia vasoconstriction
If alveolar PO2 decreases:
Pulmonary vascular smooth muscle
Contracts
Blood is directed away from poorly ventilated alveolar units towards better ventilated unit
Called hypoxic vasoconstriction; mech not clear
Local (not central) control of vascular resistance
Opposite response of systemic circulation to hypoxia