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Juerg Feldmann

Fortiori Design LLC
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Posts: 1,530
 #1 
Thanks for  the   last 4  mails I just got in  here now.
 Question?
  Can we know the  fiber situation Typ 1 and Typ 2  to make it simple by looking at moxy data's.
?
MY answer  : I do not know.  ( yet )
 Here what i try to collect now since over  8 years.
 Exactly this ideas of trends  and  in another post I showed  2 test with a very different outcome at the end of the test.
 One  with a great deoxygenation trend, indicating possibly delivery problems but as well indicating a great ability to  use O2  down to  much  lower level. ( Utilization)  different option , which may improve utilization.
 The other test  shows a  relative leveling of   at the end of SmO2  indication either a  delivery problem as well ( ins some  situations ) but for sure as well showing a different ability to use O2.  I look at the level of SmO2 %  where this happens. Are we seeing this leveling of  already by 65 %  and  higher or  is it happening by a very low SmO2  . Than there are  most likely different reasons.
 What we look is whether clear  endurance  trained athletes show  a similar  end picture compared with clear  high intensity trained athletes.
.  Here some  directions  why we look at this based on some interesting studies done in the late 1990.

 

Protein kinase C activity regulates slow myosin heavy chain 2 gene expression in slow lineage skeletal muscle fibers.

Source

Department of Cell Biology and Anatomy, The Chicago Medical School, North Chicago, Illinois 60064, USA. dimarioj@finchcms.edu

Abstract

Expression of the slow myosin heavy chain (MyHC) 2 gene defines slow versus fast avian skeletal muscle fiber types. Fetal, or secondary, skeletal muscle fibers express slow MyHC isoform genes in developmentally regulated patterns within the embryo, and this patterning is at least partly dependent on innervation in vivo. We have previously shown that slow MyHC 2 gene expression in vitro is regulated by a combination of innervation and cell lineage. This pattern of gene expression was indistinguishable from the pattern observed in vivo in that it was restricted to innervated muscle fibers of slow muscle origin. We show here that slow MyHC 2 gene expression in the slow muscle fiber lineage is regulated by protein kinase C (PKC) activity. Inhibition of PKC activity induced slow MyHC 2 gene expression, and the capacity to express the slow MyHC 2 gene was restricted to muscle fibers of slow muscle (medial adductor) origin. Fast muscle fibers derived from the pectoralis major did not express significant levels of slow MyHC 2 with or without inhibitors of PKC activity. This differential expression pattern coincided with different inherent PKC activities in fast versus slow muscle fiber types. Furthermore, over-expression of an unregulated PKCalpha mutant suppressed slow MyHC 2 gene expression in muscle fibers of the slow lineage. Lastly, denervation of skeletal muscles caused an increase in PKC activity, particularly in the slow medial adductor muscle. This increase in PKC activity was associated with lack of slow MyHC 2 gene expression in vivo. These results provide a mechanistic link between innervation, an intracellular signaling pathway mediated by PKC, and expression of a muscle fiber type-specific contractile protein gene. Dev Dyn 1999;216:177-189

MyHC II content in the vastus lateralis m. quadricipitis femoris is positively correlated with the magnitude of the non-linear increase in the VO2 / power output relationship in humans.

Source

Department of Muscle Physiology, AWF-Krakow, Poland. wfzoladz@cyf-kr.edu.pl

Abstract

In this study we have examined the relationship between the content of different isoforms of MyHC in the vastus lateralis m. quadricipitis femoris and the VO2 / power output relationship during incremental cycling exercise. Twenty-one male subjects: aged 24.0 +/- 2.5 years, body mass 73.0 +/- 7.2 kg, height 179 +/- 5 cm, BMI 22.78 +/- 1.84 kg x m(-2), VO2(max) 3697 +/- 390 ml x min(-1), 50.9 +/- 5.2 ml x kg(-1) x min(-1), participated in this experiment. The subjects performed an incremental exercise test until exhaustion. The exercise test started at power output of 30 W, followed by an increase amounting to 30 W every 3 minutes. The pedalling rate was maintained at 60 rev x min(-1). Gas exchange variables were measured continuously using breath-by-breath system Oxycon Jaeger. At the end of each step blood samples were taken for lactate concentration. Muscle biopsy samples taken from the vastus lateralis m. quadricipitis femoris, using the Bergstrom needle, were analysed for the content of different MyHC (I, IIa, IIx) using SDS-PAGE and Western blotting. The pre-exercise VO2, as a mean value of six-minute measurements, expressed both in ml x min(-1), and in ml x kg(-1) x min(-1), was positively correlated with the content of MyHC II in the vastus lateralis (p < 0.01). We have also found that the pre-exercise values of VO2 in the group of subjects with a high proportion of MyHC II (59.9 +/- 11.2 %) were significantly higher (p < 0.02, when VO2 was expressed in ml x min(-1), and p < 0.01 when VO2 was expressed in ml x kg(-1) x min(-1)) than in the group with low content of MyHC II (27.5 +/- 6.0 %) in the vastus lateralis. Moreover, we have found a significant negative correlation (r = -0.562, p < 0.01) between the slope in the VO2/PO relationship below the lactate threshold (LT) and the content of MyHC IIa in the vastus lateralis. The most interesting finding of our study was that the magnitude of the non-linear increase in the VO2 / power output relationship present above the LT was positively correlated ( r = 0.510, p < 0.02) with the content of MyHC II in the vastus lateralis. Our results show, that there is no simple relationship between the content of different types of MyHC in the vastus lateralis and the oxygen cost of work during incremental exercise test. Individuals with a high content of MyHC II in the vastus lateralis m. quadricipitisfemoris consume more oxygen in the pre-exercise conditions than subjects with a low content of MyHC II in their muscles. Subjects with a high content of MyHC II require a smaller increase in VO2 for maintaining a linear increase in power output up to the lactate threshold (lower slope in this relationship), but after exceeding the LT, they consume more oxygen above that expected from the linear relationship below the LT, than the subjects with a low content of MyHC II in their muscles. Therefore, non-linear increase in the VO2 / power output relationship, present above the LT, is more pronounced in subjects with a higher content of MyHC II in the vastus lateralis m. quadricipitis femoris.


 Now you see why we open all our presentation with the following picture, when we introduce ideas like MOXY.


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