I'm currently trying to delve a little deeper into the science of running, not just taking training programs or "common thought" for granted. To that end, I'm now reading Lore of Running by Tim Noakes. A massive 900-pager with a whole intro section steeped in anatomy and physiological models for how running and exercise truly work, this is a bigger project than the Daniels Running Formula read.
I'm attempting to grapple with this book though, so I'm tackling it like I would tackle a textbook in a class. My science background is woefully inadequate, so I'm also trying to supplement with LLMs and trusted sources like Khan Academy. Very possible I get things wrong here, but the hope is that I come out on the other side a better and more informed coach and athlete!
The primary focus of this chapter is on skeletal muscle, as this type of muscle is the biggest contributor (cardiac to a lesser extent) to athletic/running performance.
Muscles are made up of bundles of muscle fibers. Muscle fibers in turn are made up of bundles of rods called myofibrils. Myofibrils in turn are made up of sarcomeres (stacked on top of each other). Sarcomeres are made up of myofilaments which lie parallel to one another. These myofilaments are made up of a "center" thick filament made of myosin molecules and thinner "outer" filaments made of actin molecules. Myosin and actin interact with one another in a complex way (mentioned below) to produce muscle contraction (concentric shortening, eccentric lengthening).
For energy, triglycerides (fat droplets) and mitochondria, along with glycogen stores are dispersed throughout the sarcomere. Mitochondria and fat droplets can produce energy with and without the to the mitochondria, where enzymes convert this energy into lood supply. With the blood supply, blood droplets energy from food ATP (adenosine triphosphate — the body's main energy currency). Triglycerides (three fatty acid molecules linked to a glycerol molecule) are broken down by triglyceride lipase -- also broken down by mitochondria to provide energy to muscles. Again, this can happen both from the bloodstream and "non-aerobically" (NOT anaerobically, a different thing). When the fat in muscles is directly used by mitochondria, the glycerol is transported to the liver, turned into glucose. This is important for prolonged energy needs.
The glycogen stored in sarcomeres is the other non-aerobic method mitochondria gain access to energy.
The myosin molecules (making up the thick filaments) have "heads" that have a kind of attraction to the actin molecules of the thin filaments. In resting state, the attraction is blocked physically by tropomyosin molecules. To start the muscle contraction, the brain sends a neurological signal via the peripheral nerve surrounding the muscle fiber to the motor nerve end plate. This signal releases acetylcholine to a special receptor on the muscle cell, which causes a new electrical signal to travel down the transverse tubules of the muscle cell.
From this point, (unclear on the mechanism), calcium stored in the sarcoplasmic reticulum is released. This "moves" the tropomyosin molecules (via a binding to troponin-C, a receptor that is attached to the actin/tropomyosin) allowing the myosin heads to attach to the actin molecules.
At this point, the myosin head goes through a cycle, where in the ATP stored in the myosin head is broken down into ADP and Pi, the myosin head "bends" at a 45 degree angle (potentially there is a different model here, as this doesn't fully account for eccentric contraction), which pulls the actin filaments toward the center of the sarcomere.
This fully contracted position is called the "rigor complex". To break this rigor complex, mitochondria supplies fresh ATP at the ATP binder on the myosin head, and the calcium is removed from the troponin-C receptor.
The rate at which this occurs determines the speed the muscle can move. The total number of these "cross bridges" determines the power of the muscle. The speed of the contraction is determined by how fast ATP is bound and split on the myosin head. Power is also determined by the amount of calcium bound to troponin-C receptors.
Type I fibers are usually red due to the higher content of myoglobin, have a higher concentration of mitochondria, and are considered "slow twitch" meaning a lower myosin ATPase activity. Usually endurance athletes have a higher perecentage of these.
Type II fibers are a little more complex and there is a spectrum, but generally they are white, with a lower myoglobin content and lower mitochondrial concentration. Considered "fast twitch", though IIa fibers can closely resemble Type I. Type IIb are "traditional" Type II fibers.
During exercise, the brain goes through a recruitement phase where Type I are recruited first, then Type IIa, then Type IIb.
The body's composition of these fibers are somewhat genetically determined, but exercise can change the makeup here as well. The recruitment of these types and their exhaustion have various explanations, including energy depletion, but also neurological patterns, and the brain's use of different receptors to determine the body's oxygen, temperature, and glucose supply (these receptors help the body to protect itself from brain or heart damage).
Not much to say here, except that eccentric contractions produce 2x force as concentric contractions, meaning depending on their use they are more likely to be the cause of muscle or tendon injury.
Weight training (both concentric and eccentric) has been shown to aid in running performance, especially eccentric movement. Runners often benefit from weight training, but not necessarily the other way around (i.e., running can inhibit the ability to gain strength). Most likely strength training helps due to the "neuromuscular adaptations from lifting that ensure muscle activation [during running/racing] remains high."
Tagged: Lore of Running, reading, notes,