Dietary intervention and training in swimmers

Rent the article at a discount

Rent now

* Final gross prices may vary according to local VAT.

Get Access

Summary

To ascertain if muscle damage occurred in swimmers as a result of high-intensity training and to find if fluid and dietary manipulation could affect muscle damage, we studied 40 members of the University of Florida swimming team using creatine kinase (CK) and lactic dehydrogenase (LDH) as markers of muscle damage during a 6-month period of intensive training. During this time, training intensity, fluid intake during exercise and dietary supplementation were all modified one by one to examine their individual effects. During a control period of 4 weeks, all swimmers drank water before and during (120 min) workouts. CK in men at the end of this period averaged 315, SD 122 (normal < 170 IU · l−1). Half of the swimmers were then given 500 ml of a glucose-electrolyte solution (GES) (Na 21 mmol · l−1, Cl 13 mmol · l−1, K 2.5 mmol · l−1, PO4 5 mmol · l−1 and glucose 6%) before workouts and twice at intervals during the workout, while half continued to drink the same volume of water. One week after division into fluid groups, the workout intensity was increased by about 10%. Another week later CK had increased to 500, SD 180 IU · l−1 in swimmers drinking water, but fell to 280, SD 105 IU · l−1 in those drinking GES (P < 0.05). The second phase of the study began after a 4-week control period during which all athletes drank water before and during workouts. The swimmers were divided into four matched groups. Group I drank water before and during workouts and 250 ml of a 16% sucrose solution after; group II drank water before and during exercise and 250 ml of a milk protein supplement (MPS) containing 15 g lactalbumin and 16% sugar afterwards; group III drank GES before and during and the sucrose drink after exercise; group IV drank GES before and during and the MPS drink after exercise. Then during a 6-week period, the intensity of exercise was progressively increased by 25%. CK increased 61% (P < 0.01) in group I men, while it fell 12% (P < 0.05) in groups II and III, and 41% (P < 0.01) in group IV. In women, CK in group I increased 18% (P < 0.05); in group II it decreased 3.5%, in group III was unchanged, and in group IV declined 12.6% (P < 0.05). The final phase of the study was performed on 8 olympic swimmers who performed identical workouts each Saturday for 4 weeks. The 1st week they ingested water before and during exercise and the 16% sucrose solution afterwards. The 2nd week the GES solution was consumed before and during exercise and the sucrose solution afterwards. The 3rd week water was consumed before and during and MPS afterward and the 4th week GES before and during and MPS afterwards. Determination of CK and LDH before, immediately after, and at intervals afterwards showed that CK and LDH increased less when GES was the test fluid during exercise than when water was consumed. Recovery, as judged by return of CK and LDH to control values was more rapid when MPS was the post-exercise fluid than when the sucrose solution was given.