Eight male cross-country runners and five male swimmers were tested four times during their collegiate seasons. Each trial corresponded to a different training load. The runners' trials were conducted before the start of organized practice (RT1), after 3 wk of increased training (RT2), 3 wk prior to the conference championship (pre-taper, RT3), and 4 d after the conference championship (post-taper, RT4). The swimmers' trials were conducted after the first 9 wk of training (ST1), after completing 2 wk of hard training (ST2), after an additional 6 wk of training (pre-taper, ST3) and during a week following the conference championship (post-taper, ST4). Venous blood samples, heart rate (HR) and blood pressure (BP) were obtained after 15 min supine rest (0700 h). Serum was analyzed for cortisol (C), total testosterone (TT), free testosterone (FT), and creatine kinase (CK). Blood samples (lactate), HR and RPE were obtained during a fixed velocity run (75% preseason VO2max) and blood samples and RPE following a 365.8 m swim (90% preseason VO2max). The runners then completed a "performance run" to exhaustion (110% preseason VO2max) and the swimmers completed maximal 22.9 and 365.8 m swims. Serum CK, C, TT, FT, and the TT:C and FT:C ratios were not significantly different among trials for the runners. Serum TT and FT were significantly (P < 0.05) lower for the swimmers at ST2 (TT 16.7 +/- 2.5; FT 85.3 +/- 8.5) compared to ST1 (TT 30.3 +/- 2.8; FT 130.2 +/- 20.9) whereas, C, TT:C or FT:C were not significantly altered.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in cortisol concentration in response to exercise at 3 different intensities were quantified. Ten apparently healthy, recreationally active males participated. On 4 separate occasions, subjects were assigned a random order of 1-hour cycle ergometer bouts of exercise at 44.5 +/- 5.5%, 62.3 +/- 3.8%, and 76.0 +/- 6.0% (mean +/- SD) of VO2peak and a resting control session. Saliva samples were collected before exercise at 10, 20, 40, and 59 minutes of exercise and at 20 minutes of recovery. Differences in cortisol concentration were assessed via multivariate analysis of variance (alpha = 0.05) Tukey post hoc analysis when indicated. During the highest-intensity exercise session, cortisol was significantly higher at 59 minutes of exercise (p = 0.004) and at 20 minutes of recovery (p = 0.016) than at those same time points during the resting control session. No significant differences in cortisol concentration were noted among resting, low-, and moderate-intensity exercise. Exercise <40 minutes in duration elicited no significant differences at any intensity. These data indicate that only exercise of high intensity and long duration results in significant elevations of salivary cortisol.

The purpose of this study was to determine whether trained competitive runners could maintain on-land running performance using 4 wk of deep water run training instead of on-land training. Eleven well-trained competitive runners (10 males, 1 female; ages, 32.5 +/- 5.4 yr; height, 179.8 +/- 9.3 cm; weight, 70.4 +/- 6.7 kg (mean +/- SD)) trained exclusively using deep water run training for 4 wk. Subjects trained 5-6 d.wk-1 for a total of 20-24 sessions (mean +/- SD, 22 +/- 1.5 sessions). Instruction and practice sessions were conducted prior to the training period. Before and after the deep water run training, subjects completed a 5-km race on the treadmill using a computer based system, a submaximal run at the same absolute workload to assess running economy, and a combined lactate threshold and maximal oxygen consumption test. No significant differences were found for (mean +/- SEM): 5-km run time (pre, 1142.7 +/- 39.5 s; post, 1149.8 +/- 36.9 s; P = 0.28), submaximal oxygen consumption (pre 44.8 +/- 1.2 mL.kg-1.min-1; post, 45.3 +/- 1.5 mL.kg-1.min-1; P = 0.47), lactate threshold running velocity (pre, 249.1 +/- 0.9 m.min-1; post, 253.6 +/- 6.3 m.min-1; P = 0.44), or maximal oxygen consumption (pre, 63.4 +/- 1.3 mL.kg-1.min-1; post, 62.2 +/- 1.3 mL.kg-1.min-1; P = 0.11). Also no differences were found among Global Mood State pre-training, each week during training, and post-training. Competitive distance runners maintained running performance using 4 wk of deep water run training as a replacement for on-land training.

The purpose of the study was to examine ferritin, haptoglobin, and red cell indices during a competitive running and swimming season. Male runners (N = 8) and swimmers (N = 5) were tested four times during their respective seasons. The runners were tested before the start of organized practice (RT1), after 3 wk of increased training (RT2), 3 wk prior to the conference championship (pre-taper, RT3), and 3 d after the conference championship (post-taper, RT4). The swimmers were tested after the first 9 wk of training (ST1), after completing 2 wk of hard training (ST2), after an additional 6wk of training (pre-taper, ST3), and 1 wk following the conference championship (post-taper, ST4). For the runners, hemoglobin, hematocrit, and red blood cell number were lower (p < 0.05) at RT2 and were not accompanied by significant changes in other red cell indices or haptoglobin. Serum ferritin in the runners was lower at RT3 and RT4 compared to RT1 despite an adequate dietary iron intake. Hemoglobin and mean cell hemoglobin concentration were lower and mean cell volume was higher in the swimmers at ST3 and ST4. No significant changes were observed in other red cell indices for swimmers; however, serum haptoglobin tended (p = 0.07) to be reduced at ST2. In conclusion, collegiate male runners and swimmers do not demonstrate clinical hypoferritinemia, hypohaptoglobinemia, or alterations in red cell indices suggestive of the early stage of anemia with or without iron deficiency during their respective season.