In endurance athletes who are native to moderate altitude, tHb and BV were synergistically influenced by training and by altitude exposure, which is probably one important reason for their high performance.

Blood composition, hemoglobin mass (CO rebreathing method) and VO2peak were measured in 15 untrained (UT-Bogotá) and 14 trained males (TR-Bogotá) living at 2600 m of altitude, and in 14 untrained lowlanders (UT-Berlin). [Hb] amounted to 15.3 + 0.2(SE) g/dl in UT-Berlin, 17.4 + 0.2 g/dl in UT-Bogotá and 16.0 + 0.2 g/dl in TR-Bogotá. Hb mass was significantly higher in UT-Bogotá (13.2 + 0.4 g/kg, P < 0.01) and in TR-Bogotá (14.7 + 0.5 g/kg, P < 0.001) than in UT-Berlin (11.7 + 0.2 g/kg). In TR-Bogotá also plasma volume was expanded. Erythropoietin concentrations in UT-Bogotá and TR-Bogotá were not significantly increased. There was a positive correlation between blood volume and VO2peak for the pooled values of all subjects, if the oxygen uptake of UT-Berlin was corrected for an ascent to 2600 m. For the Hb mass - VO2peak relation two groups are indicated pointing to two types of altitude acclimatization with different Hb mass increases but similar distribution of aerobic performance capacity. We suggest that different genetic properties in a population of mixed ethnic origin might play a role.

Total hemoglobin mass has not been systematically investigated in females at altitude. We measured this quantity (CO-rebreathing method) as well as peak oxygen uptake in 54 young women (age 22.5 +/- 0.6 SE years) with differing physical fitness living in Bogota (2600 m) and compared the results with those of 19 subjects from 964 m in Colombia and 75 subjects from 35 m in Germany. In spite of an increased hemoglobin concentration the hemoglobin mass was not changed in highlanders (means 9.0 to 9.5 g . kg (-1) in untrained subjects at all altitude levels). Endurance trained athletes, however, showed a rise in hemoglobin mass by 2 - 3 g . kg (-1) at all sites. Erythropoietin was little increased in Bogota; iron stores were within the normal range. Aerobic performance capacity was lower at high altitude than at sea level and remained so also after correction for the hypoxic deterioration in untrained and moderately trained subjects but not in athletes; possibly the cause was reduced daily physical activity in non-athletic Bogotanians compared to lowlanders. After exclusion of the factor V.O(2peak) by analysis of covariance a mean rise of 6.6 % in hemoglobin mass at 2600 m was calculated being smaller than in males (> 12 %). The attenuated increase of hemoglobin mass in female highlanders possibly results from stimulation of ventilation improving arterial oxygen saturation or from an increased hypoxia tolerance of cellular metabolism both caused by female sexual hormones.

Under tropical conditions, we found a severe state of dehydration characterized by an extended ANP-response, which was not prevented by water intake during the race. Under hypoxic conditions, however, we found that hyponatremia had developed. This can be partly explained by pure water intake and metabolically produced water, and also, possibly, by a special hypoxia-induced effect.

Hemoglobin oxygen binding properties and acid-base status were investigated in Colombian athletes (A) and controls (C) from Cali (C-1000 m) and Bogotá (B-2600 m). [Hb] and Hct values were not influenced by altitude, but Hct was lower in the blood of athletes (in Cali 2.6%, in Bogotá 1.4%). Both training and altitude produced a right-shift of the standard oxygen dissociation curve (P50 in CC 28.5 +/- 0.9 mmHg, AC 31.0 +/- 1.4 mmHg, CB 29.6 +/- 1.5 mmHg) leading to highest P50 in blood of altitude athletes (32.3 +/- 1.1 mmHg). Opposite to the position of the ODC the slope "n" was only increased by altitude influence (delta "n" in controls 0.07, in athletes 0.28). The BCCO2 was increased in AC over the whole saturation range, whereas BCLac was neither significantly influenced by training nor by altitude. All altitude effects can be explained by higher [DPG] (delta[DPG] in controls 5.0 mumol/gHb, in athletes 3.9 mumol/gHb), but the cause for the training effects still remains unclear. The acid base status in altitude residents was characterized by low BE and pCO2, which was most pronounced in altitude athletes, the latter correcting the actual venous pH to normal values. No significant variations of the Hb-O2-binding properties could be detected in athletes one day after leaving high altitude when compared with blood samples of athletes taken at high altitude, whereas BE and venous pCO2 were already increased. It is concluded that high altitude athletes are favoured during aerobic and handicapped during anaerobic exercise after the rapid descent to low altitude.

Because of lacking ventilatory stimulation by sex hormones in postmenopausal women (PW), one might expect a lowered arterial oxygen saturation (S(O(2))) in hypoxia and therefore a stronger erythropoietic reaction than in young women (YW). Nine untrained (UTRPW) and 11 trained (TRPW) postmenopausal altitude residents (2600 m) were compared to 16 untrained (UTRYW) and 16 trained young women (TRYW) to check this hypothesis and to study the combined response to hypoxia and training. S(O(2)) was decreased in PW (89.2% +/- 2.2 vs. 93.6 +/- 0.7% in YW, p < 0.01). Hb mass, however, was similar in UT (UTRYW: 9.2 +/- 0.9 g/kg(1), UTRPW: 8.7 +/- 1.0 g/kg). But if body fat rise with age was excluded by relation to fat-free mass, Hb mass was increased in UTRPW (+1.2 g/kg, p < 0.05) compared to UTRYW. Training caused a similar rise of Hb mass in PW and YW (0.3 g/kg per mL/kg x min(1) rise in V(O(2peak))). There was no difference in erythropoietin among the groups. Ferritin was higher in PW than YW. The results show that female hormones and fitness level have to be considered in studies on erythropoiesis at altitude. The role of erythropoietin during chronic hypoxia still has to be clarified.

The assumption that buffering at altitude is deteriorated by bicarbonate (bi) reduction was investigated. Extracellular pH defense against lactic acidosis was estimated from changes (Delta) in lactic acid ([La]), [HCO3-], pH and PCO2 in plasma, which equilibrates with interstitial fluid. These quantities were measured in earlobe blood during and after incremental bicycle exercise in 10 untrained (UT) and 11 endurance-trained (TR) highlanders (2,600 m). During exercise the capacity of non-bicarbonate buffers (betanbi=-Delta[La]. DeltapH(-1)-Delta[HCO3-]. DeltapH(-1)) amounted to 40+/-2 (SEM) and 28+/-2 mmol l(-1) in UT and TR, respectively (P<0.01). During recovery beta (nbi) decreased to 20 (UT) and 16 (TR) mmol l(-1) (P<0.001) corresponding to values expected from hemoglobin, dissolved protein and phosphate concentrations related to extracellular fluid (ecf). This was accompanied by a larger decrease of base excess after than during exercise for a given Delta[La]. betabi amounted to 37-41 mmol l(-1) being lower than at sea level. The large exercise betanbi was mainly caused by increasing concentrations of buffers due to temporary shrinking of ecf. Tr has lower betanbi in spite of an increased Hb mass mainly because of an expanded ecf compared to UT. In highlanders betanbi is higher than in lowlanders because of larger Hb mass and reduced ecf and counteracts the decrease in [HCO3-]. The amount of bicarbonate is probably reduced by reduction of the ecf at altitude but this is compensated by lower maximal [La] and more effective hyperventilation resulting in attenuated exercise acidosis at exhaustion.

Introducción. La enfermedad de Chagas es una parasitosis endémica en Latinoamérica transmitida por triatominos. Está asociada a factores de riesgo como la pobreza y la ruralidad. Después de la infección aguda, un tercio de los pacientes presenta compromiso del corazón, el aparato digestivo o el sistema nervioso central, en tanto que los dos tercios restantes no presentan este tipo de compromiso secundario. La inmunosupresión farmacológica rompe el equilibrio entre el sistema inmunitario y el parásito, lo cual favorece su reactivación.Caso clínico. Se presenta el caso de un hombre de 58 años procedente de un área rural colombiana, con diagnóstico de mieloma múltiple resistente a los fármacos de primera línea de tratamiento, que requirió un nuevo esquema de quimioterapia y consolidación con trasplante autólogo de células madre.Después del trasplante, presentó neutropenia febril. Los estudios microbiológicos iniciales fueron negativos. En el frotis de sangre periférica, se demostraron tripomastigotes y se diagnosticó enfermedad de Chagas aguda posterior al trasplante. Se inició el tratamiento con benznidazol. La evolución del paciente fue satisfactoria.Conclusiones. La serología positiva para Chagas previa a un trasplante obliga a descartar la reactivación de la enfermedad en caso de neutropenia febril. Se requieren más estudios para determinar las herramientas que permitan estimar la probabilidad de reactivación de la enfermedad y decidir sobre la mejor opción de relación entre costo, riesgo y beneficio de la terapia profiláctica.