College age males performed maximal two-legged isokinetic knee extensions three times per week for 6 wk at either 60 degrees/s (slow) or 300 degrees/s (fast) or both 60 and 300 degrees/s (mixed). The velocity specific and action specific (two-leg vs. one leg) improvements in peak torque (PT) were compared to a placebo group receiving low-level muscle stimulation. The slow group improved PT significantly (P less than 0.05) more than the placebo group only at its training velocity (60 degrees/s) and more so when the specific two-legged training action was mimicked (+32% with two legs vs. +19% with one leg). The mixed group enhanced PT by 24 and 16% at their respective training velocities of 60 and 300 degrees/s. These improvements were significantly larger than placebo and also significantly larger than the 9% improvement observed at the midvelocity of 180 degrees/s. The training specificity demonstrated by the slow and mixed groups suggest that neural mechanisms contributed to their improvements in power. This is supported by their unchanging muscle morphology. Training solely at 300 degrees/s (fast) however improved PT significantly more than placebo not only at the training velocity (+18%), but also at a slower velocity of 180 degrees/s (+17%). The fast group demonstrated a significant enlargement (+11%) of type II muscle fibers. These data suggest type II fiber hypertrophy to be a plausible mechanism for the nonspecific improvement of the fast group; however, a neurological adaptation that enhances power at and below the training velocity cannot be excluded.

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Acid-base, metabolic, and ventilatory responses to repeated bouts of exercise were examined. Ten male subjects performed two (T1, T2) 5-min work tests, on a cycle ergometer, separated by a 25-min rest. The results indicate the following. 1) T2 appears to have a larger aerobic energy component than T1, due to the fact that cumulative O2 uptake (Vo2) was significantly larger for T2 and that the immediate postexercise lactic acid (HLa) and delta HLa values were both significantly smaller for T2.2) CO2 production (Vco2) and the respiratory exchange ratio were both significantly lower for T2. This is probably due to greater fat metabolism and less nonmetabolic CO2 being produced from bicarbonate (HCO-3) buffering of HLa during T2.3) Even though Vco2 was significantly lower during T2, minute ventilation (VE) was not significantly different between T1 and T2. This suggests that the ventilatory response during exercise cannot be solely mediated via CO2 flux to the lungs. 4) HLa removal and (HCO-3) regeneration appear to be sequentially linked together as indicated by the almost identical mirror image and significant -0.93 correlation. In conclusion, it appears that a bout of high-intensity exercise (T1) can alter the acid-base and metabolic responses seen during subsequent performance (T2).