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Effects of changes in hydration on protein, glucose and lipid metabolism in man: impact on health.
Keller U1, Szinnai G, Bilz S, Berneis K.
Alterations of cell volume induced by changes of extracellular osmolality have been reported to regulate intracellular metabolic pathways. Hypo-osmotic cell swelling counteracts proteolysis and glycogen breakdown in the liver, whereas hyperosmotic cell shrinkage promotes protein breakdown, glycolysis and glycogenolysis. To investigate the effect of acute changes of extracellular osmolality on whole-body protein, glucose and lipid metabolism in vivo, we studied 10 male subjects during three conditions: (i) hyperosmolality was induced by fluid restriction and intravenous infusion of hypertonic NaCl (2-5%, wt/vol) during 17 h; (ii) hypo-osmolality was produced by intravenous administration of desmopressin, liberal water drinking and infusion of hypotonic saline (0.4%); and (iii) the iso-osmolality study comprised oral water intake ad libitum. Plasma osmolality increased from 285+/-1 to 296+/-1 mosm/kg (P<0.001 during hyperosmolality, and decreased from 286+/-1 to 265+/-1 mosm/kg during hypo-osmolality (P<0.001). Total body leucine flux ([1-(13)C]leucine infusion technique), reflecting whole-body protein breakdown, as well as whole-body leucine oxidation rate (irreversible loss of amino acids) decreased significantly during hypo-osmolality. The glucose metabolic clearance rate during hyperinsulinaemic-euglycemic clamping increased significantly less during hypo-osmolality than iso-osmolality, indicating diminished peripheral insulin sensitivity. Glycerol turnover (2-[(13)C]glycerol infusion technique), reflecting whole-body lipolysis, increased significantly during hypo-osmolar conditions. The results demonstrate that the metabolic adaptation to acute hypo-osmolality resembles that of acute fasting, that is, it results in protein sparing associated with increased lipolysis, ketogenesis and lipid oxidation and impaired insulin sensitivity of glucose metabolism.
Effect of hydration state on resistance exercise-induced endocrine markers of anabolism, catabolism, and metabolism.
Judelson DA1, Maresh CM, Yamamoto LM, Farrell MJ, Armstrong LE, Kraemer WJ, Volek JS, Spiering BA, Casa DJ, Anderson JM.
Hypohydration (decreased total body water) exacerbates the catabolic hormonal response to endurance exercise with unclear effects on anabolic hormones. Limited research exists that evaluates the effect of hypohydration on endocrine responses to resistance exercise; this work merits attention as the acute postexercise hormonal environment potently modulates resistance training adaptations. The purpose of this study was to examine the effect of hydration state on the endocrine and metabolic responses to resistance exercise. Seven healthy resistance-trained men (age = 23 +/- 4 yr, body mass = 87.8 +/- 6.8 kg, body fat = 11.5 +/- 5.2%) completed three identical resistance exercise bouts in different hydration states: euhydrated (EU), hypohydrated by approximately 2.5% body mass (HY25), and hypohydrated by approximately 5.0% body mass (HY50). Investigators manipulated hydration status via controlled water deprivation and exercise-heat stress. Cortisol, epinephrine, norepinephrine, testosterone, growth hormone, insulin-like growth factor-I, insulin, glucose, lactate, glycerol, and free fatty acids were measured during euhydrated rest, immediately preceding resistance exercise, immediately postexercise, and during 60 min of recovery. Body mass decreased 0.2 +/- 0.4, 2.4 +/- 0.4, and 4.8 +/- 0.4% during EU, HY25, and HY50, respectively, supported by humoral and urinary changes that clearly indicated subjects achieved three distinct hydration states. Hypohydration significantly 1) increased circulating concentrations of cortisol and norepinephrine, 2) attenuated the testosterone response to exercise, and 3) altered carbohydrate and lipid metabolism. These results suggest that hypohydration can modify the hormonal and metabolic response to resistance exercise, influencing the postexercise circulatory milieu.
Effect of hydration state on strength, power, and resistance exercise performance.
Judelson DA1, Maresh CM, Farrell MJ, Yamamoto LM, Armstrong LE, Kraemer WJ, Volek JS, Spiering BA, Casa DJ, Anderson JM.
Although many studies have attempted to examine the effect of hypohydration on strength, power, and high-intensity endurance, few have successfully isolated changes in total body water from other variables that alter performance (e.g., increased core temperature), and none have documented the influence of hypohydration on an isotonic, multiset, multirepetition exercise bout typical of resistance exercise training. Further, no investigations document the effect of hypohydration on the ability of the central nervous system to stimulate the musculature, despite numerous scientists suggesting this possibility. The purposes of this study were to examine the isolated effect of hydration state on 1) strength, power, and the performance of acute resistance exercise, and 2) central activation ratio (CAR).
Seven healthy resistance-trained males (age = 23 +/- 4 yr, body mass = 87.8 +/- 6.8 kg, body fat = 11.5 +/- 5.2%) completed three resistance exercise bouts in different hydration states: euhydrated (EU), hypohydrated by approximately 2.5% body mass (HY25), and hypohydrated by approximately 5.0% body mass (HY50). Investigators manipulated hydration status via exercise-heat stress and controlled fluid intake 1 d preceding testing.
Body mass decreased 2.4 +/- 0.4 and 4.8 +/- 0.4% during HY25 and HY50, respectively. No significant differences existed among trials in vertical jump height, peak lower-body power (assessed via jump squat), or peak lower-body force (assessed via isometric back squat). CAR tended to decrease as hypohydration increased (EU = 95.6 +/- 4.9%, HY25 = 94.0 +/- 3.1%, HY50 = 92.5 +/- 5.1%; P = 0.075, eta(p)(2) = 0.41). When evaluated as a function of the percentage of total work completed during a six-set back squat protocol, hypohydration significantly decreased resistance exercise performance during sets 2-3 and 2-5 for HY25 and HY50, respectively.
These data indicate that hypohydration attenuates resistance exercise performance; the role of central drive as the causative mechanism driving these responses merits further research.