Hey jk...
For example, you can check any basic physiology text which shows that with altitude training there is DECREASED affinity of hemoglobin for oxygen. The hemoglobin is already almost fully saturated with oxygen in areas of high partial pressure of oxygen, such as the lungs... and has low affinity and saturation at the muscle tissue level, where the partial pressure of oxygen is low. This is so that the hemoglobin picks up the oxygen at the lungs and unloads the oxygen needed by the muscles at the tissue level.
This is seen in the physiology textbooks as the oxygen-hemoglobin disassociation/affinity curve. With altitude training, there is an increase of 2,3 DPG(diphosphoglycerate) in erythrocytes, which shifts the curve to the right, which then decreases the affinity of hemoglobin for oxygen and increases the unloading of oxygen at the low partial pressure of oxygen levels at the muscles, which is an adaptation by the body from altitude exposure to increase tissue delivery of oxygen.
Viscosity and peripheral resistance effects as well as circulation velocity effects would be negligible, until the hematocrit goes up to past 60 or 65%, when strokes or heart attacks could occur. An MCV effect on the RBCs(lorries) would also be negligible. Both RBCs and plasma volume will increase, so effects on hematocrit will usually show a moderate increase or even very little change. Hemoglobin levels will only increase about 4 to 6%, rarely up to 10%, even with prolonged altitude exposure. The most important effect of EPO is on the number of RBCs, not the size of RBCs (MCV or mean corpuscular volume).
Many of the adaptations to training in general (and altitude training) that increase VO2max (which is a measure of oxygen consumption) and increase lactate clearance and lead to increased lactate threshold levels take place inside the muscle cells....myoglobin increases, which transports oxygen inside the cell to the mitochondria. AMPK (AMP-activated protein kinase) increases levels of PGC1alpha (Peroxisome proliferator-activated receptor gamma co-activator 1-alpha), which is the major factor which controls new mitochondrial synthesis in our muscle cells. More mitochondria, with more citric acid cycle enzymes, and more oxidative phosphorylation enzymes of the electron transport chain (located on the inner mitochondrial membrane), which is where most ATP is produced, (which is the fuel for muscle contraction) and thus....more ATP fuel is generated for running faster aerobically (of course meaning-with oxygen).
So rather than greater affinity of hemoglobin for oxygen, the important adaptations are inside the muscle cells at the mitochondrial level, in addition to other changes such as a larger,stronger heart; with increased stroke volume and increased cardiac output (which then leads to the much lower resting heart rates seen in endurance athletes)....
Read more:
http://www.letsrun.com/forum/flat_read.php?thread=7142840#ixzz45Jt0wIoo