In the South American jungle, a jaguar hunts a prey that bites back, a caiman. In a show of absolute superiority, the cat makes his kill on the dangerous dinner’s turf. The jag jumps into the river and snatches the wriggling toothy reptile by its neck.
A caiman or a gator may be fast, but if he misses, he is in deep trouble, as he just shot a musket—a single-shot muzzle loader against a warm-blooded predator’s six-shooter that can be rapidly reloaded. A reptile’s weak aerobic system and reliance on glycolysis puts it at a great disadvantage against warm-blooded predators whose aerobic systems enable them to rapidly recover from their lightning strikes.
A gator needs many hours of rest and sucking wind to clear the acid produced by a single spurt of activity. Scientists believe that dinosaurs—reptiles’ cousins—had similar metabolism, which made them vulnerable to mammal predators whose aerobic systems were far superior and that enabled them to sustain their attacks.
Enter the home of the aerobic system, the mitochondria, our cells’ power plants.
This Quick and the Dead did not start out as a power-centric guide to total fitness with a health twist. The original intention was to write only about improving endurance for high-power applications by training the mitochondria.
As it turns out, the state of one’s mitochondria determines much more than the outcome of a rowing race or a judo match. The mitochondria are, in Dr. Nick Lane’s words, “the masters of life and death.”
The alternative of being “quick” to being “dead” in the African savannah or the old American West only scratches the surface of the inspiration behind the book’s title.
“Who shall give account to Him who is ready to judge the quick and the dead.” ~ 1 Peter 4:5
In the Bible, the word “quick” does not describe being quick on the draw. It means “alive.” The goal of the Q&D regimen is not just to get you to perform at a high level, but to do it in a way that does no harm to your health—and hopefully improves it a great deal.
The Old English word “quicken” meant “to come to life.” The unborn child’s first movement in the womb was called “quickening.” Fittingly, we get our mitochondrial genes from our mothers.
Healthy, strong, and abundant mitochondria make one much more resilient to a variety of stressors: cold, heat, altitude, infection, poison, radiation, etc.
On the other hand, mitochondrial dysfunction is a likely cause of cardiovascular and neurodegenerative diseases, cancer, diabetes, obesity, and aging.
Oftentimes the events leading up to these disasters involve free radical damage. Reactive oxygen species or free radicals are oxygen molecules that carry more electrons than they are supposed to. Like lactic acid, in moderate quantities, ROS perform many useful functions. In excess, they destroy performance, health, and life itself.
Mitochondria are the primary source of free radical generation in our bodies. When there is heavy traffic through the so-called electron transport chains in mitochondria, some of the electrons leak and get captured by oxygen molecules. The latter turn into highly reactive compounds like hydrogen peroxide that go on a rampage damaging the body.
You can eat blueberries until you are blue in the face, yet they are not going to save you from ROS: Antioxidant foods and supplements have turned out to be surprisingly ineffective[i] (they might even increase cancer risk.[ii])
What you need are more, bigger, and better mitochondria.[iii] They not only generate and leak fewer free radicals—they act as “net sinks,” as Dr. Alexander Andreyev put it.[iv]
If you plan on remaining quick—as in “alive”—as long as possible, you had better treat your mitochondria right.
Choices that damage mitochondria include the usual suspects of smoking, drinking, overeating, eating garbage, pollution, stress, and overtraining.
Choices that beef up mitochondria are caloric restriction, intermittent fasting, controlled hypoxia and hypothermia—and certain types of exercise.
Scientists have identified four primary signals that can lead to mitochondrial biogenesis or creation[v]:
- Mechanical strain
- Reactive oxygen species
- Increased calcium concentration
- Low energy status
One at a time.
It appears that classic Soviet anti-glycolytic training—“A+A” on our site—builds mitochondria in fast twitch fibers through the first mechanism.
The second demands “optimal”[vi] or “physiologic”[vii] concentration of free radicals. It seems to apply to intelligent and restrained interval training—as opposed to acid baths like “Tabatas”.
“Metcons” are custom made for maximizing ROS generation. You may have heard of glutathione (GSH), “the mother of all antioxidants” produced by our bodies. Scientists measure the concentrations of its “used up” version to assess oxidative stress. They found a linear relationship between its concentration and lactate concentration after exhaustive exercise[viii].
The third mechanism works only in slow twitch fibers.
The fourth is what “high intensity interval training” attempts to harness.
This mechanism was discovered by preeminent Soviet scientist Prof. Felix Meerson[ix] back when Deep Purple was recording Speed King. Unfortunately, Meerson’s discovery was overlooked and had to be made again almost half a century later.
In the XXI century, Western scientists did a very fine job of rediscovery—going beyond the Soviet professor in tracing the specific metabolic pathways starting with a low energy state and arriving at mitochondrial biogenesis or creation. Alas, other scientists, those who experimented with HIIT, paid token attention to these discoveries and viewed them out of context of the many other biochemical reactions taking place at the same time and some of the events happening in the body at large. The resulting training protocols worked, but often inefficiently and with serious side effects. Like drugs with long disclaimers in small print.
Deep soreness. Low energy. Stress. Hormones out of whack. Free radical damage. Unfavorable changes in the heart.
I became convinced there was a better way.
[i] Teixeira et al., 2009
[ii] Yun & Finkel, 2014
[iii] Hood, 2001; Boveris & Chance, 1973; Davies et al., 1981; Jenkins et al., 1983
[iv] Andreyev et al., 2004
[v] Coffey & Hawley, 2007
[vi] Lira et al., 2010
[vii] Paulsen et al., 2014
[viii] Sastre et al., 1992
[ix] Meerson, 1971