Finally some good news. Since all my life I have been overweight and have only recently become serious about loosing it and getting into shape. I’ve always been active, until probably the last 10 years I’d say. That’s when it all started to really pack on. In high school I weighed around 220 but I worked out 3x a week lifting weights, cardio, racquetball, etc.. I grew up playing football, baseball, and riding my bike everywhere.
In college it didn’t really change, I went out 3 or 4 nights a week, dancing for hours at the clubs till I’d be drenched in sweat. Running to classes, biking around campus. Generally running around to football games, basketball games. Doing any and all activities most college students do.
Met my husband and we moved out to Las Vegas, and still was active working, especially for Las Vegas MPD. We moved to Phoenix and boom. Couch-potato-itis. Now I know it’s my own fault but hey. I wasn’t looking to blame anyone. Cheetos + Large Pizza + Soda + Couch = Wide Ass … CHECK!

So now I’m changing things. Since I fell last September and sprained my ankle, and at the same time landed so hard on my right knee that I blew out (destroyed) the cartilage behind my kneecap (patella). The official diagnosis was “Partial thickness chondral defect in the lateral femoral condyle with moderately severe chondrosis of the patella”. In other words. You’ve screwed your knee but good missy. So when I walk the patella scrapes on the bones/ligaments if I don’t walk correctly. Trust me, I walk correctly.

I did my physical therapy, and without Kevin and Stephen I’d still be not walking, or walking but hopped on meds and in pain. Pushing myself through PT I think changed me. Snapped something inside me, made me realize that I’m on the downside of this lease hold of life. Time to move it or lose it. So move it I am. The total as of today is 58 lbs gone. That’s since May 4th. I’m happy with that. I was happier before the 4th of July weekend >:{ but that’s life.

I was checking my 23andMe reports looking for a genetics link for something and I found this report….

Muscle Performance
Your Data
Cynthia Kraft – CC – Two working copies of alpha-actinin-3 in fast-twitch muscle fiber. Many world-class sprinters and some endurance athletes have this genotype.

And I had a little pang of happiness inside me. Could this be why I don’t suffer DOMS (Delayed onset Muscle strain) as much as others complain about? Or is this why my muscles seem to respond when I ask them to, no matter how much I’ve abused them. I mean it only took me 3 weeks (9 sessions) to work from 2 minutes on the elliptical gasping for air, to 30 minutes on the elliptical moving along… And it’s been another week now, (3 more sessions) and I’ve just managed to complete my first 30 minute session with my Heart Rate (HR) completely in the Cardio zone for all 30 minutes. That’s HUGE. That took wicked effort. And I still did it at a 4 mph pace. ME. I weigh 408 lbs as of today, and I can set a 4 mph 15 minute mile pace. What. The. Fuck. If you’d have told me I could essentially run a marathon (that’s 26 miles) in 6.5 hours. I’d have told you. I couldn’t run one in 6.5 days… But there it is people…. in black and white…

I think I’m crazy. I think I just decided I want to try and run in a 5k. I was looking online and they have one in October. o_O I think I’ll aim for it at any rate… if I can get the elliptical down to quicker, or lesser HR or both. Hmm… yep. Can’t outrun the zombies if you can’t at least run 3 miles ;)

Anyway… more about the muscle stats below… And what it does/how it is defined etc… Information from 23andme.com in their journal section. Enjoy!

Learn More About ACTN3Marker:rs1815739

Athletic performance can be influenced by a number of factors, some of which are genetic. Genes determine between 20-80% of the variation in traits like oxygen intake, cardiac performance, and muscle fiber composition. To date, more than 150 genes have been linked to different aspects of physical performance. One of the clearest associations is seen with a gene called ACTN3 that is normally turned on in a type of muscle fiber used for power-based sports. A single SNP can turn this gene off. While this genetic change does not cause any health effects, it may contribute to whether you are a sprinter or a marathoner.

This gene produces a protein called alpha-actinin-3 that is only turned on in fast-twitch muscle fibers (the kind used for power events like sprinting or weightlifting). The protein forms part of the contractile machinery in muscle cells, where it is thought to play both structural and signalling roles.

The T version of the SNP in this gene prevents the full protein from being made. People with two copies of the T version thus have a total lack of alpha-actinin-3 in their fast-twitch muscle fibers. Those with the CT genotype have one functional copy of the gene and can still make the protein.

Surprisingly, a complete lack of the alpha-actinin-3 protein doesn’t seem to cause any type of disease. This is probably because another closely related protein can step in for alpha-actinin-3 in people without a functional copy. The substitute protein likely does not perform its job as well as alpha-actinin-3, resulting in worse performance in power exercises.

Despite lack of a disease outcome, researchers wondered if the absence of alpha-actinin-3 might have an effect on athletic performance. Studies of elite athletes in Australia and Finland showed that power athletes—those whose performance depends on fast-twitch muscle fibers—were much more likely to have at least one working copy of the gene than non-athletes. In one study of Olympic power athletes (i.e., the best of the best), all had at least one working copy. Similar results were found in a study of Spanish professional soccer players.

But does alpha-actinin-3 make a difference for non-athletes? In fact, it does.

One study looked at a group of Greek teenagers who had been tested for a variety of fitness measures related to power and endurance sports. In this group, ACTN3 genotype had no effect on the girls, but boys with the TT genotype were significantly slower in a 40 m sprint. Interestingly, running was the only power event that the different versions of ACTN3 seemed to affect. For activities like throwing a basketball or jumping into the air, performance was unaffected by genotype.

Another study looked at arm strength in a group of people before and after 12 weeks of strength training. ACTN3 genotype appeared to have no effect in men, but women with the TT genotype had lower strength at the beginning of the study. After the training program women with the TT genotype—those without a working copy of alpha-actinin-3—had made greater gains than the women with at least one functioning copy. This was true in both European and Asian women.

Scientists aren’t really sure why having alpha-actinin-3 would improve power performance. One theory is that the protein prevents damage in fast-twitch muscle fibers. The group who conducted the study of Greek teenagers thinks this explains why only running and not other power activities were affected by a lack of alpha-actinin-3. Running involves repeated use of the muscles, while jumping only uses muscles once: damage is not an issue.

The scientists who saw that women with the TT genotype were able to build up more strength than other women also think alpha-actinin-3 protects muscle fibers from damage. Muscle damage is what stimulates muscles to adapt and become stronger. Those with the TT genotype lack the protection against damage that alpha-actinin-3 normally provides, thus allowing a greater gain in strength.

Alpha-actinin-3 may also affect athletic performance by virtue of its effects on oxygen usage in muscle. Two studies (one in mice and one in humans) have shown that fast-twtich muscle fibers that lack functional copies of ACTN3 use more oxygen than those with at least one working copy. This type of metabolism might slow them down. Mice studies have also shown that these altered fibers are weaker and smaller than fibers containing alpha-actinin-3, but they are more efficient an resistant to fatigue—a situation that is better suited to endurance sports than sprinting.