you know that gcn is not ment for syclists but for people who would like to be one. 😀 same goes for most of similar running youtube content.

Yes, and it is the 'hybrid' fibres that are the one that are most flexible to change (in both directions) providing there is a consistent stimulus.

I do not know how those runners trained and I do not understand the Maffetone formula......maybe you could explain..... how much does his advisory max HR differ from you genuine maxHR? It is usually a mistake to training exclusively in one heart rate zone for any endurance sport, the best plan is one that varies according to your needs (see fft.tips/vtiz and fft.tips/tpp)

Ball park....roughly two thirds of the volume (if intensity is slightly increased) for about 6 weeks. If intensity and duration are both increased fitness will deteriorate on day 2 onwards

Jonathon Hockley a one week vacation off the bike seems to take me 3weeks to month to get back to where I was. I don’t think that’s far off. Age my have a lot to do with it also.

As you asked nicely I am happy to help. Yes there were some assumptions on this a few years back about unidirectionality perhaps linked with the difficulty conducting a study where athletes change stimulus from endurance to resistance (and back?) in one study. Common sense will tell you that a one -way system is vanishing rare in physiology so it was always perhaps a false negative due to lack of evidence. Fortunately, we have evidence from other studies regarding the flexibility of fibre 'conversion' which I am sure you realize will in reality be very complex and involve gene expression > protein signally > protein transcription and translation and finally muscle fibre compositional change over time (likely taking several months). Also remember the "conversions" maybe from faster IIx to IIb or from hybrid i/IIx to IIx etc. Remember too that less slow twitch to more fast twitch might occur in several different situations including less slow twitch stimulus as well as more fast twitch stimulus and perhaps less stimulus altogether. Now on to the actual evidence, and this is only a summary and not my own work..........

#1 DETRAINING STUDIES "From studies done on detraining and bed rest, Andersen et al. (2005) has proposed that human skeletal muscle MHC IIX (Type IIB) represents a default gene setting that is expressed in the absence physical activity or muscle contractility. This states that a previously trained individual will go through muscular changes in the direction of Type I => Type IIa => Type IIb when detraining or becomes sedentary " "Andersen et al. (2005) trained sedentary young males using knee extension exercises three times per week for 3 months using moderate to heavy resistances (from 10 to 6 repetition maximum, RM). Testing was performed before the start of training, after 3 months of training and again 3 months after detraining. Following 3 months of training, the CSA of quadriceps and EMG activity both increased by 10%. Also, isokinetic muscle strength at 30 and 240° s−1, was increased by 18% (P 

#2 INJURY STUDIES "Muscular and neural adaptations may be reversed at different rates, while muscle fiber phenotype is altered toward an increased expression of the fast MHC IIX phenotype (Andersen and Aagaard, 2000). This response is closely coupled to the progressive upregulation of chiefly the type IIx MHC and downregulation of type I MHC took as long as 90 days to be fully manifest (Huey et al)" **see** Huey KA, Roy RR, Baldwin KM, Edgerton VR.Time-dependent effects of spinal cord isolation on MHC gene expression in rodent antigravity muscles.Med Sci Sports Ex322000S80 Google Scholar "In animal experiments it has been reported that unloaded muscle does show preferential atrophy of type 1 fibres and increased proportions of type 2 fibres (Fitts et al, 2000; Jiang et al, 1992; Maier et al, 1976; Booth and Kelson, 1973). " **see**Fitts, R H, Riley, D R and Widrick, J J (2000). ‘Microgravity and skeletal muscle’, Journal of Applied Physiology, 89, 823-839. Hortobágyi et al (2000) studied 48 pain free healthy subjects and immobilised their left legs for three weeks in fibreglass casts. Proportions of type 1 fibres reduced by 9% (p < 0.05) and numbers of type 2X fibres increased by 7%, but numbers of type 2A fibres were not affected. In terms of area, however, all three fibre types were reduced significantly **see**Hortobágyi, T, Dempsey, L, Fraser, D, Zheng, D, Hamilton, G, Lambert, J and Dohm, L (2000). ‘Changes in muscle strength, muscle fibre size and myofibrillar gene expression after immobilisation and retraining in humans’, Journal of Physiology, 524, 293-304.

#3 AGING STUDIES "With the natural process of aging and its corresponding decline in muscle mass and function, a study was carried out by D’antona et al. (2003) to examine the effect of aging following immobilization on structure and function of muscle fibers. This study was performed in order to 183 inspect the differences of muscle fibers and possible shifts between young and elderly individuals after one of the elderly groups was immobilized. The subjects were divided into 3 groups: (1) healthy young individuals (n =7) with no previous record of muscular diseases or traumatic lesions, aged 30.2 ± 2.2 years, and who were not involved in any regular training or exercise; (2) elderly subjects (n=7) with same criteria as first group aged 72.7 ± 2.3 years; (3) elderly subjects (n=2) aged 70 and 72, whose right leg had been completely immobilized for 3.5 months in an extended position. Biopsies were taken from the right leg vastus lateralis. The results of this study showed an increase in MHC 2X (type IIB) and a decrease in MHC 2A (type IIA) in the order of groups 1 => 2 => 3. MHC-1 (type I) was significantly lower in the immobilized elderly than in the other two groups. As a whole, the results indicate a shift toward a faster phenotype in the elderly, and to a greater extent, in the immobilized elderly. Fiber atrophy following immobilization was more pronounced for type I fibers (-51%) than for type IIA (-26%) and IIB (-24%). Atrophy following aging was also more pronounced for type I (-22%) than type II (-12%), whereas no significant decreases in cross sectional areas were found for type IIAB and IIB (D’antona et al., 2003). This study confirms that muscular shifts favor in the direction of type IIB fibers in the absence of physical activity, but this also presents evidence of preferential aging related muscular atrophy of type IIA fibers. However with the preferential shift toward type IIB fibers in younger individuals, elderly individuals may exhibit a slower phenotype on the basis of preferential denervation of fast motor units due to aging (D’antona et al., 2003). Phenotypes exhibited are dependent on the level of physical activity since sarcopenia may be managed and even reversed through intense physical activity. Aging causes a denervation of fast twitch fibers, while lack of physical activity causes a shift toward fast twitch fibers. It remains a little unclear as to whether type I or type II muscle fibers are more abundant within the immobilized or inactive elderly population since type II fibers are affected by denervation, but inactive individuals tend to favor towards type II fibers." **see**D’Antona, G., Pellegrino, M. A., Adami, R., Rossi, R., Carlizzi, C. N., Canepari, M., Saltin, B. and Bottinelli, R. (2003). The effect of ageing and immobilization on structure and function of human skeletal muscle fibres. The Journal of Physiology, 552: 499-511. doi: 10.1111/j.1469-7793.2003.00499.x

#4 DOES RESISTANCE TRAINING REDUCE TYPE I ST fibres? The jury is out, but in humans, resistance training has been shown to reduce fast type IIx MHC that is downregulated and the fast IIa MHC that is upregulated (2, 7, 22, 63). If the subjects are detrained for several weeks, it appears that this process is reversed and the reexpression of the fast type IIx appears to be even greater than the level that was originally expressed in the pretraining period (5). "Numerous studies have shown that heavy resistance exercise training will decrease the expression of MyHC IIX in human skeletal muscle and simultaneously increase the expression of MyHC IIA, whereas the expression of MHC I is much more unaffected by the resistance exercise (Hather et al., 1991; Adams et al., 1993; Andersen & Aagaard, 2000). This is a highly solid observation and a general consensus on this point exists among people working in the field (Fry, 2004; Folland & Williams, 2007). Likewise, cessation of resistance training will induce, or re‐induce MyHC IIX at the expense of MyHC IIA (Andersen & Aagaard, 2000; Andersen et al., 2005). Whether or not the number of fibers expressing MyHC I is increased or decreased after strength training is debateable, but most likely, there is no or only very subtle changes in the number of fibers expressing MyHC I (Andersen & Aagaard, 2000; Fry, 2004)." **see**Fry AC. The role of resistance exercise intensity on muscle fibre adaptations. Sports Med 2004: 34: 663-679. **see**Hather BM, Tesch PA, Buchanan P, Dudley GA. Influence of eccentric actions on skeletal muscle adaptations to resistance training. Acta Physiol Scand 1991: 143: 177-185. #5 SPACE (LOW GRAVITY STUDIES) There is some evidence in this category too.

I answered your question here: medium.com/@alexfastfitnesstips/vo2-max-and-body-weight-cb7b500700a2

Medicine (MD) and Coaching. How about you?

@@Fastfitnesstips Thanks. My background quickly is Masters in Sport and Exercise Science, 20 years coaching experience in Professional High Performance Strength and conditioning/ Sport Science and Medicine.