The increase in urine osmolality in all races (R1-R4) might be due to an increase in water permeability in the kidney, matching the fact that athletes urinated less frequently [2]. This could lead to impairments of free water CH5183284 cell line excretion in R1, R2 and R4 with indicators of a more chronic than an acute dehydration. Post-race symptoms reported by finishers in all races indicated this hypothesis. Glomerular filtration race significantly decreased and urine osmolality increased and it seemed to be a result in a change in renal function. Arginine vasopressin secretion, aldosterone activity and the prevalence of EAH SIADH

is also considered as a potentional Ro 61-8048 molecular weight mechanism to develop EAH [39], because arginine vasopressin (AVP) regulates body’s retention PSI-7977 of water. Changes in sodium and potassium concentrations and osmolality in plasma and urine are also indirect markers for the activity of aldosterone [2, 4, 16, 19, 45] and AVP-secretion [12, 42, 43, 45, 57, 59]. Urine [K+] significantly increased in R1 and R4, and urine specific gravity was associated with post-race urine [K+] in R4. On the contrary, urine [K+] in R2 and R3 remained stable, and urine [Na+] significantly

decreased in R2 and R3, although the K+/Na+ ratio in urine was < 1 only in R3. The increased urinary [Na+] losses could be compatible with SIADH in R2 and R3. In all races, the transtubular potassium gradient increased and was > 10 in R1, R3 and R4, probably due to an increased aldosterone activity. This change in aldosterone is associated with a change in the K+/Na+-ratio in urine, a positive ratio suggests an increased aldosterone activity [16, 18]. In all races (R1-R4), the K+/Na+-ratio in urine increased. The K+/Na+-ratio in urine was < 1.0 only in R3, suggesting Rolziracetam that more potassium

than sodium was excreted through the kidney, however the K+/Na+-ratio in urine was > 1 in R1, R2 and R4. Body water increase with simultaneous dehydration (R2-R4) might be possibly due to endocrine-induced renal water retention, in order to maintain the metabolic processes that are required for energy supply and blood flow during prolonged exercise [54]. Finishers were more hyperhydrated than dehydrated in R3. Apart from fluid overload, however, other mechanisms may have lead to water retention in R3, such as protein catabolism [54]. In a 24-hour running race, Fellmann et al. [59] found an increase in plasma volume, aldosterone and AVP. Stuempfle et al. [24] showed an increased activity of both aldosterone and AVP after an ultra-endurance race. Alternatively, there might be also an impairment in mobilization of osmotically-inactive sodium stores or inappropriate inactivation of osmotically-active sodium [11, 18]. These cannot be determined from the present study. Fluid overload and the prevalence of EAH Fluid overload is considered as the main risk factor for EAH [39, 48].