Original episode & show notes | Raw transcript
This document provides a detailed analysis of the core concepts discussed in the “Empirical Cycling Podcast” transcript. It aims to dissect the physiological and biomechanical principles behind common fitness myths, offering a comprehensive understanding for an educated student audience.
This is perhaps one of the most persistent myths in cycling. The idea is that pushing a large gear at a low cadence (e.g., 50 RPM) creates high muscular tension, thereby mimicking the effects of lifting heavy weights in a gym. The podcast correctly refutes this, and the reasons lie in the fundamental principles of how muscles adapt to become stronger.
First, we must define strength in this context as the maximal force a muscle can produce. Building this capacity is not merely about creating tension; it’s about creating a specific type of stimulus that signals the muscle fibers to adapt. The two most critical components of this stimulus are:
High Mechanical Load: The force exerted on the muscle must be significant relative to its maximum capacity.
Muscle Stretch Under Load (Eccentric Contraction): This is the most crucial and often overlooked factor.
Muscles can contract in two primary ways during movement:
Concentric Contraction: The muscle shortens as it produces force (e.g., the “up” phase of a bicep curl or pushing the pedal down).
Eccentric Contraction: The muscle lengthens while under tension (e.g., the “down” phase of a bicep curl or a squat, where you are controlling the weight against gravity).
The podcast highlights that specialized sensory structures in the muscle called costameres are highly sensitive to being stretched while under a heavy load. When this happens, it sends a powerful signal to the muscle cell’s nucleus, essentially saying, “The current load exceeds our structural capacity; we must rebuild stronger to handle this in the future.” This triggers the protein synthesis and neural adaptations that lead to true strength gains.
Lack of Eccentric Contraction: Cycling is an almost purely concentric activity. When you push down on the pedal, your quadriceps are contracting and shortening. They are never put into a state of lengthening under high tension, which is the primary driver of strength adaptation. In a squat, your muscles are loaded as they lengthen, providing the necessary stimulus that pedaling lacks.
Ineffective Mechanical Tension & Kinetic Chain: While big gear work feels hard, the actual tension on the leg muscles is limited by the stability of the kinetic chain.
In a squat, the kinetic chain is stable and direct: the load is on your shoulders, transmitted through a braced core and spine to your hips and down to your feet.
On a bike, the chain is much longer and less stable, running from your hands on the handlebars, through your arms, core, and finally to your feet. Any instability or flex in this long chain dissipates force, preventing you from ever achieving the truly maximal mechanical tension on your leg muscles that you could in a controlled gym lift.
Conclusion: Big gear work is not useless. It is a form of sport-specific strength application. It helps translate the maximal strength you’ve built in the gym into on-bike power. However, it cannot build that foundational strength because it lacks the critical eccentric-loading component and the ability to apply a truly maximal mechanical load.
This myth is the foundation for dietary strategies like fasted training and ketogenic diets. The logic seems intuitive: if you force your body to use fat for fuel, it will become better at it, leading to improved endurance. While the premise is partially true (you do adapt to use the fuel you’re given), it fails to translate into improved performance for a key reason: it ignores the real drivers of aerobic adaptation.
Your muscles primarily use carbohydrates and fats for fuel. The decision of which to use is a complex process governed by intensity and substrate availability. The podcast correctly identifies a key gatekeeper in fat metabolism:
The rate at which CPT1 can transport fats is a major limiting factor for fat oxidation. At low intensities, this transport rate can easily keep up with energy demand. As intensity increases, however, energy demand skyrockets. The CPT1 transport system becomes a bottleneck, unable to supply fat quickly enough. Simultaneously, the breakdown of carbohydrates ramps up dramatically. This high flux of carbohydrate-derived fuel effectively “out-competes” fat at the mitochondrial level, further down-regulating fat oxidation.
The Dietary Hack: When you adopt a keto diet or ride fasted, your body responds to the high availability of fat and low availability of carbohydrates by up-regulating the machinery for fat transport (including CPT1). It becomes measurably “better” at burning fat. However, this comes at the cost of down-regulating the enzymes and pathways needed for high-rate carbohydrate metabolism, which is essential for high-intensity racing efforts. As the referenced Louise Burke studies on elite race walkers showed, this adaptation leads to no improvement in performance.
The True Driver of Adaptation: The real signal for improving aerobic performance isn’t the type of fuel you burn, but the training stress itself. As the podcast mentions, the following signals are what truly drive adaptation:
Low Glycogen Stores: Training with depleted muscle glycogen activates key signaling molecules.
Calcium Flux: The release of calcium during muscle contraction is a powerful signal.
AMPK Activation: Often called the “cellular energy sensor,” AMPK is activated when energy levels (ATP) are low, signaling the need to create more mitochondria.
PGC-1α (The Master Regulator): All these signals converge on PGC-1α, a molecule that orchestrates the creation of new mitochondria (mitochondrial biogenesis).
More mitochondria means more CPT1 transporters, more aerobic enzymes, and a greater capacity to use both fat and carbohydrates. Therefore, it is the training volume and intensity that makes you a better fat-burner as a byproduct of becoming a fitter athlete, not the dietary manipulation itself.
This adage, often attributed to cycling legend Eddy Merckx, suggests that all “base season” training should be done at a very low intensity. The podcast correctly frames the answer as, “It depends.” This rule is an oversimplification that ignores the most important principle of training: context.
For a professional cyclist with a 20+ year training history who can ride 25-30 hours per week, purely low-intensity riding provides an enormous amount of training stimulus. The sheer volume creates the necessary stress to trigger the aerobic adaptations discussed in the previous section (AMPK, PGC-1α, etc.). For them, a period of low-intensity riding is also a crucial mental and physical recovery from a grueling race season.
For a time-crunched amateur riding 10-12 hours a week, this approach is ineffective.
Lack of Progressive Overload: Training adaptations only occur when the body is stressed beyond what it’s accustomed to. An amateur athlete will quickly adapt to 10-12 hours of low-intensity riding. Once they plateau, if they cannot add more hours (the “volume” lever), the only way to continue creating an adaptive stress is by increasing the intensity.
Insufficient Stimulus: The total weekly stimulus from 10 hours of low-intensity riding is simply not enough to drive significant long-term adaptation for a reasonably fit individual. By incorporating moderate-intensity work (e.g., tempo, sweet spot), they can achieve a greater metabolic stress in their limited time, leading to more effective adaptations.
Conclusion: The “little ring” philosophy is not inherently wrong, but its application is highly dependent on the athlete’s training history, fitness level, and, most importantly, the amount of time they have available to train. For most non-professional athletes, a base period that strategically blends low-intensity volume with moderate-intensity work will yield far superior results.