Despite a fraction of the time commitment, run SIT induces similar body composition, VO(2max), and performance adaptations as ET, but with no effect on Q(max). These data suggest that adaptations with ET are of central origin primarily, whereas those with SIT are more peripheral

We assessed whether 10-s sprint interval training (SIT) bouts with 2 or 4 min recovery periods can improve aerobic and anaerobic performance. Subjects (n = 48) were assigned to one of four groups [exercise time (s):recovery time (min)]: (1) 30:4, (2) 10:4, (3) 10:2 or (4) control (no training). Training was cycling 3 week(-1) for 2 weeks (starting with 4 bouts session(-1), increasing 1 bout every 2 sessions, 6 total). Pre- and post-training measures included: VO(2max), 5-km time trial (TT), and a 30-s Wingate test. All groups were similar pre-training and the control group did not change over time. The 10-s groups trained at a higher intensity demonstrated by greater (P < 0.05) reproducibility of peak (10:4 = 96%; 10:2 = 95% vs. 30:4 = 89%), average (10:4 = 84%; 10:2 = 82% vs. 30:4 = 58%), and minimum power (10:4 = 73%; 10:2 = 69%; vs. 30:4 = 40%) within each session while the 30:4 group performed ~2X (P < 0.05) the total work session(-1) (83-124 kJ, 4-6 bouts) versus 10:4 (38-58 kJ); 10:2 (39-59 kJ). Training increased TT performance (P < 0.05) in the 30:4 (5.2%), 10:4 (3.5%), and 10:2 (3.0%) groups. VO(2max) increased in the 30:4 (9.3%) and 10:4 (9.2%), but not the 10:2 group. Wingate peak power kg(-1) increased (P < 0.05) in the 30:4 (9.5%), 10:4 (8.5%), and 10:2 (4.2%). Average Wingate power kg(-1) increased (P < 0.05) in the 30:4 (12.1%) and 10:4 (6.5%) groups. These data indicate that 10-s (with either 2 or 4 min recovery) and 30-s SIT bouts are effective for increasing anaerobic and aerobic performance.

Morphometry and oxidative capacity of slow-twitch (type I) and fast-twitch (type IIa and IIb) muscle fibers obtained from vastus lateralis needle biopsies were compared between younger (21-30 yr) and older (51-62 yr) normal fit (maximal O2 uptake = 47.0 vs. 32.3 ml.kg-1.min-1) and endurance-trained (66.3 vs. 52.7 ml.kg-1.min-1) men (n = 6/group). The older groups had smaller type IIa (31%) and IIb (40%) fiber areas and fewer capillaries surrounding these fibers than did younger groups. The reduced type II fiber areas and capillary contacts associated with aging were also observed in the older trained men. However, the capillary supply per unit type II fiber area was not affected by age but was enhanced by training. Additionally, on the basis of quantitative histochemical analysis, succinate dehydrogenase activities of type IIa fibers in the older trained men [4.07 +/- 0.68 (SD) mmol.min-1.l-1] were similar to those observed in younger trained men (4.00 +/- 0.48 mmol.min-1.l-1) and twofold higher than in older normal fit men (2.01 +/- 0.65 mmol.min-1.l-1; age x fitness interaction, P < 0.05). Type I muscle fibers were unaffected by age but were larger and had more capillary contacts and higher succinate dehydrogenase activities in the trained groups. The findings of this study suggest that aging results in a decrease in type II fiber size and oxidative capacity in healthy men and that this latter effect can be prevented by endurance training. Conclusions regarding the effects of age and training status on muscle capillarization depend largely on how these data are expressed.

Serum urea increases with exercise duration suggest prolonged exercise may be analogous to starvation where protein catabolism is known to occur. The purpose of this investigation was to alter muscle glycogen levels and to study the effect on protein catabolism. Six subjects (27-30 yr) pedaled a cycle ergometer for 1 h at 61% VO2max (mean VO2 = 2.33 +/- 0.7 1 . min-1) 1) after CHO loading (CHOL) and 2) after CHO depletion (CHOD). The following urea N measures were made: pre-exercise serum and urine, exercise serum and sweat (15-min serial samples), and serum and urine during 240 recovery min. Results demonstrated that 1) exercise serum urea N increased in CHOD attaining significance (P less than 0.01) at 60 min; 2) serum urea N increases continued into recovery at all measurement points of CHOD (P less than 0.01) and at 240 min of CHOL (P less than 0.05); 3) sweat urea N increased 154.2-fold (CHOD) and 65.6-fold (CHOL) (P less than 0.05). Calculations indicate that CHOD sweat urea N excretion was equivalent to a protein breakdown of 13.7 g . h-1 or 10.4% of the total caloric cost. It was concluded that protein is utilized during exercise to a greater extent than is generally assumed and that under certain conditions protein carbon may contribute significantly to exercise caloric cost.

This randomized double-blind cross-over study assessed protein (PRO) requirements during the early stages of intensive bodybuilding training and determined whether supplemental PRO intake (PROIN) enhanced muscle mass/strength gains. Twelve men [22.4 +/- 2.4 (SD) yr] received an isoenergetic PRO (total PROIN 2.62 g.kg-1.day-1) or carbohydrate (CHO; total PROIN 1.35 g.kg-1.day-1) supplement for 1 mo each during intensive (1.5 h/day, 6 days/wk) weight training. On the basis of 3-day nitrogen balance (NBAL) measurements after 3.5 wk on each treatment (8.9 +/- 4.2 and -3.4 +/- 1.9 g N/day, respectively), the PROIN necessary for zero NBAL (requirement) was 1.4-1.5 g.kg-1.day-1. The recommended intake (requirement + 2 SD) was 1.6-1.7 g.kg-1.day-1. However, strength (voluntary and electrically evoked) and muscle mass [density, creatinine excretion, muscle area (computer axial tomography scan), and biceps N content] gains were not different between diet treatments. These data indicate that, during the early stages of intensive bodybuilding training, PRO needs are approximately 100% greater than current recommendations but that PROIN increases from 1.35 to 2.62 g.kg-1.day-1 do not enhance muscle mass/strength gains, at least during the 1st mo of training. Whether differential gains would occur with longer training remains to be determined.