Freethought & Rationalism Archive

Tara · 04-23-2003, 02:26 AM

This topic came up on a track and field message board where signal to noise ratio is ever leaning towards predominance of noise. But against all odds, in the face of tremendous idiocy, a brief, but ostensibly scientific discussion of skeletal muscle fibre types did proceed... piquing my interest. Saddly, I�m ignorant of physiology, and biology in general for that matter, but I�m very curious to find out more on this specific topic. So on stumpling upon this site and I thought presenting my query here might yield some valuable input. Suggestions of where I could follow up on this would be most helpful as well.

Here�s the most scientific seeming post from Letsrun.com on the topic in review. Go here for a full look at a group of runner's pseudo-scientific physiology/genetics discussion...

Quote:

I am nearly half-way through a Ph.D. program in physiology and developmental biology. I specialize in exercise biochemistry and am working with an internationally renowned professor in this area.

AH nailed it right on.

As for muscle "tuning" to a specific activity there are a number of ways it can adapt. Everyone talks about it being a certain percentage of slow twitch and fast twitch being set and never changing. This is false. The myosin heavy chain (not myosin light chain as GW said) composition of single fibers adapts to the specific activity imposed upon it. Myosin is the main contractile protein of skeletal muscle and exists in three major isoforms in humans. Type I, IIa, and IIx (used to be called IIb), sometimes called slow, fast oxidative, and fast glycolytic respectively.

There are some old-school studies saying that fiber type is set at birth and doesn't change. This is false and is mostly based off histochemical studies. Separating myosin heavy chain (MHC) by gel electrophoresis shows that "fiber-type" does indeed change with training within.

Any activity imposed upon skeletal muscle leads to a drop-out of type IIx myosin and an increase in type IIa myosin. Additionallly, myosin expression pattern in elite athletes has been examined. What research is out there show that elites tend to have more hybrid fibers than moderately trained individuals. A hybrid fiber is a muscle fiber that expresses more than one type of myosin. In one study by Kligaard et. al. on elite cross country skiers it was found that they had a large number of hybrid fibers co-expressing MHC type I and IIa. In other words they had a large number of fibers with both high oxidative and contractile capabilities.

No longitudinal studies have been done to show this process taking place, rather it has always been observed ex post. So, maybe they were elite because they had a greater genetic endowment to produce hybrid fibers. Did the chicken or the egg come first here? Nobody knows yet.

Studies done on animals with chronic electrical stimulation of muscles can convert slow to fast and vice versa depending on the frequency of stimulation. In humans and rats the soleus muscle tends to be most slow twitch. Even with artifical electrical stimulation the soleus will not full convert to fast twitch muscle. This indicates that certain boundaries were set during cell differentiation. This is why flo-jo would never win an olympic marathon. She does have the gene for type 1 mysosin but during cell differentiation chromatin structure etc. was set-up so that it is more difficult for here to express that gene. (Thats really an over simplification--it could be diffent alleles for differnt transcription factors etc. Interestingly, the major transcription factor for type I and IIa mysosin is Myo-D.)

Additionally, pennation angle can change with training too. Pennation angle is the angle of the myosin/fibers relative to diretion of force transmission and can be optimized to a certain degree for force output of a certain type.

But the age old question as to what is changing over YEARS that allows someone to get continually get fast--nobody knows the full answer. Change in MHC composition happens fairly quickly initially--a few months.

Recently, some of the signaling that causes mitochondrial biogenesis has been unraveled with a major study coming out of the lab I work in. I tell about that some other time if anybody cares. You won't find it out from runningart or anybody else on this board for that matter.

For a good review on myosin heavy chain adaptation with exercise see the following review by Dirk Pette (he's the world leader in fiber type changes induced by electrica stimulation--no I don't work in his lab. I'm based in the U.S.
-----------------------------------------------------------
Can J Appl Physiol 2002 Aug;27(4):423-48 Related Articles, Links

The adaptive potential of skeletal muscle fibers.

Pette D.

Department of Biology, University of Konstanz, Germany.

Mammalian skeletal muscle fibers display a great adaptive potential. This potential results from the ability of muscle fibers to adjust their molecular, functional, and metabolic properties in response to altered functional demands, such as changes in neuromuscular activity or mechanical loading. Adaptive changes in the expression of myofibrillar and other protein isoforms result in fiber type transitions. These transitions occur in a sequential order and encompass a spectrum of pure and hybrid fibers. Depending on the quality, intensity, and duration of the alterations in functional demand, muscle fibers may undergo functional transitions in the direction of slow or fast, as well as metabolic transitions in the direction of aerobic-oxidative or glycolytic. The maximum range of possible transitions in either direction depends on the fiber phenotype and is determined by its initial location in the fiber spectrum.

Wounded King · 04-23-2003, 02:49 AM

Did you manage to get the reference provided in that post?

If not there is a review by the same author available online.

Pette D. The adaptive potential of skeletal muscle fibers.
Can J Appl Physiol. 2002 Aug;27(4):423-48

Reading the primary literature or reviews like this are probably the best way to find out about muscle type plasticity.

Tara · 04-23-2003, 04:12 AM

I was actually just looking for that reference. Thanks a lot. That should go far in helping... I thought maybe only the abstract was available online at first.

While I'm at this, if I'm allowed to go off on a different topic, apologies for the bad message board etiquette, but I only need a few good responses (or just one) and don�t want to start a new thread for such a simple question� So in an effort to dispel one of the "scientific truths" I've heard spouted, it's entirely false to say you can "go beyond your genetic endowment," correct?

Someone, supposedly of some credibility on the subject, was trying to tell me that this is possible because athletic training can induce the expression of different genes... but uh, that's hardly going beyond your genetic endowment, correct? The DNA contained in a person's 46 chromosomes is set, hard and fast, ever after recombination, spontaneous mutations and all that might happen in meiosis... no?

Some have already told me this idea of being able to go beyond genetics is misguided, but if someone could reiterate I'd be thankful. I just want to hear a clearer, more convincing argument against this.

Wounded King · 04-23-2003, 04:27 AM

I think it was more badly worded than misguided. He doesnt seem to be suggesting you gain genes, simply that you can up/down regulate the expression of specific sets. It seems to be more a case of going beyond a baseline muscle character determined by your normal levels of gene expression. Genes obviously are not sufficient to make someone a top athlete a lot of hard 'nurture' is required.

Godot · 04-23-2003, 04:43 AM

First off, I think you need to get this point clarified:

Quote:

I am nearly half-way through a Ph.D. program in physiology and developmental biology. I specialize in exercise biochemistry and am working with an internationally renowned professor in this area.

And I'm a 300-ft tall pink elephant. If this is the case, they should be willing to at least divulge the institution at which they are studying as well as the name of their "internationally renowned professor". That would provide you with a name to search for on Highwire.
Your genetic endowment is all you have. Going beyond it is incomprehensible. Hell, most people don't even approach their potential by a couple of light years! To be idiomatic, training can only help you "unlock" your potential.
The concept of endurance training (or any form of training for that matter) being able to effect a spontaneous, random and positive mutation is certainly a novel one for me.

Wounded King · 04-23-2003, 04:56 AM

Why should they be willing to divulge that information? Who he is is hardly germane as long as his references are relevant and the information is accurate. Besides, he only claimed to be half way through a PhD, its not as if he was saying that he was an internationally renowned professor.

ps418 · 04-23-2003, 07:46 AM

Quote:

Originally posted by Tara
So in an effort to dispel one of the "scientific truths" I've heard spouted, it's entirely false to say you can "go beyond your genetic endowment," correct?

. . .

Some have already told me this idea of being able to go beyond genetics is misguided, but if someone could reiterate I'd be thankful. I just want to hear a clearer, more convincing argument against this.

Its obviously true in a sense that you can not go 'beyond' your genetic endowment. But its also true that your genetic endowment can be expressed in different ways, depending upon non-genetic, environmental differences.

That said, genetic differences clearly account for a substantial portion of all sorts of athletics-relevant individual differences, including things like the ratio of fast-twitch/slow-twitch muscle fibers, muscle-fiber number, muscle-fiber response to resistance training, heart volume, the blood concentration of hemoglobin, hematocrit and red blood cell count, long bone lengths, strength and proportion, muscle insertion points, plasma testosterone levels (which influence how much muscle mass you can add through training), and so on.

This does not mean that none of these things can be altered by training, because many of them can be. Muscles for one are extraordinarily plastic. But it does mean that because of genetic differences, individuals will respond to the training differentially. Genetics does contribute in many different ways to both actual and potential athetic ability.

To take the example of muscle fiber type proportions, both genetic endowment and training play signficant roles. Training does significantly alter fiber proportions. But differential training alone does not explain all differences in the fiber proportions, or in the absolute number of muscle fibers (see below).

Quote:

Skeletal muscle fiber type distribution is quite heterogeneous, with about 25% of North American Caucasian men and women having either less than 35% or more than 65% of type I fiber in their vastus lateralis muscle. To what extent human skeletal muscle fiber type proportion is under the control of genetic factors is examined in this paper. The results summarized here suggest that about 15% of the total variance in the proportion of type I muscle fibers in human is explained by the error component related to muscle sampling and technical variance, that about 40% of the phenotype variance is influenced by environmental factors, and the remaining variance (about 45%) is associated with inherited factors. These estimates suggest that a difference of about 30% in type I fibers among individuals could be explained exclusively by differences in the local environment and level of muscular contractile activity. However, unidentified genetic factors would have to be invoked to account for the observation that the skeletal muscle of about 25% of the North American Caucasian population have either less than 35% or more than 65% of type I fibers.

Simoneau JA, Bouchard C., Genetic determinism of fiber type proportion in human skeletal muscle. FASEB J 1995 Aug;9(11):1091-5.

Quote:

The purpose of the study was to estimate the genetic effect for skeletal muscle characteristics using pairs of nontwin brothers (n = 32), dizygotic (DZ) twins (n = 26), and monozygotic (MZ) twins (n = 35). They were submitted to a needle biopsy of the vastus lateralis for the determination of fiber type distribution (I, IIa, IIb) and the following enzymes were assayed for maximal activity: creatine kinase, hexokinase, phosphofructokinase (PFK), lactate dehydrogenase, malate dehydrogenase, 3-hydroxyacyl CoA dehydrogenase, and oxoglutarate dehydrogenase (OGDH). For the percentage of type I fibers, intraclass correlations were 0.33 (p less than 0.05), 0.52 (p less than 0.01), and 0.55 (p less than 0.01) in brothers and DZ and MZ twins, respectively. MZ twins exhibited significant within-pair resemblance for all enzyme activities (0.30 less than or equal to r less than or equal to 0.68). In spite of these correlations, genetic analyses performed with the twin data alone indicated that there was no significant genetic effect for muscle fiber type I, IIa, and IIb distribution and fiber areas. Although there were significant correlations in MZ twins for all muscle enzyme activities, the often nonsignificant intraclass coefficients found in brothers and DZ twins suggest that variations in enzyme activities are highly related to common environmental conditions and nongenetic factors. However, genetic factors appear to be involved in the variation of regulatory enzymes of the glycolytic (PFK) and citric acid cycle (OGDH) pathways and in the variation of the oxidative to glycolytic activity ratio (PFK/OGDH ratio). Data show that these genetic effects reach only about 25-50% of the total phenotypic variation when data are adjusted for age and sex differences.

Bouchard et al, Genetic effects in human skeletal muscle fiber type distribution and enzyme activities. Can J Physiol Pharmacol 1986 Sep;64(9):1245-51.

Quote:

The role of heredity in the response of maximal anaerobic capacities and skeletal muscle histochemical and biochemical characteristics to a 15-week cycle ergometer training program involving both continuous and interval work patterns was investigated in 14 pairs of monozygotic twins. The training program consisted mainly of series of ergocycle supramaximal exercises lasting from 15 s to 90 s and performed 4 and 5 times a week. The subjects were submitted to 10 s and 90 s all-out ergocycle tests to estimate maximal anaerobic alactacid (AAC) and lactacid (ALC) capacities, respectively. Muscle fiber types and creatine kinase (CK), hexokinase (HK), phosphofructokinase (PFK), lactate dehydrogenase (LDH), malate dehydrogenase (MDH), 3-hydroxyacyl CoA dehydrogenase (HADH), and oxoglutarate dehydrogenase (OGDH) activities were determined in a biopsy from the vastus lateralis. Training increased AAC, ALC, fiber type I proportion, MDH, HADH, and OGDH (P less than 0.05) and decreased fiber type IIb proportion and the PFK/OGDH ratio. No significant change was observed for CK, HK, PFK, and LDH. Large interindividual differences in the response to training were observed for all variables. However, intraclass correlations indicated that the extent of the response of ALC and CK, HK, LDH, MDH, and OGDH activities and of the PFK/OGDH activity ratio to training were significantly similar within pairs of twins. Although the role of heredity appeared absent for the changes in fiber type proportions and in anaerobic alactacid capacity, the present results suggest that the response of anaerobic lactacid capacity and most enzyme activities to high-intensity intermittent training is significantly determined by the genotype.

Simoneau et al, Inheritance of human skeletal muscle and anaerobic capacity adaptation to high-intensity intermittent training. Int J Sports Med 1986 Jun;7(3):167-71.

Another important component of athletic ability that is signficantly genetically influenced is the VO2 max, which is the maximum amount of oxygen in milliliters that can be utliized in one minute, per kilogram of body weight. VO2max is a major factor in aerobic endurance. As with muscle fiber type proportions, VO2max can be increased by training, but the response to training is significantly inluenced by genotype, and not all individual or population-level differences are the result of differential training (see below). Also, there is at least one genetic polymorphism (the I variant of the angiotensin I-converting enzyme) that has been associated with variation in aerobic endurance (Woods et al, 2002)

Quote:

PURPOSE: This study investigates the familial resemblance of VO2 at the ventilatory threshold (VO2vt) from 199 nuclear families (100 White and 99 Black) participating in the HERITAGE Family Study. METHODS: VO2vt (mL x min(-1)) was determined in the sedentary state and again after 20 wk of aerobic cycle ergometer exercise training in 339 individuals (131 parents and 228 of their offspring), aged between 17 and 65 yr. VO2vt was adjusted for weight, age, fat mass, and fat-free mass by using regression methods. RESULTS: There was evidence for significant familial resemblance in the sedentary state for VO2vt (maximal heritability = 58% in White and 54% in Black families) and VO2vt/VO2max (maximal heritability = 38% in White and 39% in Black families). Spouse, sibling, and parent-offspring relationships for VO2vt were significant at baseline, suggesting that both genetic and shared environmental factors may contribute to the familial resemblance in the sedentary state. There was a moderate familial component in the response of VO2vt to aerobic exercise training in Whites (22%) and a larger component in Blacks (51%). In Blacks, the familial effect for VO2vt/VO2max appeared to be accounted for by fat and fat-free mass. CONCLUSION: These results show a strong familial contribution to VO2vt in the sedentary state and to the response of VO2vt to aerobic exercise training.

Gaskill et al, Familial resemblance in ventilatory threshold: the HERITAGE Family Study. Med Sci Sports Exerc 2001 Nov;33(11):1832-40.

Quote:

Quechua natives of the highland Andes may be genetically adapted to high altitude and thus able to resist decrements in maximal O2 consumption in hypoxia (DeltaVO2max). This evolutionary hypothesis was tested via the repeated measures of VO2max (sea level versus 4,338m) in 30 young male Peruvians of mixed Spanish and Quechua origins. Genetic admixture level (% Spanish ancestry) was estimated on each individual using a panel of 22 ancestry-informative DNA markers. Genetic admixture explained a significant proportion of the variability in DeltaVO2max after control for major covariate effects including sea level VO2max and the decrement in arterial O2 saturation measured at VO2max (DeltaSPO2max) (R(2) for admixture and covariate effects ~0.80). The genetic effect reflected a main effect of admixture on DeltaVO2max (P=0.041), as well as the interaction between admixture and DeltaSpO2max (P=0.018). Admixture was predictive of DeltaVO2max only in subjects with a large DeltaSpO2max at 4,338 m (P=0.031). In such subjects, DeltaVO2max was 12-18% larger in the highest versus lowest subgroup of Spanish genetic ancestry, with least square mean values (+/-S.E.) of 739+/-71 ml(.)min(-1) versus 606+/-68 ml(.)min(-1) (11.1+/-1.3 ml(.)min(-1.)kg(-1) versus 9.7+/-1.3 ml(.)min(-1.)kg(-1)), respectively. A suggestive trend for interaction (P=0.095) was also noted between admixture and the decrease in ventilatory threshold at 4,338 m (DeltaVEthresh). Similar to the previous interaction, admixture was predictive of DeltaVO2max only in subjects with a large DeltaVEthresh. Together, these interactions suggest that the putative genetic effect on DeltaVO2max depends on a subjects' aerobic fitness level. In particular, genetic effects may be more important (or easier to detect) in very athletic subjects who are more likely to show gas exchange impairment during exercise. In summary, the results of this study are consistent with the evolutionary hypothesis, and point to a better gas exchange system in Quechua as a possible explanation for the admixture effect detected.

Brutsaert et al, in press, Spanish genetic admixture is associated with larger VO2max decrement from sea level to 4,338 meters in Peruvian Quechua. J Appl Physiol 2003 Apr 11; [epub ahead of print].

Quote:

Human physical performance is strongly influenced by genetic factors. We have previously reported that the I variant of the human angiotensin I-converting enzyme (ACE) gene is associated with greater endurance performance in mountaineers and Olympic runners and improved performance in army recruits. In this study we examined whether this effect is mediated by improvements in cardiovascular fitness with training in 58 army recruits homozygous for the insertion (I, ACE genotype II) or deletion (D, ACE genotype DD) allele. A submaximal and maximal exercise protocol was used to calculate both the heart rate/oxygen uptake (VO2) relationship and changes in maximal oxygen uptake (VO2max), respectively. There was no significant intergroup difference in VO2max at baseline (P=0.19) or after training (P=0.22). There was no difference between genotypes with training in the heart rate/VO2 elevation (P = 0.79 for the mean difference in mean adjusted heart rates). However, VO2 at all exercise intensities in the submaximal test was lower for all subjects after training and at 80 W the reduction in VO2 was greater for the II subjects compared to DD subjects [mean(SEM)] [1.6 (0.27) and 0.68 (0.27) ml kg(-1) min(-1), respectively; P = 0.02 for mean difference]. The I/D polymorphism may play a role in enhanced endurance performance but this is not mediated by differences in VO2max or the heart rate/VO2 relationship in response to training.

Woods et al, Endurance enhancement related to the human angiotensin I-converting enzyme I-D polymorphism is not due to differences in the cardiorespiratory response to training. Eur J Appl Physiol 2002 Jan;86(3):240-4.

Patrick

Godot · 04-23-2003, 07:58 AM

Quote:

Originally posted by Wounded King
Why should they be willing to divulge that information? Who he is is hardly germane as long as his references are relevant and the information is accurate. Besides, he only claimed to be half way through a PhD, its not as if he was saying that he was an internationally renowned professor.

Who he is is of no consequence. If he's claiming to have an internationally renowned professor as his supervisor (supposedly in this field), then he's doing it to either name drop or because it is true. Divulging the name of the renowned professor may turn up some interesting papers in this field; that was my point.

Wounded King · 04-23-2003, 08:42 AM

He did give a name to search for, not his professors but then he doesnt claim that he works on this specific field so his supervisors work is not neccessarily going to be at all relevant.

Your pink elephant quote did suggest that you felt the poster was unreliable becuase he didnt give out his personal details, or at least details which may have allowed him to be identified.

Godot · 04-23-2003, 09:27 AM

Quote:

Originally posted by Wounded King
He did give a name to search for, not his professors but then he doesnt claim that he works on this specific field so his supervisors work is not neccessarily going to be at all relevant.

I have to disagree with you on this point. To wit:

Quote:

I am nearly half-way through a Ph.D. program in physiology and developmental biology. I specialize in exercise biochemistry and am working with an internationally renowned professor in this area.

Not to be a prick about it, but this sounds like it's his field.

Quote:

Your pink elephant quote did suggest that you felt the poster was unreliable becuase he didnt give out his personal details, or at least details which may have allowed him to be identified.

Agreed and understood. It was intended more as an indictment of the anonymity of the internet.

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04-23-2003, 02:49 AM	#2
Wounded King Veteran Member Join Date: Mar 2003 Location: Edinburgh Posts: 1,211	Did you manage to get the reference provided in that post? If not there is a review by the same author available online. Pette D. The adaptive potential of skeletal muscle fibers. Can J Appl Physiol. 2002 Aug;27(4):423-48 Reading the primary literature or reviews like this are probably the best way to find out about muscle type plasticity.

04-23-2003, 04:12 AM	#3
Tara Junior Member Join Date: Apr 2003 Location: Florida US Posts: 67	I was actually just looking for that reference. Thanks a lot. That should go far in helping... I thought maybe only the abstract was available online at first. While I'm at this, if I'm allowed to go off on a different topic, apologies for the bad message board etiquette, but I only need a few good responses (or just one) and don�t want to start a new thread for such a simple question� So in an effort to dispel one of the "scientific truths" I've heard spouted, it's entirely false to say you can "go beyond your genetic endowment," correct? Someone, supposedly of some credibility on the subject, was trying to tell me that this is possible because athletic training can induce the expression of different genes... but uh, that's hardly going beyond your genetic endowment, correct? The DNA contained in a person's 46 chromosomes is set, hard and fast, ever after recombination, spontaneous mutations and all that might happen in meiosis... no? Some have already told me this idea of being able to go beyond genetics is misguided, but if someone could reiterate I'd be thankful. I just want to hear a clearer, more convincing argument against this.

04-23-2003, 04:27 AM	#4
Wounded King Veteran Member Join Date: Mar 2003 Location: Edinburgh Posts: 1,211	I think it was more badly worded than misguided. He doesnt seem to be suggesting you gain genes, simply that you can up/down regulate the expression of specific sets. It seems to be more a case of going beyond a baseline muscle character determined by your normal levels of gene expression. Genes obviously are not sufficient to make someone a top athlete a lot of hard 'nurture' is required.

04-23-2003, 04:56 AM	#6
Wounded King Veteran Member Join Date: Mar 2003 Location: Edinburgh Posts: 1,211	Why should they be willing to divulge that information? Who he is is hardly germane as long as his references are relevant and the information is accurate. Besides, he only claimed to be half way through a PhD, its not as if he was saying that he was an internationally renowned professor.

04-23-2003, 08:42 AM	#9
Wounded King Veteran Member Join Date: Mar 2003 Location: Edinburgh Posts: 1,211	He did give a name to search for, not his professors but then he doesnt claim that he works on this specific field so his supervisors work is not neccessarily going to be at all relevant. Your pink elephant quote did suggest that you felt the poster was unreliable becuase he didnt give out his personal details, or at least details which may have allowed him to be identified.

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