The so-called Norwegian method describes a form of training that is not actually that new, but has only become increasingly popular in cycling in recent years. In fact, many cyclists are still unaware of it, which is why I would like to introduce it here.
It is important to note that the method originates from running. The functioning and physiology of the body are identical in every sport, so fundamental processes can be transferred. Different requirements in individual sports and disciplines can sometimes lead to different conclusions for training. Transferring this training method 1:1 to cycling can backfire. The main reason for this is the different strain on the muscles. But more on that later.
Hyped today – outdated tomorrow – myths
As an athlete, you should regularly remind yourself that the latest training and nutrition methods will be outdated in 10-20 years and that in the future you will wonder how you could have trained in such a “primitive” way. For example, ten to fifteen years ago, it was recommended to consume 60 to 90 grams of carbohydrates per hour during competitions, whereas today this is laughed at and dosages of over 120 grams per hour are even being discussed. What I’m trying to say is that you should always approach the latest hype with a certain amount of skepticism and be aware that some of what is currently considered the best will soon be outdated or disproved. The golden rule is: listen to your own body and take its signals seriously.
Sports science is still in the dark about many physiological processes, and only assumptions can be made. Direct measurements in the body and muscles are usually not possible, and we have to rely on indirect measurements and alternative parameters. Even with the Norwegian method, there are only indications of what the success is based on. One point is the improved energy production from lactate. So-called experts still claim that spiroergometry can be used to determine the metabolism of fat and carbohydrates from respiratory gases using the respiratory factor. However, proteins/amino acids, which can cover up to 10 percent of energy requirements, have always been neglected here. And the energy production from lactate and the change in respiratory gases due to the bicarbonate buffering of the blood have been completely neglected. In short: the respiratory factor cannot be used to determine exactly which energy sources are metabolized in what proportions. It only provides rough indications. A second myth should also be dispelled at this point: measuring blood lactate cannot directly show what the lactate formation rate looks like. Especially when the use of lactate as an energy source increases—such as in the muscles and heart muscle—the measured blood lactate values are lower EVEN THOUGH a lot of lactate is being produced.
Results of the Norwegian method in long-distance running and conclusions for cycling
In addition to higher-intensity intervals, the Norwegian method focuses primarily on volume. Unlike classic polarized training, the intervals are not in the VO2max range or above. HIIT is rarely performed and tends to be avoided, as the fatigue caused by increased release of catecholamines (noradrenaline, adrenaline, and dopamine), among other things, is too great to complete the correspondingly high volumes. The intervals in the Norwegian method consist primarily of longer periods of exertion in the threshold range. A special feature here is double threshold training, whereby two of these threshold units take place on one day, with the intensity just below the threshold in the sweet spot range. This improves lactate tolerance and raises the threshold. VO2max intervals are used to tolerate high peaks of exertion in competitions and are not used for the purpose of increasing VO2max. For the latter, low to medium intensity training is more suitable for well-trained athletes.
Improving endurance performance through extensive low- to moderate-intensity training is achieved in two ways. Firstly, an increased cardiac output is maintained over a longer period of time, which increases the oxygen supply to the working skeletal muscles. Secondly, the improvement is achieved through increased capacity for oxidative metabolism via mitochondrial biogenesis and capillarization in type I skeletal muscle fibers. It is important to note that the mosaic-like architecture of human skeletal muscle means that increased capillarization in type I skeletal muscle fibers also serves to increase oxygen supply to type II muscle fibers. The oxygen supply to the muscles and within the muscles themselves is improved by increased formation of capillaries and mitochondria.
There are two primary signaling pathways for mitochondrial proliferation. One is based on calcium signaling, which is more commonly used in high-volume training. The other is based on signal transmission via the AMP (adenosine monophosphate)-activated protein kinase (AMPK) signaling pathway, which tends to occur during high-intensity training, as a great deal of energy (ATP) is consumed in a short period of time or converted into AMP. Thus, high-intensity competitive training leads to an increase in mitochondrial density and an improvement in aerobic metabolism to a certain extent.
However, most studies in the field of long-distance running on this topic conclude that the majority of training volume for long-distance runners should be completed at low intensity in order to optimize performance development. The adaptation potential of the calcium signaling pathway is much greater than that of the AMPK signaling pathway. Endurance runners therefore cannot avoid high training volumes and cannot replace them with HIIT. Accordingly, only a relatively low training volume of the latter is required to achieve saturation of the adaptation response via this signaling pathway.
The (elite) runners considered in the studies on the Norwegian method are mostly runners who cover more than 160 kilometers per week! If you assume a slow pace/average speed for the kilometers covered and ignore the altitude covered, you would end up with less than 15 hours of training per week. In contrast, cyclists train for 30 hours at high volumes. These loads are hardly comparable. Unlike cycling, running does not involve coasting in the slipstream or downhill, there is no significant relief from tailwinds, and the strain on tendons, ligaments, etc. is much greater. At the same time, running on flat terrain requires much less strength than pedaling on a bike. Different stresses on the bike due to different cadences cannot be equated with the demands of a changed running or stride frequency.
In short:
In addition to higher-intensity intervals, the Norwegian method focuses primarily on volume. Studies suggest that HIIT intervals only increase mitochondria to a certain extent. “More and harder” HIIT intervals do not lead to corresponding success. The situation is different when it comes to training volume: more volume leads to more and more effective mitochondria. The challenge, however, is to ensure the necessary recovery. Therefore, a high training volume is often not feasible for amateur athletes with additional everyday stress. Those who are unable to train for a large number of hours should switch to other training methods. The extreme increase in cell powerhouses (mitochondria) through high-volume training cannot be achieved or replaced by high-intensity intervals. For cyclists who compete in short criterium races, this is not so relevant. However, those who want to master long and intense efforts such as cycling marathons will not be able to avoid higher training volumes.
Literature:
Casado A, Foster C, Bakken M, Tjelta LI. Does Lactate-Guided Threshold Interval Training within a High-Volume Low-Intensity Approach Represent the „Next Step“ in the Evolution of Distance Running Training? Int J Environ Res Public Health. 2023 Feb 21;20(5):3782. doi: 10.3390/ijerph20053782. PMID: 36900796; PMCID: PMC10000870.
Bishop DJ, Botella J, Granata C. CrossTalk opposing view: Exercise training volume is more important than training intensity to promote increases in mitochondrial content. J Physiol. 2019 Aug;597(16):4115-4118. doi: 10.1113/JP277634. Epub 2019 Jul 15. PMID: 31309570.
Egan B, Zierath JR. Exercise metabolism and the molecular regulation of skeletal muscle adaptation. Cell Metab. 2013 Feb 5;17(2):162-84. doi: 10.1016/j.cmet.2012.12.012. PMID: 23395166.
Böning D. Vorwärts immer, rückwärts nimmer. Probleme wissenschaftlichen Fortschritts. Dtsch Z Sportmed. 2013; 64: 350-351. doi:10.5960/dzsm.2013.109
Antico Arciuch VG, Elguero ME, Poderoso JJ, Carreras MC. Mitochondrial regulation of cell cycle and proliferation. Antioxid Redox Signal. 2012 May 15;16(10):1150-80. doi: 10.1089/ars.2011.4085. Epub 2012 Jan 13. PMID: 21967640; PMCID: PMC3315176.
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