How cadence plays into cycling
I recently published a post on the ATP Performance Instagram page detailing the implications of cadence and the impacts of that on aerobic training adaptations. It’s a fascinating topic, and so I wanted to share further details around that in a far more in-depth post.
The most intriguing aspect around this is that the research around the topic is somewhat indirect, but the studies support the notion that adapting cadence around training can have a big impact on aerobic training adaptations.
I will start by asserting that there is no one correct cadence, power, heart rate, or duration of training that will get the most gains in terms of training adaptations. It is far more nuanced than that. Allostasis (blog on that coming) is the process of adapting to external stressors in an attempt to achieve homeostasis. Essentially, your body adapts to the stresses that it experiences. Novel training stimulus has a greater impact on this, so using differing training stimulus to target training adaptations is key. This is why you don’t want to be stagnant with your training, and vary the stimulus for specific training blocks.
This is why using cadence as a variation tool for adapting stimulus can have important implications to training adaptations. That can be high torque intervals, high cadence intervals, or varying cadence averages over longer durations of riding.
As mentioned in the post I shared, preferred cadence actually tends to be the most efficient. At low power, low cadence often requires a lower cardiac output and can be more efficient without excessive torque build-up which can promote the onset of muscular fatigue. At higher powers, a higher cadence tends to be more efficient so as to remain below the critical torque boundary. This is why WorldTour riders tend to target being able to withstand intervals of around ~10minutes long at 1Nm/Kg body weight for males and 0.88Nm/Kg for females. These are high torque targets, and require building up to, and are not appropriate for amateurs. You also require a certain muscular and structural resilience to do these while limiting injury risk.
However high cadence is often neglected as a focus point for training stimulus. I used to work with Neal Henderson, Sufferfest creator, Wahoo Sports Science officer, and coach to the US and AUS track cycling squads during his prolific career. One of the interesting facts I learnt from working with him and others at Wahoo Sports Science was the use of high cadence training for specific training adaptations. Namely, using high cadence for shorter intervals leads to a greater muscle activation pattern (EMG testing confirms this) and can have implications on greater pedalling efficiency and co-activation patterns.
This then links to another interesting principle, which is using higher cadences for aerobic training gains over longer durations. I need to go into some scientific principles first to loop back around to this point.
How cadence might link to aerobic adaptations
When it comes to aerobic performance, there are a few key factors that are of priority for us to focus on. There is mitochondrial function and numbers, as having more of these working more efficiently is key to producing ATP from primarily aerobic sources such as fat metabolism or oxidative carbohydrate metabolism. That is how WorldTour riders can maintain such high power for such long durations. There are then factors linked somewhat to this such as fat oxidation, and also the use of lactate as a fuel source, which involves lactate clearing and shuttling. Another key factor of endurance training is oxygen delivery. This starts in how we breath, and oxygen perfusion in the lungs, blood flow via the strength of the heart, and then delivery to the muscle. We improve delivery to the muscles in one way via muscle capillarisation, and angiogenesis, the creation of new capillaries. More capillaries, more oxygenated blood delivered to more of the muscle and the mitochondria to use to create ATP via oxidative pathways.
VEGF
This occurs via VEGF (vascular endothelial growth factor) and this is signaled in various different ways. ‘Training for skeletal muscle capillarization: a Janus-faced role of exercise intensity?’ by Lasse Gliemann covers this in some great detail and explains how the frictional or sheer forces against the luminal side (internal) of blood vessels stimulate VEGF and angiogenesis. This is present during higher intensity exercise as well, due to higher blood pressure and therefore sheer forces exerted on the blood vessels. However, two factors mean that lower intensity training is more beneficial in this instance. Firstly, high intensity is not sustainable over longer durations. Long low intensity rides have the potential for far greater total shear stress applied to the blood vessels over time than short bout high intensity, thus those rides have a greater impact on VEGF stimulation. Secondly, there are several anti-angiogenic factors that are activated during high intensity exercise so as to stop uncontrolled proliferation of VEGF. Essentially, higher intensity blunts some elements of angiogenesis adaptations.
But this leads on to some interesting principles. If you ride at 70 RPM normally at 200w for long endurance rides, that is likely the most efficient cadence and power combination, and results in a lower heart rate and easier perception, and higher gross efficiency. However, by increasing the cadence of endurance rides to a comfortable but higher level, this could have implications on VEGF activation. At higher cadences, heart rate is increased, and blood flow is increased. This means greater sheer forces exerted on the luminal side of blood vessels, and potentially greater angiogenic adaptations due to VEGF signalling. This is supported by Gotshall et al., 1996 as they found that as cadence increased to levels of 90 and 110 RPM from 70 RPM that heart rate, stroke volume, cardiac output and blood pressure also increased. This increased blood flow pressure is also one of the principles in how blood flow restricted (BFR) training can assist in VEGF stimulation as a meta-analysis by Li, S et al., 2022 showed.
This then leads on to another factor as to why increased cadence for low intensity could impact VEGF, and that is localised hypoxia. Again this was found by Li, S et al., 2022 to be a factor in VEGF stimulation via BFR, but a study by Skovereng, K et al., 2016 found that increased cadence led to increased deoxygenation of blood in prime locomotor muscles in the legs, essentially the muscles used more oxygen. Localised hypoxia can increase the oxygen uptake of the muscles and, although this is slight conjecture, higher cadence demonstrated a greater muscle oxygen consumption (mVO2) of certain locomotor muscles in the legs, and it could be inferred this this has a benefit on VEGF stimulation via localized hypoxia. Greater mVO2 is not necessarily an indicator of greater hypoxia though, more studies would be required to confirm this suggestion and the mechanisms at play. This means that this is admittedly a less supported inference than the links to increased cadence and impacts on luminal blood vessel shear forces.
PGC-1α
We now move on to another activator of VEGF, which is PGC-1α (Peroxisome proliferator-activated receptor gamma coactivator 1-alpha). This is one of the overriding mechanisms for many aerobic training adaptations such as angiogenesis and mitochondrial biogenesis. It is triggered via multiple pathways, and these pathways can be activated via high intensity intervals, repeat bouts, or long duration sessions.
A study by Zhang et al., 2014 though found that PGC-1α promoter activity has shown to be more sensitive to Ca2+ (cytosolic calcium) levels compared with adenosine monophosphate-activated protein kinase (AMP-K), ROS (reactive oxygen species) or p38 MAPK (Mitogen-Activated Protein Kinase) signalling. The Ca2+ levels in the muscle is partly linked to the number of muscle contractions, as well as the intensity of them. But as mentioned, long duration low intensity allows for greater stimulation due to the total volume producing a greater overall stimulus than a smaller bout of higher intensity. We can potentially hypothesise from this that a higher cadence could increase the levels of Ca2+ and therefore have a greater impact on PGC-1α activity. This is mediated via Ca2+-calmodulin-dependant kinase 2 (CaMKII) and calcineurin enzymes, and this hypothesis is supported by research from Ferraro, E., et al., 2014.
The reason this is important for angiogenesis is that PGC-1α is a strong activator of VEGF as supported by Ishan, M et al., 2014. So using lower intensity cycling for longer durations with a greater volume of muscle contractions has the potential to increase the activation of PGC-1α and therefore increase the VEGF stimulation and therefore have greater impacts of angiogenesis adaptation of training.
It is certainly an area of research that requires more study, but based on the currently available scientific literature, there is a strong supportive case for the suggestion that increasing cadence to a sensible amount during longer duration lower intensity exercise could have a beneficial impact on the angiogenesis training adaptations that are one of the key goals of this type of training.
Of course optimal cadence, and what is appropriate for riders, is highly multifaceted. There are biomechanical considerations in regards to mobility of joints, namely hip and knee but also ankle, along with lever length and distribution of mass across the legs, crank length,intensity being worked at, and other various factors. However, when used appropriately in a training plan for road cyclists, and in conjunction with other power, heart rate, and cadence driven varied stimuli, higher cadences during low intensity training sessions could assist in certain aerobic training adaptations as well as providing a somewhat novel stimulus.
References
Gliemann, L. (2016). Training for skeletal muscle capillarization: a Janus-faced role of exercise intensity?. European journal of applied physiology, 116(8), 1443-1444.
Gottshall, R. W., Bauer, T. A., & Fahrner, S. L. (1996). Cycling cadence alters exercise hemodynamics. International Journal of Sports Medicine, 17(01), 17-21.
Li, S., Li, S., Wang, L., Quan, H., Yu, W., Li, T., & Li, W. (2022). The effect of blood flow restriction exercise on angiogenesis-related factors in skeletal muscle among healthy adults: a systematic review and meta-analysis. Frontiers in Physiology, 13, 814965.
Skovereng, K., Ettema, G., & van Beekvelt, M. C. (2016). Oxygenation, local muscle oxygen consumption and joint specific power in cycling: the effect of cadence at a constant external work rate. European journal of applied physiology, 116(6), 1207-1217.
Zhang, Y., Uguccioni, G., Ljubicic, V., Irrcher, I., Iqbal, S., Singh, K., … & Hood, D. A. (2014). Multiple signaling pathways regulate contractile activity‐mediated PGC‐1α gene expression and activity in skeletal muscle cells. Physiological reports, 2(5), e12008.
Ferraro, E., Giammarioli, A. M., Chiandotto, S., Spoletini, I., & Rosano, G. (2014). Exercise-induced skeletal muscle remodeling and metabolic adaptation: redox signaling and role of autophagy. Antioxidants & redox signaling, 21(1), 154-176.
Ishan, M., Watson, G., & Abbiss, C. R. (2014). PGC-1α mediated muscle aerobic adaptations to exercise, heat and cold exposure.
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