Reply To: 50's at 100 pace

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USRPT promotes the conversion of type 2b muscle fibers to type 2a muscle fibers. Type 2 muscle fibers are the fast twitch fibers with b being anaerobic and a being oxidative. When glycogen is used by the type 2a fibers, it breaks down to water and carbon dioxide, not lactate like in the type 2b fibers. Rushall explains that lactate build up does not reach maximum levels as it does in some other sports and USRPT is sufficient to deal with the amount of lactate produced in a race.

From page 22 of bulitin 39 – “Maximal lactate capacities are not taxed in swimming races and so need not be trained with many “lactate sets” for maximal lactate tolerance capacities. [When maximal lactate tolerance is reached in an individual has not been explained and so such training is purely guess work.] The stimulation of the lactacid energy system with more appropriate and beneficial race-pace training is likely to be more than enough and would not demand specialized overload training.”

He also says that abnormally high levels of lactate can be explained by improper pacing. Going out too hard can start producing lactate early and build up too high before the finish causing you to die at the end of a race. As long as the swimmer swims at the proper pace that he trained at, he should be fine as long as he paces/splits the race properly.

Another reason that USRPT doesn’t advocate lactate tolerance sets is that it interferes with neuromuscular patterning. In a lactate tolerance set you are going to be swimming below race pace for part of the set. These sets will also produce some accumulated fatigue that will take longer to recover from. This means that you won’t be able to get in as many actual race pace repetitions latter in that practice and in the following days. You can’t form neuromuscular patterning from swimming at varying speeds or if you are too exhausted to get in an adequate amount of actual race pace repetitions.