© Borgis - New Medicine 2/2006, s. 39-42
Ilona Pokora
Heat stress responses in men after ingestion of a low-sodium diet
Faculty of Physiological-Medical Sciences, Department of Physiology, Academy of Physical Education, Katowice, Poland
Head of Department: Prof. Józef Langfort, MD, PhD
Summary
Summary
Aim: The aim of this study was to examine the physiological and metabolical responses to exogenous heat stress after ingestion of a low-sodium diet (580 mg Na/24 h/person).
Material and method: The study included 11 healthy males non-exercising and non-acclimating to heat. The participants were volunteers (aged 21.44±0.91 years, body height 178.3±2.28 cm, body weight 72.54±4.97 kg). The participants took part in two research tasks. Before the experiment, after diet, heat stress and the 24 hour long recovery period, the samples of vein blood were collected. They also assessed the changes in body mass and body composition after receiving the diet and after the heat stress in both tasks (weight, bioimpedance TANITA, Poland) and the changes in water distribution in body water compartments.
Results: The obtained results indicate that the reduction of sodium availability after ingestion of low sodium diet, increases heat accumulation during thermal stress as the result of decrease in water availability to sweating.
Conclusions: Diminution of sodium amount in adult males obstructs the proper rehydration during recovery despite of strong activation of sodium-saving mechanisms.
Introduction
Physical activity and/or exposure to heat results in some thermal homeostasis disorders. Maintaining a constant internal temperature under such conditions and active defence against the threat of hyperthermia triggers a lot of compensation reactions aiming at recovering the functional balance of the organism. Under a thermal stress affecting the organism its defence against the excess of heat is performed mainly by sweating. Unfortunately, the sweat evaporation from the skin surface involves some loss of water and electrolytes, which can lead (without refilling liquids) to hyperosmotic dehydration. The increase in osmolality and reduction of the systemic liquid volume results in reducing the efficiency of heat dissipation from the body, which can cause hyperthermia. Relatively little is known how effective can be the thermoregulatory mechanism in defence against hyperthermia and dehydration under the conditions of low-sodium diet.
Daily sodium consumption ranges from 700 to 3,600 mg/24h/person. Under the conditions of increased ambient temperature because of the possibility of abundant sweating, the content of this element in food and beverages should be doubled.
The main source of sodium for humans are meat dishes and table salt added to meals and to preserved food during its preparation. Sodium can also come from such sources as: baking soda, local spices or neutralizing agents. The minimum human demand for this element ranges from 500 to 1000 mgNa/24h, though average daily amount we deliver in food ranges from 2,500-5,000 mg Na/24h and it frequently reaches the value of 6,000 mg/24h.
The increase in sodium intake up to approx. 16,000 mg/24 h does not result in any significant changes in blood pressure and such amount of Na often in food is recommended to long-distance runners taking exercises in high ambient temperatures [1]. The delivery of 21-27 g/24h per day in food increases the risk of hypertension.
Decreasing the amount of consumed sodium leads to the reduction in blood pressure. The hypotensive effect of low-sodium diet is a result of changes in electrolyte and water content and hormonal changes accompanying the drop in sodium concentration in the body [5].
The currently available literature provides a lot of information concerning water-electrolyte changes occurring in the body under the influence of thermal stress. Although, relatively little is known about the changes in systemic response to heat load under the conditions of low-sodium diet. The studies of Armstrong et al. [2] show that low-sodium diet does not exclude the development of thermal acclimation in people and it seems that it should not disable body to efficiently respond to a single heat stress, though presumably different may be the response model to the thermal stress under the shortage of sodium ions.
The aim of this paper was to assess the changes of physiological and metabolic markers after a single thermal stress in the participants being on a low-sodium diet.
Material and method
The study included 11 healthy males non-exercising and non-acclimating to heat. The participants were volunteers (aged 21.44±0.91 years, body height 178.3±2.28 cm, body weight 72.54±4.97 kg) and before the experiment they were informed about the aim and investigation schedule. The investigation schedule was given a permission from the Bioethical Investigation Commission at the Academy of Physical Education, Katowice.
The participants took part in two research tasks.
In the first of them (C-HS) 3 days before the planned impact of thermal stress they consumed mixed food (diet) (C) in which they received 3,200 mgNa/24 h/person and 4,300 mgK/24h/person. In the second task (L-Na-HS) for 3 days they received a low-sodium diet (L-Na) with significantly reduced sodium concentration: down to 539 mgNa/24h/person. The sodium content in this diet amounted to 3,900 mgK/24h/person. The caloric value of both diets was similar and amounted to 3200kcal?75kg-1?24h-1. While receiving both diets participants drank low-electrolyte liquids at the amount of approx. 3 l/24h. The diet type taken by participants was subject to randomization.
On the third day of consuming a particular diet, participants were subject to heat stress. The heat stress (HS) was always applied by staying in dry sauna (sauna temperature amounted to 85°C, whereas its relative humidity did not exceed 25%) for approx. 90 minutes with two several minute brakes for taking a cold shower) [7]. After the stay in sauna and cooling down the body participants recovered for 2h (at that time they did not refill the water loss resulted from staying in sauna). After completing the rest till to the end of 24h recovery they received in particular groups: C-HS – control diet, whereas L-Na-HS a low-sodium diet and they drank low-electrolyte liquids at the amount of at least 3 l/24h.
Before the experiment, after diet, heat stress and the 24 hour long recovery period, the samples of vein blood were collected in order to test the following values: aldosterone concentration (Aldo)-RIA DSL8600 USA, cortisol (Cort)-RIA DSL2100, USA, haemoglobin (Hb) by spectrophotometric method HEMOCUE, Sweden, total protein content (TP) by spectrophotometric method, ANALCO, Poland, and the haematocrite index. In the blood plasma the tests assessed the following concentration levels: sodium (Na+) and potassium (K+) by using a flame spectrophotometer manufactured by EPENDORF-EFOX, Germany. Prior to and after heat stress internal temperature (ELLAB, Denmark) and systolic and diastolic blood pressure were measured. They also assessed the changes in body mass and body composition after receiving the diet and after the heat stress in both tasks (weight, bioimpedance TANITA, Poland) and the changes in water distribution in body water compartments [4].
The results were subject to standard statistical analysis using the packet of Statistica (ANOVA) software. Checking the difference in significance between obtained values were based on the variance analysis and the Newman-Keuls post-hoc test. Corrected values were subject to assessment, where the correction included the changes in plasma volume resulting from diet and heat stress, affecting the assessed blood plasma parameters.
Results
The applied low-sodium diet resulted in a significant body mass reduction of participants (approx. 2%) (Table 1) and a considerable increase in cell volume (CV). (Figure 1) that maintained within the whole experiment.
Table 1. Changes in body mass caused by diet and heat stress.
| Impact type | [kg] | [%] |
| 1. Low-sodium diet (L-Na) | 1.55 | 1.98 |
| 2. Heat stress after control diet (C-HS) | 1.35 | 1.89 |
| 3. Heat stress after low-sodium diet (L-Na-HS) | 1.0 | 1.34 |
Fig. 1. Percentage changes of extra- (DPV%) and intracellular (DCV%) water volumes after diet, heat stress and after 24h recovery, in control and experimental group.
The changes in water distribution in water compartments (spaces) involved slight changes in the concentration of Na and a significant increase in the concentration of K and Aldo (3x) (Figure 1). A slight increase was also observed in the case of Cort concentration (the reduction in plasma volume connected with diet was taken into account) (Figure 2). The internal temperature, though slightly lower after the L-Na diet did not significantly differ before heat stress in both investigation tasks (Figure 4). The arterial blood pressure was lower by 5 mmHg after the L-Na diet than after the C type. The difference in blood pressure values between groups maintained also after heat stress.
Fig. 2. Changes of blood aldosterone and cortysole concentration after diet, heat stress and after 24h recovery, in control and experimental group.
Fig. 3. Changes of plasma sodium concentration after diet, heat stress and after 24h recovery, in control and experimental group.
Fig. 4. Changes of plasma potassium concentration after diet, heat stress and after 24h recovery, in control and experimental group.
Fig. 5. Body temperature at rest (before diet) after ingestion control or low-sodium diet after heat stress and after 24h recovery in control and experimental group.
The heat stress caused an increase in internal temperature (Figure 4) and the loss of water in the control group from both water compartments, while in the L-Na group mainly from extra-cellular space (ECV). In addition, the applied heat stress (HS) resulted in the increase of aldosterone concentration in both investigation tasks reaching 406±83 in the C-HS task, whereas 997±227 pg/ml in the L-Na-HS tasks. After a 24h recovery, the concentration of Aldo in the control group returned to the pre-stress level and was still 3 times higher in the L-Na group. The concentration of cortisol increased after the HS only in the control group. After the 24h recovery its concentration returned to the rest value in the control group, whereas in the L-Na-HS group decreased below the levels registered at rest, and went down even below the levels noted for the control group. The heat stress applied did not cause any significant changes in the concentration of Cort in the L-Na-HS group (Figure 2).
The rest concentration of potassium was higher in the group being on L-Na diet than in the control group while in the case of sodium it did not differ much between both groups. Heat stress resulted in similar growth of Na concentration in both groups. The concentration of potassium after HS increased by 3% in the control group and by 6% in the group being on the L-Na diet. After the 24h recovery under the condition of taking the same amount of low-electrolyte liquids the tests showed: a drop in sodium blood plasma level (its concentration reached a similar level as at rest) whereas in the L-Na-HS group the deficiency of sodium still maintained (that was not seriously increased by heat stress) (Figure 3). The concentration of K decreased after the 24h recovery in both tasks, though it was still significantly higher in the L-Na-HS group than in C-HS.
Discussion
The heat stress applied during this study resulted in a significant body mass reduction in both groups (Table 1). The amount of water lost was higher in the group on the mixed diet. In this group the water lost came from both body volumes. Hayes et al. [6] think that failing to refill the lost liquids within 2 hours of rest does not exclude the possibility of decreasing the level of ECV after heat stress caused by physical exercise. After the 2h rest in the mixed diet group (without supplementing water deficiency) the tests showed a progressing improvement in re-hydration resulted from moving water from inactive body areas.
The ingestion of L-Na diet was accompanied by typical sodium reduction in diet, body mass reduction and shifting water to the intracellular volume. The heat stress applied under such conditions resulted in increased water loss from extra-cellular space, at the same time it did not decrease the amount of intracellular volume (ICV). Within the 2h rest no decrease in water deficiency in ECV was observed, whereas there was some water excess in ICV. Making up for water loss caused by HS (drinking liquids at the amount not less than 3 l/24h) at the lack of sodium intake did not contribute to efficient re-hydration in ECV. Only increasing the sodium intake during recovery could improve the state of hydration and recover a proper water distribution in water compartments of the body.
In earlier studies the author found that [8] the total sodium deficiency caused by a low-sodium diet (L-Na) amounted to 70.72 mmol which involved the loss of approx. 530 ml of water from intracellular space (ICV) and 690ml from extra-cellular (ECV). Hargreaves et al. [5] believe that reducing sodium in diet down to the level of 50-150 mmol/24h/person does not reduce the ability to physical effort at high ambient temperatures despite increased rennin activity and intensified sodium-saving.
Some latest studies show a significant increase in aldosterone concentration after a L-Na diet. Francesconi et al. [9] think that the increase in secretion of Aldo during heat stress is proportional to the initail liquid deficiency. The level of Aldo secretion observed in current investigations stays in contrast to the above-mentioned information. A loss in body mass induced by the diet or sauna was similar (Table 1), which shows a similar water shortage in the body in both cases but in the group being on L-Na diet the secretion of Aldo was by 3 times higher than in the participants being on the control diet. It seems that under the conditions of similar loss in systemic water the stronger impulse to increased aldosterone secretion was the clear difference in proportion Na:K in the blood plasma of the L-Na-HS group than in the C-HS.
As shown by the results, the volume of plasma decreased by diet and HS was not compensated despite recovery and refilling systemic liquids. That is why sodium deficiency maintained and contributed to: keeping water deficiency in the extra-cellular volume and triggering volume receptors. The created conditions should stimulate the body to activate water and electrolyte-saving mechanisms.
The heat stress in participants being on the L-Na diet resulted in a higher internal temperature during HS, thus showing that sodium deficiency is accompanied by reducing the effect of heat dispersion by sweat evaporation, as a result of reduced water availability to sweat glands.
Conclusions
Summing up, we can show that receiving a low-sodium diet has a significant impact on a lot of responses triggered by the body during heat stress including the reduction in sweat released, thus contributing to heat accumulation in the body. Despite triggering the sodium- and water-saving reactions very limited re-hydration was observed during the 24 hour recovery period.
Piśmiennictwo
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