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Clinical Science ( 1989)76,553-557 553 Exercise tolerance in the heat on low and normal salt intakes M. HARGREAVES", T. 0. MORGAN", R. SNOWt AND M. GUERINS *Department of Physiology, University of Melbourne, Parkville, +Departmentof Physical Education and Recreation, Footscray Institute of Technology, Footscray, and +Departmentof Biochemistry, Repatriation General Hospital, Heidelberg, Australia (Received 6 June/22 August 1988; accepted 4 October 1988) SUMMARY 1. Salt restriction is recommended in the treatment of hypertension and is included in national dietary guidelines, but its effect on exercise in hot conditions has not been extensively studied. 2. The effects of 2 weeks on two levels of salt intake (50 and 150 mmol/day) on the ability to exercise (60% of maximal oxygen uptake) in a. hot environment (35°C) were studied in eight healthy normotensive subjects. 3. All subjects were able to complete the exercise load on the two levels of salt intake. No differences in mean oxygen uptake, heart rate or rectal temperature during exercise were observed between the two salt intakes. 4. Plasma sodium, potassium and osmolality were similar on the two salt intakes both before and during exercise. Plasma renin activity and aldosterone concentration were elevated after 2 weeks on the reduced salt intake and remained so during exercise. 5. The estimated sweat rate during exercise was similar on the two salt intakes but the loss of sodium was less on the low salt intake. 6. On the basis of these results it is concluded that moderate salt restriction does not impair the ability to exercise in a hot environment. Key words: aldosterone, diet, exertion, renin, sodium restriction. Abbreviations: ANG I, angiotensin I; Vo, max., maximal oxygen uptake. INTRODUCTION In recent years dietary salt restriction has been advocated in the management of hypertension [ 1, 21. Restriction of sodium intake has also been included in the nutritional goals of a number of countries [3,4]. It has been suggested that this approach may increase the risks associated with the physiological stress of exercise, heat exposure or Correspondence: Professor T.O. Morgan, Department of Physiology, University of Melbourne, Parkville, 3052, Australia. volume depletion [5, 61. Since regular exercise has also been shown to lower blood pressure [7], and may be used in combination with salt restriction [8], it is important to determine whether individuals on a reduced salt intake are at increased risk during exercise, especially when performed in a hot environment. Early work examining this question [9] suggested that exercise-heat tolerance was impaired on a 'low' salt intake (103 mmol/day) compared with a 'moderate' intake (259 mmol/day). In contrast, Armstrong et al. [lo]have demonstrated that the ability to exercise in the heat on repeated days is unaffected by a reduction in salt intake from 400 to 100 mmol/day. The present study was undertaken to further examine the effect of moderate salt restriction (50 mmol/day) on the physiological responses to combined exercise and heat stress. METHODS Eight male adults [23.4f 1.1 years, maximal oxygen uptake ( vo, max.) = 4.05 k 0.24 I/&, mean fSEMI with normal blood pressure (see Table 1)agreed to take part in this study after being informed of the risks and stresses associated with the protocol and having given written consent. The study was approved by the ethics committees of the University of Melbourne and Footscray Institute of Technology. The subjects were physically active but were neither specifically trained nor heat acclimatized, and were familiar with the exercise procedures used in the laboratory. In consultation with a dietitian, subjects selected a range of foods to produce a daily sodium intake of approximately 50 mmol and maintained this diet for 4 weeks. For two 2-week periods subjects ingested either slow sodium (Ciba-Geigy, 100 mmol/day; CON) or placebo tablets (LOW), with a randomized, double-blind cross-over design, so that sodium intakes of 150 and 50 mmol/day, respectively, would be obtained. Four subjects received slow sodium tablets first; the remaining four received placebo. Dietary adherence was checked by 24 h urine collections on the last 2 days of each 2-week period. At the end of each 2-week period exercise-heat tolerance M. Hargreaves et al. 554 was assessed during 60 min of cycling exercise at a workload requiring approximately 60% of maximal oxygen uptake ( Vo2max.), in a heat chamber maintained at 35°C and 25% relative humidity. Subjects reported to the laboratory on the morning of a trial after an overnight fast and were weighed nude on a Sauter balance ( k5 g). A thermistor probe (Yellow Springs Instrument) was positioned to a depth of 10 cm to monitor rectal temperature. A catheter was inserted into a forearm vein and after sitting quietly for 15-20 min the resting blood sample was obtained. Subjects then entered the chamber and commenced exercise on a Monark bicycle ergometer. Heart rates (cardiac auscultation) and rectal temperatures were recorded every 10 min during exercise. Expired air was collected in Douglas bags for oxygen uptake determination using Applied Electrochemistry oxygen and carbon dioxide gas analysers and a Parkinson-Cowan gas meter, calibrated against a Tissot spirometer. Venous blood samples were obtained at 15, 30 and 60 min of exercise and these, together with the resting sample, were analysed for sodium, potassium, osmolality, plasma renin activity and plasma aldosterone concentration. On completion of the exercise subjects exited the chamber, sweat samples were obtained using a washdown technique [ 111, and post-exercise body weight was measured. No fluid was ingested during exercise. Blood for electrolytes, osmolality and aldosterone was collected in chilled tubes containing a small amount of lithium heparin; the tubes for plasma renin activity contained ethylenediaminetetra-acetate. These samples were centrifuged and the plasma stored at -80°C until analysis, except that for electrolytes which remained on ice and was analysed later on the same day. Plasma sodium and potassium were measured using indirect reading ion-selective electrodes, while urine and sweat samples were analysed by flame photometry. Osmolality was measured on a vapour pressure osmometer (Wescor Inc, Logan, UT, U.S.A.). Plasma renin activity (Biodata Labs, Rome, Italy) and plasma aldosterone concentration (Diagnostic Products Corporation, Los Angeles, CA, U.S.A.) were measured by radioimmunoassay. On the day before the exercise-heat tolerance test, maximal exercise performance was assessed during a 30 s maximal effort on an air-braked cycle ergometer (Repco, Melbourne, Australia). Peak power and total work were obtained from an Exertech work monitor unit, interfaced with the ergometer. The data from the two trials were compared using a paired t-test and where appropriate analysis of variance for repeated measures. The slopes of the aldosteronetime plots were obtained using linear regression analysis. Data are reported as means fSEM. RESULTS All subjects successfully modified their dietary sodium intakes and achieved the target sodium intake on placebo, 49 f7 mmol/day. When slow sodium tablets (100 mmol/ day) were given the 24 h urinary sodium excretion increased to a mean of 155 k 18 mmol/day, significantly greater ( P < O . O O l ) than on placebo. Body weight on placebo was 70.9 f 1.8 kg, which was not different from the value of 71.4 f 1.6 on slow sodium tablets. Resting blood pressures were similar after 2 weeks on the two diets [CON= 129/66 mmHg (17.2/8.8 kPa), LOW= 123/ 6 3 mmHg (16.4/8.4 kPa)J. The effects of 100 mmol of sodium/day on baseline variables are summarized in Table 1. Table 1. Baseline variables after 2 weeks on either a normal (CON) or reduced (LOW) sodium intake Values are means k SEM ( n = 8). Statistical significance: *P<0.05, **P<0.01, ***P<0.001 compared with CON. Blood pressure: to convert mmHg to kPa, divide by 7.5. CON Body weight (kg) Heart rate (beats/min) Blood pressure (mmHg) Systolic Diastolic Urine electrolytes (mmol/day) Sodium Potassium Chloride Creatinine Urea Plasma electrolytes (mmol/l) Sodium Potassium Chloride Creatinine Urea Plasma osmolality (mosmol/kg) Plasma renin activity(pmo1of ANG I h - ' ml-I) Plasma aldosterone (pmol/l) LOW 71.4k 1.6 59-13 70.9 k 1.8 64+4* 129k4 66-13 123-14 63+3 155+ 18 83-19 159k 16 14.5 k 0.8 380 k 27 49 7*** 9 4 k 13 63 k 5*** 15.1 -1 1.2 354 -1 35 + 138.6 0.4 4.0k0.1 102.8 k 0.8 0.09 k 0.001 5.8 k 0.5 275k 1 1.5 k 0.2 277 f 36 + 139.3 k 0.5 4.0-10.1 100.4 f 0.6 0.10 -10.00 1 5.6 k 0.5 275 k 2 2.6 k 0.2*** 780 k 144** Sodium intake and exercise-heat tolerance The subjects reported no side effects on either diet and did not complain of any tiredness or lethargy while on the reduced sodium intake. All subjects were able to complete the full 60 min of exercise in the heat on both low and normal sodium intakes. Oxygen uptake (CON=2.30f0.14 l/min, LOW=2.35+0.12 I/min), heart rate (CON = 158 f5 beats/min, LOW= 161 f3) and rectal temperature (CON = LOW= 38.0 fO.l°C) during exercise were similar on the two sodium intakes. Body weight loss during exercise was similar on the two diets (CON= 1.27 f 0.1 1 kg, LOW= 1.26 f0.09 kg). There were no differences between diets in plasma sodium or potassium either before or during exercise (Fig. 1).The exercise-heat exposure resulted in significant elevations in these plasma electrolytes, the greater being in potassium. The concentration of sodium in the sweat on the low sodium intake (38.4k5.2 mmol/l) was lower (P<0.01) than the corresponding value of the normal sodium intake (49.7 f 4.3 mmol/l). The concentration of potassium in the sweat did not differ between diets (Table 2). The sweat rate, estimated from the body weight loss corrected for respiratory and metabolic water losses, did not differ between the two diets (Table 2); however, the amount of sodium lost during exercise on the low sodium intake was lower than on the normal sodium intake (Table 2). Plasma aldosterone was higher at rest after 2 weeks on a low sodium intake (LOW=780+ 144 pmol/l, CON = 277 k 36 pmol/l, P< 0.01) and remained so during exercise (Fig. 2). Plasma r e i n activity demonstrated a similar pattern with both resting [LOW=2.6+0.2 pmol of angiotensin I (ANG I) h-' ml-l, CON=1.5+0.2 pmol of ANG I h-I ml-l P<O.OOl] and exercise levels being higher after 2 weeks on the low sodium intake (Fig. 2). Maximal exercise performance was similar on the two diets, being unaffected by the level of sodium intake. There were no differences in either peak power (LOW= 926 f 50 W, CON = 974 f38 W) or total work (LOW= 2 1.2 k 1.1 kJ, CON = 21.6 f0.8 kJ). DISCUSSION In the present study the exercise workloads and the environmental conditions did not differ for the two levels of sodium intake. Exercise-heat tolerance was assessed by 555 the physiological response to the combined exercise and heat stress under these standardized conditions, i.e. an exaggerated heart rate and rectal temperature response or an inability to complete the 60 min of exercise after the reduced sodium intake would indicate impaired exerciseheat tolerance. All subjects completed the full 60 min of exercise on both diets and there were no differences in 142 1 T T / d 6 I T /=- I t f !! 0 I I I 15 30 60 Exercise time (min) Fig. 1. Plasma sodium and potassium before and during exercise in the heat after 2 weeks on either a normal (CON, 0 ) or reduced (LOW, 0)sodium intake. Values are means fSEM (n= 8). No differences were seen between trials; however, all exercise values were higher (P<0.05) than the respective value before exercise. Table 2. Sweat rate and composition during exercise after 2 weeks on either a normal (CON) or reduced (LOW) sodium intake Values are means f SEM (n= 7). Statistical significance: *P<0.01, **P< 0.001, compared with CON. CON ~~ LOW ~ Estimated sweat rate (I/h) Sweat sodium (mmol/l) Sodium loss (mmol/h) Sweat potassium (mmol/l) Potassium loss (mmol/h) 1.15 f 0.1 1 49.7f 4.3 54.8f 2.9 3.7f 0.4 4.2f 0.5 1.12 f 0.09 38.4f5.2* 40.6 3.6** 4.0f 0.3 4.5f 0.6 * M. Hargreaves et al. 556 T * * , *** $/f d 6 although plasma volume was not measured, the similarity in body weights before exercise suggests that the hydration state of the subjects was similar on the two sodium intakes. It has been reported that severe salt restriction in rats increases the risks associated with certain kinds of stress (e.g. trauma, haemorrhage) by modifying cardiovascular and sympathetic function [14]. In the present study, we observed no differences in the heart rate response to exercise between diets. Furthermore, the level of sodium restriction was fairly modest (50 mmol/day). Perhaps more severe sodium restriction would produce the negative effects that have been observed in rats. A potential limitation in the present study may be the inability to detect differences between diets with a relatively small sample size ( I I = 8). The differences between the diets for maximal heart rate and rectal temperature were 3.75 f2.8 beats/min and 0.08 0.09”C (mean fSEM), respectively. With 80% power these differences would have been as high as 7 beats/min and 0.22”C, these values being 4% and O.6%, respectively, of the observed maximal responses. Thus, if there were differences in responses betweeen diets in the present study they were probably minor and of little physiological significance. Plasma renin activity and aldosterone levels were higher after the low sodium intake and increased during the exercise-heat exposure in both trials (Fig. 2), the increases being similar in magnitude to those previously reported for an equivalent exercise-heat stress [15]. The exercise-induced increase in plasma renin activity is closely related to the enhanced sympathoadrenal activity during exercise [ 161, although alterations in plasma volume and osmolality may also be important [17]. It has been shown that plasma renin activity during exercise can be influenced by the level of dietary sodium [18, 191; a similar result was obtained in the present study (Fig. 2). The increase in angiotensin I1 levels [ 191, resulting from an increase in renin activity, is a major stimulus for aldosterone secretion during exercise [ 191, but increases in plasma potassium (Fig. 1) and adrenocorticotropic hormone levels are also likely to be involved in stimulating aldosterone release. The absolute increase in plasma aldosterone during exercise (CON = 1.227f 175 pmol/l, LOW=2325+336 pmol/l) and the slope of the aldosterone-time relationship were greater ( P < 0.05) on the reduced sodium intake. Previously, in humans, it has been demonstrated that the stimulatory effect of angiotensin I1 on aldosterone release is attenuated with increasing dietary sodium intake [ 191. Furthermore, sodium restriction alters the adrenal sensitivity and response to angiotensin I1 stimulation [20].The results of the present study are in line with these observations. Another. hormone that may be important is antidiuretic hormone. In the present study there were no differences in plasma osmolality either before or during exercise. Since the increase in plasma antidiuretic hormone levels during exercise is closely related to the increase in plasma osmolality [ 171, it is likely that antidiuretic hormone levels during exercise on the two diets were similar. Furthermore, a previous study has shown little effect of sodium depletion, more * 32220 3301 t 1 I 1 0 15 30 60 Exercise time (min) Fig. 2. Plasma renin activity (PRA) and plasma aldosterone concentration (PAC) before and during exercise in the heat after 2 weeks on either a normal (CON, 0 ) or reduced (LOW, 0)sodium intake. Values are means fSEM ( n= 6-8). Statistical significance: *P<O.O5, **P< 0.01, ***P<0.001, compared with CON. exercise heart rates or rectal temperatures between trials. Thus, it appears that moderate salt restriction did not impair exercise-heat tolerance. Recently it has been demonstrated that the process of heat acclimatization in man is unaffected by the level of dietary sodium [lo]. Furthermore, rats placed on an extremely sodiumdeficient diet did not exhibit circulatory hyponatraemia or decrements in endurance exercise performance in the heat [12]. These authors suggested that the hormonal responses to the low sodium intake were important in maintaining plasma sodium levels and exercise performance. In the present study there were no differences in plasma sodium either before or during exercise (Fig. 1) despite the threefold difference in dietary sodium intake, most likely the result of the increases in plasma renin activity and aldosterone (Fig. 2). Two important factors influencing thermal balance during exercise are plasma volume and osmolality [ 131. In the present study no differences in plasma osmolality were observed between diets either before or during exercise. Furthermore, Sodium intake and exercise-heat tolerance severe than in the present study, on plasma antidiuretic hormone levels 1211. It has been suggested that alterations in sodium intake may influence the intracellular calcium level in vascular smooth muscle cells and, as a result, the blood pressure [22]. Thus, an increase in sodium intake ultimately leads to an increase in intracellular calcium in smooth muscle and a more forceful contraction when stimulated [22].It is presumed that a reduction in sodium intake results in an opposite effect [22]. Whether such a mechanism operates in skeletal muscle, where intracellar calcium is well buffered by the sarcoplasmic reticulum, is speculation. Nevertheless, we though it of interest to examine whether a reduction in sodium intake had any negative effect on muscle performance during maximal dynamic exercise. While there was no differencebetween diets in total work output during maximal exercise, peak power was slightly lower (P=O.lO) after 2 weeks on the reduced sodium intake. Thus, the effect of alterations in sodium intake on muscle performance may warrant further investigation. The results of the present study indicate that moderate dietary sodium restriction does not impair the ability to exercise in a hot environment and infer that advice to reduce salt intake can be given safely. ACKNOWLEDGMENTS We thank Rosemary Snowden, Caryl Nowson and Janet Cripps for their assistance during this study. M.H. was supported by the National Health and Medical Research Council of Australia. REFERENCES 1. Morgan, T.O., Gillies, A., Morgan, G., Adam, W., Wilson, M. & Carney, S. (1978)Hypertension treated by salt restriction. Lancet, ii, 473-476. 2. Macgregor, G.A., Markandu, N.D., Best, F.E., Elder, D.M., Cam, J.M., Sagnella, G.A. & Squires, M. (1982) Doubleblind randomized crossover trial of moderate sodium restriction in essential hypertension. Lancet, i, 351-355. 3. U.S. Department of Agriculture and Department of Health and Human Services (1985) Dietary Guidelines for Americans, 2nd edn. Human Nutrition Information Service, U.S. Department of Agriculture, Washington, D.C. 4. National Health and Medical Research Council of Australia (1987) Recommended Dietary Intakes for Use in Australia. Australian Government Publishing Service, Canberra. 5. Brown, J.J., Lever, A.F., Robertson, J.I.S., Semple, P.F., Bing, R.F., Heagerty, A.M., Swales, J.D., Thurston, H., Ledingham, J.G.G., Laragh, J.H., Hansson, L., Nicholls, M.G. & Espiner, A.E. (1984)Salt and hypertension. Lancer, ii, 456. 6. Laragh, J.H. & Pecker, M.S. (1983) Dietary sodium and essential hypertension: some myths, hopes, and truths. Annals of Internal Medicine, 98,735-743. 557 7. Nelson, L., Jennings, G.L., Esler, M.D. & Korner, P.I. (1986) Effect of changing physical activity on blood pressure and haemodynarnics in essential hypertension. Lancet, ii, 473-476. 8. Nomura, G., Kumagai, E., Midorikawa, K., Kitano, T., Tashiro, H. & Toshima, H. 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