The article you posted can be very interesting, because is the clear demonstration that the most part of these researches can give different results if carried out with different subjects.
At first, we need to consider that athletes running 10000m in 28'27" ARE NOT ELITE. For example, in 2016 with this time a runner was number 170 in the world and 55 in Kenya. If these athletes run ONLY 28'27" because are not strong like the best in the world, or because their training is not enough in both the direction (volume and intensity), is something we don't know, but the fact they are by far (2 minutes) worse than the best is evident, so they are not part of the subjects I'm speaking about.
Secondly, the fact they change their blood values going at sea level is correct, but it's an absolute bullshit that this happens after 2-3 days. This change is very gradual, and top athletes living and training in altitude reach this level 2-3 months after going (and staying) at sea level.
Now, I want to show how the conclusions NEVER have validity for everyone, depending on the system of the research, and on the subjects who are investigated.
Look at the next two abstracts about the role of Folic Acid in connection with Erythropoietin :
Folic acid supplementation improves erythropoietin response.
Pronai W1, Riegler-Keil M, Silberbauer K, Stockenhuber F.
Author information
1
Department of Internal Medicine, Krankenhaus der Barmherzigen Brüder, Eisenstadt, Austria.
Abstract
Therapy with recombinant human erythropoietin (rhEPO) has become most valuable for the treatment of renal anemia in patients with various chronic renal diseases. For the first time this study presents data showing that rhEPO affects the metabolism of folic acid. There were 13 patients enrolled; they suffered from different chronic renal diseases and showed an impaired responsiveness to rhEPO therapy. Before starting rhEPO therapy the mean corpuscular volume of erythrocytes (MCV) was measured; MCV was 90.4 fl. During rhEPO therapy the MCV increased significantly by 14.8 fl (p `` 0.05). The developing macrocytic anemia was overcome when folic acid was administered additionally for a mean period of 3.14 +/- 3 months. Hematocrit (Hct) also responded accordingly. Whereas Hct did not increase adequately during the exclusive treatment with rhEPO, an increase in Hct from 23 +/- 3.3 to 30 +/- 4.2% (p < 0.01) was observed after the addition of folic acid. These results are rather remarkable as folic acid serum levels were clearly within the normal range during the whole study period. So it can be concluded that rhEPO therapy results in an increased demand for folic acid. Even if serum concentrations are within the normal range, the administration of folic acid will enhance the effectiveness of rhEPO therapy so that the rhEPO dosage can be reduced.
How you can say, the research brings to the conclusion that
FOLIC ACID SUPPLEMENTATION IMPROVES ERYTHROPOIETIN RESPONSE.
Now, go to read the following research :
Abstract
Pronai et al. [1995] published an article in Nephron which claimed that folic acid supplementation improves erythropoietin (EPO) response. The authors studied 13 patients who were resistant to EPO given at a dosage of 75 U/kg (per week or per dose?). Eight patients responded with a fall in mean corpuscular volume (MCV) and a rise in hematocrit when they were given folic acid.
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Dear Sir,
Pronai et al. [1995] published an article in Nephron which claimed that folic acid supplementation improves erythropoietin (EPO) response. The authors studied 13 patients who were resistant to EPO given at a dosage of 75 U/kg (per week or per dose?). Eight patients responded with a fall in mean corpuscular volume (MCV) and a rise in hematocrit when they were given folic acid.
Based on this experience, we selected 14/71 patients on chronic hemodialysis who revealed an elevated MCV (%%99 fl). Hemodialysis had been performed for 4–216 months; all patients were receiving 3 × 4–5 h/week of hemodialysis with a high-flux, large surface area (>1.8 m2) dialyzer. All patients were on EPO treatment (duration 4 months to 10 years) given subcutaneously twice weekly in 12 (mean dose 100.5 U/kg/week) and 3 times weekly intravenously in 2 (mean dose 286 U/kg/week). Iron was intravenously replaced regularly whenever serum ferritin fell below 100 µg/l. The patients were studied before and after 1 month of a folic acid replacement of 5 mg/day orally.
The results (mean ± SD) are shown in table 1.
Table 1
Results
Before folic acid supplementation, plasma folate was slightly lowered in 5 patients but only 1 of them had a low red cell folate level (which is a better indicator of tissue folate), Plasma vitamin B12 concentrations were normal in all patients. Folate replacement increased plasma folate levels significantly. The EPO dose remained unchanged (98.0 s.c. and 286 i.v. U/kg/week). Neither mean MCV nor hemoglobin concentration changed significantly. Two patients of 13 had a moderate decrease of MCV (from 100 to 96 and 109 to 104 fl), but only 1 of the 2 patients showed a slight rise in hemoglobin from 136 to 141 g/l. The patient with low plasma and red cell folate levels showed a rise in plasma folate concentration from 4.3 to 21.5 nmol/l but her MCV (103 before, 101 fl after) and hemoglobin (132 before, 130 g/gl after) remained unchanged.
Although we agree with Pronai et al. that means of economizing EPO should be sought,
our own results favor the conclusion that folic acid supplementation only rarely improves response to EPO in hemodialysis patients with an elevated MCV.
How you can say again, this research goes to the conclusion that
FOLIC ACID SUPPLEMENTATION ONLY RARELY IMPROVES RESPONSE TO EPO.
I continue to repeat, from years, that we can only study DIRECTLY WITH SPECIFIC SUBJECTS SOMETHING REGARDING THE SUBJECTS THEMSELVES.
But, of course, for all blind people, whose experience is to read some book, or to work with people with specific diseases, or toe see the reactions in some average person, a pharma can produce on a champion at the top of his training the same improvement that produces in a person with a bad disease.