Three Independent Biological Mechanisms Cause Exercise-Associated Hyponatremia: Evidence from 2,135 Weighed Competitive Athletic Performances
To evaluate the role of fluid and Na+ balance in the development of exercise-associated hyponatremia (EAH), changes in serum Na+ concentrations ([Na+]) and in body weight were analyzed in 2,135 athletes in endurance events. Eighty-nine percent of athletes completed these events either euhydrated (39...
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| Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 102; no. 51; pp. 18550 - 18555 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
National Academy of Sciences
20.12.2005
National Acad Sciences |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0027-8424 1091-6490 |
| DOI | 10.1073/pnas.0509096102 |
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| Abstract | To evaluate the role of fluid and Na+ balance in the development of exercise-associated hyponatremia (EAH), changes in serum Na+ concentrations ([Na+]) and in body weight were analyzed in 2,135 athletes in endurance events. Eighty-nine percent of athletes completed these events either euhydrated (39%) or with weight loss (50%) and with normal (80%) or elevated (13%) serum [Na+]. Of 231 (11%) athletes who gained weight during exercise, 70% were normonatremic or hypernatremic, 19% had a serum [Na+] between 129-135 mmol/liter, and 11% a serum [Na+] of <129 mmol/liter. Serum [Na+] after racing was a linear function with a negative slope of the body weight change during exercise. The final serum [Na+] in a subset of 18 subjects was predicted from the amount of Na+ that remained osmotically inactive at the completion of the trial. Weight gain consequent to excessive fluid consumption was the principal cause of a reduced serum [Na+] after exercise, yet most (70%) subjects who gained weight maintained or increased serum [Na+], requiring the addition of significant amounts of Na+ (>500 mmol) into an expanded volume of total body water. This Na+ likely originated from osmotically inactive, exchangeable stores. Thus, EAH occurs in athletes who (i) drink to excess during exercise, (ii) retain excess fluid because of inadequate suppression of antidiuretic hormone secretion, and (iii) osmotically inactivate circulating Na+ or fail to mobilize osmotically inactive sodium from internal stores. EAH can be prevented by insuring that athletes do not drink to excess during exercise, which has been known since 1985. |
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| AbstractList | To evaluate the role of fluid and Na+ balance in the development of exercise-associated hyponatremia (EAH), changes in serum Na+ concentrations ([Na+]) and in body weight were analyzed in 2,135 athletes in endurance events. Eighty-nine percent of athletes completed these events either euhydrated (39%) or with weight loss (50%) and with normal (80%) or elevated (13%) serum [Na+]. Of 231 (11%) athletes who gained weight during exercise, 70% were normonatremic or hypernatremic, 19% had a serum [Na+] between 129-135 mmol/liter, and 11% a serum [Na+] of <129 mmol/liter. Serum [Na+] after racing was a linear function with a negative slope of the body weight change during exercise. The final serum [Na+] in a subset of 18 subjects was predicted from the amount of Na+ that remained osmotically inactive at the completion of the trial. Weight gain consequent to excessive fluid consumption was the principal cause of a reduced serum [Na+] after exercise, yet most (70%) subjects who gained weight maintained or increased serum [Na+], requiring the addition of significant amounts of Na+ (>500 mmol) into an expanded volume of total body water. This Na+ likely originated from osmotically inactive, exchangeable stores. Thus, EAH occurs in athletes who (i) drink to excess during exercise, (ii) retain excess fluid because of inadequate suppression of antidiuretic hormone secretion, and (iii) osmotically inactivate circulating Na+ or fail to mobilize osmotically inactive sodium from internal stores. EAH can be prevented by insuring that athletes do not drink to excess during exercise, which has been known since 1985. To evaluate the role of fluid and Na + balance in the development of exercise-associated hyponatremia (EAH), changes in serum Na + concentrations ([Na + ]) and in body weight were analyzed in 2,135 athletes in endurance events. Eighty-nine percent of athletes completed these events either euhydrated (39%) or with weight loss (50%) and with normal (80%) or elevated (13%) serum [Na + ]. Of 231 (11%) athletes who gained weight during exercise, 70% were normonatremic or hypernatremic, 19% had a serum [Na + ] between 129-135 mmol/liter, and 11% a serum [Na + ] of <129 mmol/liter. Serum [Na + ] after racing was a linear function with a negative slope of the body weight change during exercise. The final serum [Na + ] in a subset of 18 subjects was predicted from the amount of Na + that remained osmotically inactive at the completion of the trial. Weight gain consequent to excessive fluid consumption was the principal cause of a reduced serum [Na + ] after exercise, yet most (70%) subjects who gained weight maintained or increased serum [Na + ], requiring the addition of significant amounts of Na + (>500 mmol) into an expanded volume of total body water. This Na + likely originated from osmotically inactive, exchangeable stores. Thus, EAH occurs in athletes who ( i ) drink to excess during exercise, ( ii ) retain excess fluid because of inadequate suppression of antidiuretic hormone secretion, and ( iii ) osmotically inactivate circulating Na + or fail to mobilize osmotically inactive sodium from internal stores. EAH can be prevented by insuring that athletes do not drink to excess during exercise, which has been known since 1985. To evaluate the role of fluid and Na+ balance in the development of exercise-associated hyponatremia (EAH), changes in serum Na+ concentrations ([Na+]) and in body weight were analyzed in 2,135 athletes in endurance events. Eighty-nine percent of athletes completed these events either euhydrated (39%) or with weight loss (50%) and with normal (80%) or elevated (13%) serum [Na+]. Of 231 (11%) athletes who gained weight during exercise, 70% were normonatremic or hypernatremic, 19% had a serum [Na+] between 129-135 mmol/liter, and 11% a serum [Na+] of <129 mmol/liter. Serum [Na+] after racing was a linear function with a negative slope of the body weight change during exercise. The final serum [Na+] in a subset of 18 subjects was predicted from the amount of Na+ that remained osmotically inactive at the completion of the trial. Weight gain consequent to excessive fluid consumption was the principal cause of a reduced serum [Na+] after exercise, yet most (70%) subjects who gained weight maintained or increased serum [Na+], requiring the addition of significant amounts of Na+ (>500 mmol) into an expanded volume of total body water. This Na+ likely originated from osmotically inactive, exchangeable stores. Thus, EAH occurs in athletes who (i) drink to excess during exercise, (ii) retain excess fluid because of inadequate suppression of antidiuretic hormone secretion, and (iii) osmotically inactivate circulating Na+ or fail to mobilize osmotically inactive sodium from internal stores. EAH can be prevented by insuring that athletes do not drink to excess during exercise, which has been known since 1985.To evaluate the role of fluid and Na+ balance in the development of exercise-associated hyponatremia (EAH), changes in serum Na+ concentrations ([Na+]) and in body weight were analyzed in 2,135 athletes in endurance events. Eighty-nine percent of athletes completed these events either euhydrated (39%) or with weight loss (50%) and with normal (80%) or elevated (13%) serum [Na+]. Of 231 (11%) athletes who gained weight during exercise, 70% were normonatremic or hypernatremic, 19% had a serum [Na+] between 129-135 mmol/liter, and 11% a serum [Na+] of <129 mmol/liter. Serum [Na+] after racing was a linear function with a negative slope of the body weight change during exercise. The final serum [Na+] in a subset of 18 subjects was predicted from the amount of Na+ that remained osmotically inactive at the completion of the trial. Weight gain consequent to excessive fluid consumption was the principal cause of a reduced serum [Na+] after exercise, yet most (70%) subjects who gained weight maintained or increased serum [Na+], requiring the addition of significant amounts of Na+ (>500 mmol) into an expanded volume of total body water. This Na+ likely originated from osmotically inactive, exchangeable stores. Thus, EAH occurs in athletes who (i) drink to excess during exercise, (ii) retain excess fluid because of inadequate suppression of antidiuretic hormone secretion, and (iii) osmotically inactivate circulating Na+ or fail to mobilize osmotically inactive sodium from internal stores. EAH can be prevented by insuring that athletes do not drink to excess during exercise, which has been known since 1985. To evaluate the role of fluid and Na + balance in the development of exercise-associated hyponatremia (EAH), changes in serum Na + concentrations ([Na + ]) and in body weight were analyzed in 2,135 athletes in endurance events. Eighty-nine percent of athletes completed these events either euhydrated (39%) or with weight loss (50%) and with normal (80%) or elevated (13%) serum [Na + ]. Of 231 (11%) athletes who gained weight during exercise, 70% were normonatremic or hypernatremic, 19% had a serum [Na + ] between 129-135 mmol/liter, and 11% a serum [Na + ] of <129 mmol/liter. Serum [Na + ] after racing was a linear function with a negative slope of the body weight change during exercise. The final serum [Na + ] in a subset of 18 subjects was predicted from the amount of Na + that remained osmotically inactive at the completion of the trial. Weight gain consequent to excessive fluid consumption was the principal cause of a reduced serum [Na + ] after exercise, yet most (70%) subjects who gained weight maintained or increased serum [Na + ], requiring the addition of significant amounts of Na + (>500 mmol) into an expanded volume of total body water. This Na + likely originated from osmotically inactive, exchangeable stores. Thus, EAH occurs in athletes who ( i ) drink to excess during exercise, ( ii ) retain excess fluid because of inadequate suppression of antidiuretic hormone secretion, and ( iii ) osmotically inactivate circulating Na + or fail to mobilize osmotically inactive sodium from internal stores. EAH can be prevented by insuring that athletes do not drink to excess during exercise, which has been known since 1985. endurance exchangeable Na+ stores fluid overload overdrinking syndrome of inappropriate ADH secretion To evaluate the role of fluid and Na super(+) balance in the development of exercise-associated hyponatremia (EAH), changes in serum Na super(+) concentrations ([Na super(+)]) and in body weight were analyzed in 2,135 athletes in endurance events. Eighty-nine percent of athletes completed these events either euhydrated (39%) or with weight loss (50%) and with normal (80%) or elevated (13%) serum [Na super(+)]. Of 231 (11%) athletes who gained weight during exercise, 70% were normonatremic or hypernatremic, 19% had a serum [Na super(+)] between 129-135 mmol/liter, and 11% a serum [Na super(+)] of <129 mmol/liter. Serum [Na super(+)] after racing was a linear function with a negative slope of the body weight change during exercise. The final serum [Na super(+)] in a subset of 18 subjects was predicted from the amount of Na super(+) that remained osmotically inactive at the completion of the trial. Weight gain consequent to excessive fluid consumption was the principal cause of a reduced serum [Na super(+)] after exercise, yet most (70%) subjects who gained weight maintained or increased serum [Na super(+)], requiring the addition of significant amounts of Na super(+) (>500 mmol) into an expanded volume of total body water. This Na super(+) likely originated from osmotically inactive, exchangeable stores. Thus, EAH occurs in athletes who (i) drink to excess during exercise, (ii) retain excess fluid because of inadequate suppression of antidiuretic hormone secretion, and (iii) osmotically inactivate circulating Na super(+) or fail to mobilize osmotically inactive sodium from internal stores. EAH can be prevented by insuring that athletes do not drink to excess during exercise, which has been known since 1985. To evaluate the role of fluid and Na+ balance in the development of exercise-associated hyponatremia (EAH), changes in serum Na+ concentrations ([Na+]) and in body weight were analyzed in 2,135 athletes in endurance events. Eighty-nine percent of athletes completed these events either euhydrated (39%) or with weight loss (50%) and with normal (80%) or elevated (13%) serum [Na+]. Of 231 (11%) athletes who gained weight during exercise, 70% were normonatremic or hypernatremic, 19% had a serum [Na+] between 129-135 mmol/liter, and 11% a serum [Na+] of <129 mmol/liter. Serum [Na+] after racing was a linear function with a negative slope of the body weight change during exercise. The final serum [Na+] in a subset of 18 subjects was predicted from the amount of Na+ that remained osmotically inactive at the completion of the trial. Weight gain consequent to excessive fluid consumption was the principal cause of a reduced serum [Na+] after exercise, yet most (70%) subjects who gained weight maintained or increased serum [Na+], requiring the addition of significant amounts of Na+ (>500 mmol) into an expanded volume of total body water. This Na+ likely originated from osmotically inactive, exchangeable stores. Thus, EAH occurs in athletes who (i) drink to excess during exercise, (ii) retain excess fluid because of inadequate suppression of antidiuretic hormone secretion, and (iii) osmotically inactivate circulating Na+ or fail to mobilize osmotically inactive sodium from internal stores. EAH can be prevented by insuring that athletes do not drink to excess during exercise, which has been known since 1985.[PUBLICATION ABSTRACT] |
| Author | Myers, Norman T. D. Noakes J. Dugas T. Hew P. Wharam K. Sharwood D. Speedy S. Reid C. Almond L. Weschler |
| AuthorAffiliation | University of Cape Town/Medical Research Council Research Unit for Exercise Science and Sports Medicine, Department of Human Biology, University of Cape Town/Sports Science Institute of South Africa, Newlands, 7700, South Africa; ‡ Department of General Practice and Primary Care, University of Auckland, Aukland 1020, New Zealand; § Sports Medicine Practice, St. Helen's Hospital, Hobart 7216, Tasmania, Australia; ¶ Department of Cardiology, Children's Hospital, Boston, MA 02115; and ∥ 161 Richdale Road, Colts Neck, NJ 07722 |
| AuthorAffiliation_xml | – name: University of Cape Town/Medical Research Council Research Unit for Exercise Science and Sports Medicine, Department of Human Biology, University of Cape Town/Sports Science Institute of South Africa, Newlands, 7700, South Africa; ‡ Department of General Practice and Primary Care, University of Auckland, Aukland 1020, New Zealand; § Sports Medicine Practice, St. Helen's Hospital, Hobart 7216, Tasmania, Australia; ¶ Department of Cardiology, Children's Hospital, Boston, MA 02115; and ∥ 161 Richdale Road, Colts Neck, NJ 07722 |
| Author_xml | – sequence: 1 fullname: T. D. Noakes – sequence: 2 fullname: K. Sharwood – sequence: 3 fullname: D. Speedy – sequence: 4 fullname: T. Hew – sequence: 5 fullname: S. Reid – sequence: 6 fullname: J. Dugas – sequence: 7 fullname: C. Almond – sequence: 8 fullname: P. Wharam – sequence: 9 fullname: L. Weschler – sequence: 10 givenname: Norman surname: Myers fullname: Myers, Norman |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/16344476$$D View this record in MEDLINE/PubMed |
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| Notes | SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 Conflict of interest statement: No conflicts declared. Abbreviations: TBW, total body water; EAH, exercise-associated hyponatremia; EAHE, exercise-associated hyponatremic encephalopathy; SIADH, syndrome of inappropriate ADH secretion. Author contributions: T.D.N., K.S., D.S., T.H., S.R., J.D., C.A., and P.W. designed research; T.D.N., K.S., D.S., T.H., S.R., J.D., C.A., and P.W. performed research; T.D.N., C.A., and L.W. contributed new reagents/analytic tools; and T.D.N., K.S., D.S., T.H., S.R., J.D., C.A., P.W., and L.W. analyzed data and wrote the paper. Communicated by Norman Myers, University of Oxford, Oxford, United Kingdom, October 26, 2005 To whom correspondence should be addressed at: University of Cape Town/Medical Research Council Research Unit for Exercise Science and Sports Medicine, Department of Human Biology, Sports Science Institute of South Africa, Boundary Road, Newlands, 7700, South Africa. E-mail: tdnoakes@sports.uct.ac.za. |
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| SubjectTerms | Athletes Biological Sciences Body Weight Body weight changes Dehydration Exercise Exercise - physiology Fluids Humans Hyponatremia Hyponatremia - blood Hyponatremia - classification Hyponatremia - etiology Hyponatremia - physiopathology Medical research Racing Secretion Sodium Sodium - blood Sports - physiology Weight gain Weight loss |
| Title | Three Independent Biological Mechanisms Cause Exercise-Associated Hyponatremia: Evidence from 2,135 Weighed Competitive Athletic Performances |
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