If ~20% of muscle fibres are 'undecided' at birth -- when/how do they become 'decided'? And is there still undecided/transitional fibres throughout later years?


Why don't fat cells hypoxiate, rather than empty of fat? How does this affect weight gain/regain?

Usually when your hormones start to take off 9 or so for boys, younger for girls. You can "boost" or encourage that growth as a child if you're active enough. Most of the time it's genetics though.
I've gone from fast twitch muscle fibers to slow twitch ( when I was doing ultra marathons and triathlons ) but they always revert back to what is natural for me.
Sprinting is king

lol have you had muscle biopsies to confirm or are you just assuming because you ran for longer time?



muscle fibers are not nearly as simple as you would assume. honestly even myofibrils have blends of MHC class proteins and the predominant type determines how the fiber usually responds. genetic transcription factors will influence the predominant MHC proteins expressed in a myofibril which is determined by genetic code but you can influence MHC expression to some degree via training/detraining. for example, quadriplegic patients have very predominantly fast twitch fibers because of a lack of stimulation. age increases slow twitch proportion

Iirc girls generally start puberty at 9 and boys 11. Give/take 1 yr


@cloudkicker - interesting.. I remember watching a Jason Blaha video and he mentioned that you don't want to do Low intensity cardio after a high intensity anaerobic bout of leg training, because to a small degree you're short-changing yourself, in that you're essentially 'confusing' transitional fibres. Would this actually occur? (Again, only to a very small but still appreciable degree)


Also, can I get an answer for the adipose question?

I'm not quite sure what you mean by fat cells hypoxiating rather than emptying of fat? Clarify that and I'll answer you. Because hypoxic death is a well known phenomenon of adipocytes that happens during obesity and augments inflammation

fiber composition wont ever really become significantly more fast twitch. your type II fibers may develop in size but typically training adaptation will simply make all of your fibers more oxidative. MHC expression will shift towards MHC I in majority of circumstances, very specific artificial stim may convert some slow twitch to fast but very unlikely. i dont think there are transitional fibers in the sense that you (or jason blaha, sorry hes pretty bad) understand them. all fibers exist on a continuum of MHC compositions, and the standard fiber classifications that we have (I, IIa, IIx, IIb, IIc, etc) vaguely encompass a range of MHC compositions. there are no finite properties to muscle fibers, all behave slightly differently when innervated

e: that said i also wouldnt rely on MHC expression changes due to exercise as a very primary adaptation mechanism in strength training.

This post was edited by cloudkicker on Aug 30 2015 09:08pm

Ok. Thankyou for clarifying that. But what is MHC?



@balla, I read that fat cells don't die, they just empty themselves when you lose weight

...MHC=myosin heavy chain. Doesn't seem like you did much reading before your queries. Though I'll still oblige

This myth is partly true, partly untrue. Irrespective of weight loss/gain, there's a constant turnover of adipocytes. This may not necessarily reflect a net gain/loss but occurs nonetheless, thus effectively debunking the dogma.
However, it's also true that the preponderance of studies found no net loss of adipocytes in chronic fat loss. There does seem to be an increased reliance on hyperplasia, ergo increasing total adipocyte number, as obesity worsens and perpetuates, though. However, even if these adipocytes stay there post-weight loss, and just in general, don't fret. It's actually a protective mechanism from obesity-induced derangements. Effectively, the adipocyte becoming "overfull" so to speak, will be more insulin resistant and less able to do its job. Smaller, but more total, adipocytes, are more effective and insulin sensitive and thereby attenuate lipid spillover/ectopic fat storage.
I've heard some musings that long term fat loss results in some adipocyte apoptosis and therefore overall less numbers, but I've yet to actually see a study denoting that. If anyone has one though, I'd love to see it. I could also bring up a lot of interesting animal and in-vitro data, but I'm hesitant to draw many conclusions from them so I'll leave them out.

http://www.nature.com/nature/journal/v453/n7196/full/nature06902.html
http://www.sciencedirect.com/science/article/pii/S0006291X10004067
http://www.sciencedirect.com/science/article/pii/S0300595X76800230
http://advances.nutrition.org/content/4/1/67.full

shane got it, but yeah if you take two type IIa fibers from a human and stim them both at 10hz you will almost certainly find that there are very nuanced differences in their contractile profiles, because one might have 56 percent type IIx MHC proteins and the other might only have 53% (or so the theory goes). these minute variations in isoform expression lead to a blend of blends, so fiber types vary within a muscle belly but MHC isoforms vary even within a single fiber. this is part of the reason why i dont like people using excuses like "oh he must have more fast twitch fibers than me" or "its just his genetics". its so much more complex than that

You guys are great! Cheers