The Combined Effects of Exercise and Post Dehydration Water Drinking on Plasma Argenine Vasopressin, Plasma Osmolality and Body Temperature in Healthy Males
Subgroup: Volume 3, Issue 2, Spring
Date: June 2005
Type: Original Article
Start Page: 80
End Page: 86
- Khamnei s Applied Drug Research Center, Tabriz University of Medical Sciences, Tabriz, I.R.Iran
- Alipour MR Applied Drug Research Center, Tabriz University of Medical Sciences, Tabriz, I.R.Iran
- Ahmadiasl N Applied Drug Research Center, Tabriz University of Medical Sciences, Tabriz, I.R.Iran
City, Province: Tabriz,
The purpose of this study was to inves tigate the effect of exercise and post dehydration water drinking on varia tions in plasma arginine vasopressin (P A VP), plasma osmolality (Posm) and tympanic temperature (Ttym) in healthy males.
Materials and Methods: Eight healthy young males (27.4+/-0.8 yrs old) volunteered for the study. They performed constant work exercise, at a rate of 60 rpm at 50% of individual work load for V02 peak for 30 minutes. Six blood samples (at minutes 0, 15 and 30 during exercise and at minutes 3, 15 and 30 after termination of exer cise) were obtained through an indwelling ve nous cannula. Plasma concentrations for Na+, and AVP were determined. Posm was calculated using Na+ concentrations. Simultaneous varia tions in Ttym were also determined.
Results: Our results demonstrated a positive cor relation between increase in P A VP and both Posm and Ttym during exercise but not during the re covery period. When exercise was combined with water drinking a fast and significant sup pression in P A VP occurred (P<0.05). Conclusions: These results suggest that Posm and Ttym have no significant effect on AVP secretion post exercise, and thus other factors must be in volved in AVP secretion during post exercise re covery period.
Keywords: Arginine vasopressin;Plasma osmolality;Tympanic temperature;Water drinking; exercIse.
Exercise is known to influence intravascular water and electrolyte balance in an exertion dependent manner, and to increase plasma osmolality (P osm) and arginine vasopressin level (PAvp).I During exercise, water loss through hyper-perspiration and hyperpnea results in an increase in P osm. Alterations in plasma osmolality are sensed by osmoreceptors in the hypothalamus, which in tum initiate mechanisms that affect water intake (via thirst) and water excretion (via AVP secretion) to return plasma osmolality to normal?-9 Other factors motivated by exer·· cise modify this response. I Increases in Posm and core temperature are two significant factors of this kind. 15 ,16 On the other hand, post dehydration water drinking is another factor, which manipulates PAVp.16.18
It has been shown that the increase in P A VP per unit rise in P osm tends to be higher than that induced by hypertonic saline infusion during exercise suggesting that mechanisms other than osmoregulation are involved. 10,1 I
One possible mechanism is increased body temperature. 1 Several studies have suggested that heat exposure elevates plasma A VP concentration and reduces urinary excretion rate,12-14 suggesting that increased body temperature, per se, can stimulate A VP secretion. 15 Takamata et al 16 reported that the effect of increased body core temperature on A VP secretion was P osm dependent; i. e. , the effect of increased core temperature was greater at a higher P osm. They also demonstrated that in humans the osmotic inhibition of thermal sweating and the associated reduction in A VP secretion were reversed by consumption of a small amount of water before occurrence of any change in plasma osmolality or volume. Simi liar results have also been reported earlier by the authors. 17 Thrasher and colleagues have shown that the plasma A VP fall to basal levels within 15 min after water drinking (significant fall after 6 min) in dogs that had been deprived ofwater for 24 h. 18 Geelen et al demonstrated a rapid fall in P A VP after drinking in dehydrated humans, in the absence of changes in serum Na+, osmolality, or plasma volume. Therefore, they suggested that oropharyngealgastric stimuli mediated by the central nervous system are most likely responsible for the depressed AVp. 19 In further studies, Greenleaf et al showed that the act of drinking in dehydrated humans, alone or combined with gastric stimuli, independent of the composition and osmolality of the fluid consumed, leads to prompt inhibition of A VP secretion.2o
Despite relatively extensive information regarding the effects of exercise and post dehydration water drinking on P A vp, their combined effect has not been reported so far. In practice, drinking of water at cessation of exercise is common behavior, making the present issue an important research topic. The present study investigates the combined effect of exercise recovery and water drinking on A VP secretion.
Materials and Methods
Eight healthy male subjects (27.4±0.8 years old) participated in the study. All volunteers were initially familiarized with the experimental procedures and written informed consent was obtained.
Subjects underwent two exercise protocols (Prot A. without water drinking and Prot B. with water drinking) on separated days. Experiments started at 15:00 hours. Pretest instructions included eating a light lunch, refraining from drinking any beverage after 1 :00 pm and any exercise on the day of experiment.
During the first session, each subject had his peak oxygen uptake (V02 peak) measured. This was determined by an incremental work rate protocol on a bicycle ergometer (ergo-metrics 800S Sensormedics, USA) interfaced with a personal computer (V max 29C Sensormedics, USA). It was preprogrammed to begin at a load of 25 w for an initial 2 minute warm up stage, increase to 50 w for the second stage, and increases by 20 w each minute until the subject achieved volitional fatigue. Subjects were requested to maintain a pedal cadence of 60 rpm for the duration of the test. In the second and third sessions, the protocols conducted were as follows:
Protocol A. An indwelling cannula was inserted into a large superficial vein in the forearm initially. Then subjects rested in the sitting position for 30 minutes in the laboratory (28.4±0.4 ambient temperature, 45.5±0.03 relative humidity, and natural convection). 9mL of blood sample was obtained through the indwelling cannula at the end of resting period, after which they performed a constant work rate exercise test (60 rpm at 50% of their determined V02 peak) for 30 minutes. Second and third blood samples were collected at 15 and 30 minutes respectively after the onset of the exercise. During the recovery period, blood samples were taken at 3, 15 and 30 minutes. The samples were immediately centrifuged at 3000 g and 4°c for 5 minutes and then plasma concentrations of sodium and A VP were measureq.
Tympanic temperature was measured at 0, 15 and 30 minutes during exercise and again every consecutive 3 minutes, for 30 minutes into the recovery.
Protocol B. The same procedure, described above, was followed except that subjects consumed a desired amount of water (425±25 ml) just after exercise cessation.
Change in tympanic temperatures was measured using the Ear Thermometer (Braun Pro 3000, Ireland).
Plasma sodium concentration was determined by Eppendorf flame photometr (Efox 5054, instrumentation laboratory). Because sodium and its associated anions account for about 94 percent of the solute in the extracellular compartment, plasma osmolality could be roughly approximated as Posm=2.1
PA VP was determined by radioimmunoassay (vasopressin RIA, IBL Hamburg RIA kit).
All values are presented as means±SE. The average response of the different physiological variables was compared using ANOVA with repeated measures. In the event of statistical significance (P < 0.05), a Tukey's test was used to identify significant differences. Independent-sample t-test was used for differences between Protocols A and B. Results obtained in the two groups were assessed for statistically significant differences by the Pearson correlation test (P<0.05).
Inter-and intraassay coefficients of variation were 3.4% and 2.3%, respectively. Changes in plasma osmolality, AVP and tympanic temperature during exercise and subsequent recovery are given below:
Arginine vasopressin: Before the onset of exercise, mean PAVP was 2.26±0.21 pg/mL in Prot. A and 2.50±0.12 pg/mL in Prot B. In both protocols, significant increases in P AVP were observed during exercise (Table 1). In
Table 1. Plasma concentration of arginine vasopressin (PAVP), plasma osmolality (Posm) and tympanic temperature (Ttym) before, during and after cessation of exercise (50% of V02peak) with and without after cessation water drinking (protocols A and B, respectively) in eight subjects. P values for significant differences with control (0 time) are shown under mean values.
|PA Vp (pg/mL)||B||2.50±0.12||2.95±0.17||
Prot A, it increased to an even higher level in the first sample taken 3 minutes after exercise (3.73±0.20 pg/mL, P=O.OO) and then fell to lower levels recovering to values not significantly different from the baseline. In contrast, in Prot. B, P A VP decreased rapidly during recovery period and became significantly lower than baseline in the second sample taken IS minutes after the termination of exercise (1.93±0.l4 pg/mL, P=0.04). There was also a significant difference in PAVP between the two protocols during the recovery period (PPlasma osmolality: Before the onset of exercise, Posmwas 298.7±1.8 mosmlkg H20 in Prot. A and 300.3±l mosmlkg H20 in Prot. B, which were not significantly different. In both protocols, there were significant increases in P osm during exercise (311.6±2.S mosmlkg H20, P=O.OO in Prot. A and 309.S±2.1 mosmlkg H20, P=0.02 in Prot. B), followed by a significant decrease by exercise termination (290.3±1.9 mosmlkg H20, P=O.OI in Prot. A and 290.3±2.9 mosmlkg H20, P=O.Ol in Prot. B), and then recovered to baseline values. There was no significant difference in Posm between counterpart values of the two protocols during recovery period. As shown in figure lA and lC, there were significant positive correlations between P AVP and P osm (r = 0.48, P=0.02 in Prot A and r = 0.42, P= 0.04 in Prot B) during exercise but not during recovery (Table 1 and Fig.l and 2), (Figs 2A and 2C).
Tympanic temperature: Baseline values for Ttym were 37. 08±0.OS °C and 37. OS±0.08 °C for Prot. A and Prot. B, respectively, which were not significantly different. In both protocols, these values increased significantly during exercise, (37.36±0.OS °C, P=0.03 in Prot. A and 37.34±0.OS °C, P=O.OI in Prot. B) and remained elevated up to the first post exercise measurement (37.38±0.06 °C, P=0.02 in Prot. A and 37.4S±0.03 °C, P=O.OO in Prot. B), and then recovered to the baseline values. There were significant correlations between P A Vp and T tym in both protocols during exercise (r = 0.S6, P=O.OI in Prot. A and r=0.3S, P= 0.04 in Prot. B) (Fig IB and ID); this was not the case during recovery in either of the protocols (Figs 2B and 2D) (Fig. 1 and 2 and Table 1).
Drinking water on termination of exercise is a common behavior. In the present study, we examined the combined effect of exercise and post dehydration water drinking on P A Vp variations. Our results demonstrate that in the face of similar changes in P osm and Ttym, when exercise is combined with water drinking a fast and significant suppression in PAVP occurs. (Table 1).Several researchersIA have reported that the primary stimulus for A VP release during exercise is increased P osm resulting from enhanced sweat production and respiratory water loss. Alterations in P osm are sensed by osmoreceptors in the hypothalamus, which initiate the thirst mechanism and A VP secretion, thereby affectin~ water intake and urinary water excretion. -9 Takamata et all have suggested that the main cause of the increased Posm during moderate to heavy exercise of short duration is the hypotonic fluid movement from intra to extra vascular space. This may explain the rapid improvement in P osm seen during the recovery period in the present study (Table 1), which seems to be due to the redistribution of water and retrievement of hypotonic fluid lost into interstitial compartments. More reductions in Posm 30 minutes after exercise in Prot. B can be attributed to absorption of the water consumed by the subjects. In agreement with these reports, results obtained in the present study indicate a positive correlation between P AVp and P osm during exercise (r= 0.48, P=0.02 and r= 0.42, P=0.04 in Prot. A and B, respectively) (Fig.l). During recovery, however, our results failed to show any significant correlation between PA Vp and P osm in either of the two protocols (Fig.2).
Fig.I. Relations between plasma concentration for arginine vasopressin and plasma osmolality and tympanic temperature during exercise (50% of V02peak) in Prot. A (panels A and R) and Prot. B (panels C and D).
Another possible mechanism involved in AVP secretion is increased body temperature. Takamata et ae6 demonstrated that A VP secretion is enhanced by increased body core temperature. Our conclusion drawn from the result, obtained in the present study was similar to that of Posm, i. e. ; P A Vp and Ttym were significantly correlated during exercise only, a correlation that later became non significant. According to the results of this study, it seems that P osm and Ttym which are assumed to be two first line factors involved in A VP secretion, although effective during exercise, do not seem to have a significant role in P AVP changes during its recovery.
Fig.2. Relations between plasma concentration for arginine vasopressin and plasma osmolality and tympanic temperature during recovery from exercise (50% of V02peak) in Prot. A (panels A and B) and Prot. B (panels C and D).
The sharp reduction in PA VP in Prot B by initiation of recovery period suggests possioffble contribution of oropharyngeal18 and gastricl9 receptors in A VP secretion. These receptors are assumed to be stimulated by wa ter drinking and studies performed on dehy drated humanl9 and animals.22-24 In other words, it seems that the inhibitory effect of water drinking on A VP secretion gains dominance on the stimulatory effects elicited by increase in P osm and Ttym seen at the off transient of exercise. More confirmatory data particularly from animal models are required for the inference made above.
We would like to thank Dr MR Bonyadi,and Mr. H Ibrahimi for their technical ass is tance, Dr. H Salimi Khaligh for reviewing the article and the Drug Applied Research Center of Tabriz University of Medical Sciences for financial support.
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