I sometimes get the response that our approach completely overlooks what we know about muscle pH relative to the increases in the duration of effort: “Acid is building up, and that’s what is slowing athletes down. How can you guys dismiss that for an event like the 400, 800, and even much longer events?”
So where did the focus on lactic acid begin in the first place?
A.V. Hill’s frog research noted that fatigued muscle fibers accumulated large quantities of lactic acid. He also discovered that cells returned to their vigor once this lactic acid dissipated.
Hill drew the following conclusion: intracellular lactic acid was the principal cause of fatigue. And maybe this is where all the lactic acid stuff really began.
But as I noted in the previous blog, does correlation equal causation? Does lactic acid truly promote what we often describe as tiredness in muscles? The occurrence of two things happening together does not “prove” causation, especially in the world of performance training where all kinds of things may be acting together.
So what does the research tells us? One study noted that individuals who cannot produce lactic acid actually experience fatigue more quickly than those who generate great quantities of lactic acid (Journal of Physiology (London),why is that the case? Vol. 418, p. 311, 1989) This should lead us to the obvious question:
Another study noted that acidic conditions have no effect on fatigue (Journal of Applied Physiology, Vol. 85, p. 478, 1998).This should lead us to another obvious question: how can that be?
More current research offers that Hill’s hypothesis may have been wrong. Researchers have noted that lactic acid actually benefits force production in fatigued muscles. (Science, Vol. 305, p. 1144, 2004) The research offers that increased levels of lactic acid influence the activity of chloride-ion "channels" in muscle cells. This process actually sustains force production in muscles.
So, where is this taking us? If we follow what the research is suggesting, lactic acid may not be the enemy at the gates of performance that needs buffering or reduction via the more conventional methods of training.
That is certainly not a popular notion, at least as evidenced by those who continue to argue that the development of a large aerobic capacity is the best way to control acidosis.
Yet it may be what Owen Anderson once described as “sizzling, red-hot workouts” that result in a far greater benefit. Flooding the blood with lactic acid actually does a far better job because it compels the muscle cells to clear the acid more effectively.
And why might this be the case? Lactic acid can accumulate even when the muscles have adequate supplies of oxygen. Barry has alluded to the myth of oxygen in his analysis of the hypoxic/normoxic studies. It appears to be more a matter of “mitochondrial shuttling ability” than oxygen supply, and if that is indeed the case, than one solution may be to enhance this mitochondrial shuttling.
So how does one do that? As Owen Anderson noted: “Running lots of miles at a moderate pace just won't do the trick, because your shuttles can handle such exertion quite easily (inward hydrogen movement through the shuttles is moderate during moderate running, and so there is no stimulus for the shuttles to undergo a make-over). What you need instead is training which really taxes your shuttles.”
And what becomes “taxing training”?
As Anderson concludes:
“Any workout conducted at 10-K speed or faster will place a nice surcharge on your mitochondrial shuttles, but one particularly effective shuttle session involves going to your favorite place for a workout, warming up thoroughly, and then alternating one-minute intervals at close-to-max speed with two-minute, easy-jog recoveries.”