article hyperplasia
- Thread starter faz
- Start date
Interesting Faz. But then I got to the first two paras of 'The Hypertrophic Phase' and it kind of turned me off to the rest of the article. I skimmed the rest about the approach to hyperplasia and it just seemed to be a lot of subjective musings. Perhaps I'll read it properly later.
Wow, he is almost as long winded as me
First question would be, even if mature human muscle can grow via fiber splitting would resistance exercise even cause it? Most models showing hyperplasia in animals have shown a higher occurance during extreme stretching (see Kelley's excellent review JAP Vol. 81, No. 4, pp. 1584-1588, Oct 1996).
Next would be, what about innervation?
At some point during the splittling process there would need to be neural path growth concomittantly in order for this new fiber to be able to produce contractional force.
Interestingly there is a study that looked at Congenital generalized lipodystrophy (an autosomal recessive genetic disorder characterized by almost complete absence of adipose tissue, above average muscular appearance, and severe insulin resistance since birth). What was found is the GCL subjects had more type II fibers, smaller cross sectional areas of both tyoe I and II and higher fiber counts but were not any stronger than their non-GCL counterparts. In fact they were weaker. So were some of the fibers a result of GCL somehow causing hyperplasia (what the study suggested) and were these fibers innervated? They did test the bio-energetic capacity and found nothing abnormal and these GCL patients had a normal shift in the balance of high-energy phosphates across a range of exercise, indicating the strength deficits were not metabolic in nature. Interersting
First question would be, even if mature human muscle can grow via fiber splitting would resistance exercise even cause it? Most models showing hyperplasia in animals have shown a higher occurance during extreme stretching (see Kelley's excellent review JAP Vol. 81, No. 4, pp. 1584-1588, Oct 1996).
Next would be, what about innervation?
At some point during the splittling process there would need to be neural path growth concomittantly in order for this new fiber to be able to produce contractional force.
Interestingly there is a study that looked at Congenital generalized lipodystrophy (an autosomal recessive genetic disorder characterized by almost complete absence of adipose tissue, above average muscular appearance, and severe insulin resistance since birth). What was found is the GCL subjects had more type II fibers, smaller cross sectional areas of both tyoe I and II and higher fiber counts but were not any stronger than their non-GCL counterparts. In fact they were weaker. So were some of the fibers a result of GCL somehow causing hyperplasia (what the study suggested) and were these fibers innervated? They did test the bio-energetic capacity and found nothing abnormal and these GCL patients had a normal shift in the balance of high-energy phosphates across a range of exercise, indicating the strength deficits were not metabolic in nature. Interersting
QuantumPositron
New Member
Wow.