The effects of exercise training on riboflavin requirements and of riboflavin intake on endurance were examined in 14 women, 50-67 y of age, who participated in a 10-wk, two-period crossover exercise study at two riboflavin intakes, 0.15 micrograms/kJ (0.6 micrograms/kcal) and 0.22 micrograms/kJ (0.9 micrograms/kcal). Subjects exercised 20-25 min/d, 6 d/wk, for 4-wk periods on a cycle ergometer at 75-85% of their maximal heart rate. Riboflavin status was assessed by measuring the erythrocyte glutathione reductase activity coefficient (EGRAC) and urinary riboflavin excretion. Physical performance was evaluated by using a walking treadmill test to determine maximal oxygen capacity (VO2max) and anaerobic threshold by gas exchange (ATGE). Exercise significantly affected riboflavin status as EGRAC increased (P less than 0.001) and riboflavin excretion decreased (P less than 0.01) in both groups. VO2max increased significantly with exercise (P less than 0.01). However, changes in VO2max (L/min) and ATGE with exercise training were not different in the two groups. Riboflavin requirements of older women increased with exercise training, but increased riboflavin intake did not enhance improvements in endurance.
Cat thyroid slices were employed to determine whether preincubation with excess iodide, a procedure previously reported to depress subsequently measured iodide transport activity, is associated with any alteration in the relationship between sodium and iodide transport. Kinetic analysis revealed that the inhibition of iodide-concentrating activity by iodide pretreatment was accompanied by a reduction in the apparent affinity of the iodide transport for iodide as reflected by increase in the value of KA, the concentration of iodide required to achieve half-maximal transport activity. A reduction in extracellular sodium concentration was also accompanied by an increase in the value of KA for iodide transport. Thus, the KA of iodide transport in control thyroid tissue was increased from a value of 8.6 +/- 1.2 to 16.5 +/- 2.4 microM, by a reduction in extracellular sodium from 144 to 52 mM. In contrast, in thyroid tissue subjected to a 2-h preincubation with 30 microM NaI, a similar reduction in extracellular sodium concentration was associated with only a 20% increase in KA from a value of 17.7 +/- 2.4 to 21.7 +/- 2.2 microM. Analysis of the kinetic data suggests that the autoregulatory effect of excess iodide results in a decline in the sodium dependency of iodide transport. This loss of sodium dependency is accompanied by an increase in the affinity of the process for sodium, as well as a reduction in the affinity of the transport system for iodide.
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