Marathon running: physiological and chemical changes accompanying late-race functional deterioration.

Twenty-one experienced runners were studied before, during and immediately after a marathon race to ascertain whether either depletion of energy substrate or rise in body temperature, or both, contribute to late-race slowing of running pace. Seven runners drank a glucose/electrolyte (GE) solution ad libitum (Na+ 21 mmol l-1, K+ 2.5 mmol l-1, Cl- 17 mmol l-1, PO4(2-) 6 mmol l-1, glucose 28 mmol l-1) throughout the race; 6 drank water and 8 drank the GE solution diluted 1:1 with water. Although average running speeds for the three groups were not significantly different during the first two-thirds (29 km) of the race, rectal temperature was significantly higher (P < 0.05) and reduction of plasma volume was greater (P < 0.05) in runners who replaced sweat losses with water. During the last one-third of the race, the average running pace of the water-replacement group slowed by 37.2%; the pace slowed by 27.9% in the 8 runners who replaced their sweat loss with GE diluted 1:1 with water (1/2 GE) and 18.2% in runners who replaced fluid loss with full-strength solution (GE). Eleven runners (5 in the water group, 4 in the 1/2 GE group and 2 in the GE group) lapsed into a walk/run/walk pace during the last 6 miles of the race. Ten of these had a rectal temperature of 39 degrees C or greater after 29 km of running, and plasma volume in these runners was reduced by more than 10%.(ABSTRACT TRUNCATED AT 250 WORDS)

Dietary intervention and training in swimmers.

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 less than 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 less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of phosphate loading on 2,3-diphosphoglycerate and maximal oxygen uptake.

Increased concentration of red blood cell 2,3-diphosphoglycerate (RBC 2,3-DPG) shifts the hemoglobin-oxygen dissociation curve to the right, thus theoretically allowing better oxygenation of tissues. To determine whether such a shift is physiologically significant, we investigated the effects of oral phosphate loading on several parameters including plasma phosphate concentration, RBC 2,3-DPG, hematocrit and hemoglobin concentration, maximal oxygen uptake (VO2max), and degree of lactic acidemia in 10 well-trained distance runners. After control determinations were made, either a phosphate load or a placebo was given for 3 d before the athlete was restudied. A placebo and two phosphate-loading studies were performed at weekly intervals, followed by 2 wk of rest and another post-intervention control study. Blood samples for control values were drawn before and after a standard warm-up period, after treadmill exercise at a 10% grade, and at the completion of the VO2 determination. After oral phosphate loading there was a significant increase in serum phosphate and RBC 2,3-DPG. Maximal oxygen uptake was significantly increased and correlated with the rise in RBC 2,3-DPG (r = 0.81). The increase in blood lactate after exercise on the 10% grade was attenuated during sessions which followed phosphate loading.