Oxidación de Cu(I) en agua de mar

La cinética de oxidación de Cu(I) con oxígeno, a concentración nanomolar, se ha estudiado en función de la concentración de cobre (I), pH, concentración de bicarbonato y de la temperatura, al objeto de obtener las ecuaciones de dependencia de la constante de velocidad con cada variable, en NaCl (0.7M) con bicarbonato (2mM) y en agua de mar. Los estudios a escala nanomolar se han comparado con los estudios realizados por otros autores a escala micromolar. El tiempo de vida medio a nivel nanomolar es superior en ambos medios, lo que justifica la presencia de concentraciones medibles de Cu(I) en aguas superficiales. La constante de velocidad de segundo orden (k) es independiente de la concentración de Cu(I), en el rango de 20 a 200 nM, con lo que los resultados permiten una visión más realista de lo que ocurre en el océano. En los estudios del efecto del pH en la cinética de oxidación se obtienen rectas próximas para disolución de NaCl (0.7M) con bicarbonato (2mM) y en agua de mar, por lo que las interacciones específicas pueden despreciarse o quedar compensadas entre sí. La ecuación obtenida para cada caso es: Logk(NaCl) = −2.453(±0.341) + 0.611(±0.044)pH (para NaCl) Logk(sw) = −1.484(±0.266) + 0.489(±0.034) pH (para agua de mar) La concentración de bicarbonato produce un aumento en la constante de segundo orden (k) hasta 5mM, comportándose de acuerdo con la ecuación siguiente: [ ] [ ]2 3 2 3 3 2 2 ( ) 1.54 10 ( 3.518 10 ) 3.963( 58.17 10 ) 0.212( 3.242 10 ) 3 NaHCO Logk NaHCO NaHCO − − − ⋅ ± ⋅ = − ± ⋅ + ± ⋅ − El aumento de la temperatura produce un aumento en la constante de velocidad relacionándose este efecto con la entalpía y entropía de activación del proceso. Oxidación de Cu(I) en agua de mar 8 El trabajo realizado supone un mejor conocimiento de los procesos que controlan la cinética de oxidación del Cu(I) en medios naturales y servirán de base para futuros experimentos.

The re-establishment of the normal blood lactate response to exercise in humans after prolonged acclimatization to altitude

[EN] 1. One to five weeks of chronic exposure to hypoxia has been shown to reduce peak blood lactate concentration compared to acute exposure to hypoxia during exercise, the high altitude 'lactate paradox'. However, we hypothesize that a sufficiently long exposure to hypoxia would result in a blood lactate and net lactate release from the active leg to an extent similar to that observed in acute hypoxia, independent of work intensity. 2. Six Danish lowlanders (25-26 years) were studied during graded incremental bicycle exercise under four conditions: at sea level breathing either ambient air (0 m normoxia) or a low-oxygen gas mixture (10 % O(2) in N(2), 0 m acute hypoxia) and after 9 weeks of acclimatization to 5260 m breathing either ambient air (5260 m chronic hypoxia) or a normoxic gas mixture (47 % O(2) in N(2), 5260 m acute normoxia). In addition, one-leg knee-extensor exercise was performed during 5260 m chronic hypoxia and 5260 m acute normoxia. 3. During incremental bicycle exercise, the arterial lactate concentrations were similar at sub-maximal work at 0 m acute hypoxia and 5260 m chronic hypoxia but higher compared to both 0 m normoxia and 5260 m acute normoxia. However, peak lactate concentration was similar under all conditions (10.0 +/- 1.3, 10.7 +/- 2.0, 10.9 +/- 2.3 and 11.0 +/- 1.0 mmol l(-1)) at 0 m normoxia, 0 m acute hypoxia, 5260 m chronic hypoxia and 5260 m acute normoxia, respectively. Despite a similar lactate concentration at sub-maximal and maximal workload, the net lactate release from the leg was lower during 0 m acute hypoxia (peak 8.4 +/- 1.6 mmol min(-1)) than at 5260 m chronic hypoxia (peak 12.8 +/- 2.2 mmol min(-1)). The same was observed for 0 m normoxia (peak 8.9 +/- 2.0 mmol min(-1)) compared to 5260 m acute normoxia (peak 12.6 +/- 3.6 mmol min(-1)). Exercise after acclimatization with a small muscle mass (one-leg knee-extensor) elicited similar lactate concentrations (peak 4.4 +/- 0.2 vs. 3.9 +/- 0.3 mmol l(-1)) and net lactate release (peak 16.4 +/- 1.8 vs. 14.3 mmol l(-1)) from the active leg at 5260 m chronic hypoxia and 5260 m acute normoxia. 4. In conclusion, in lowlanders acclimatized for 9 weeks to an altitude of 5260 m, the arterial lactate concentration was similar at 0 m acute hypoxia and 5260 m chronic hypoxia. The net lactate release from the active leg was higher at 5260 m chronic hypoxia compared to 0 m acute hypoxia, implying an enhanced lactate utilization with prolonged acclimatization to altitude. The present study clearly shows the absence of a lactate paradox in lowlanders sufficiently acclimatized to altitude.