Genotype and Phenotype Muscle Fibers

Elite athletes are born, and no matter how hard an athlete trains, changing their genotype is unlikely. There are mainly two types of genes, genotype and phenotype. Genotypes are the muscle type you are born with that will not change, and phenotypes are highly influenced by the environment or exercise adaptations. This literature review will be looking at phenotype and discovering if fiber types have the capability to convert from one muscle type to the next with aerobic endurance training. Research had done a good job proving that resistance training will increase type II fibers, as well have increase cross sectional area (CSA) and cause hypertrophy. The research studying fiber type conversion is a little more scattered.

There are mainly 4 different types of muscle fibers: type I, type IIa, type IIx, and type IIb. Type I fibers or slow twitch fibers are highly oxidative, fatigue resistant, are mitochondria rich, have an intermediate color, and used for posture during rest or for long endurance/aerobic type exercise (Brooks, Fahey, & Baldwin, 2005). Type IIb muscle fibers, found in rodents not humans, are the complete opposite of type I. They are fast twitch highly glycolytic, fatiguable, low mitochondria, have a whitish color, and used during anaerobic high intensity exercise. As for type IIa, they are fast twitch fibers with oxidative and glycolytic properties, and a redish color. Humans can also develop type IIx muscle fibers, which are fast twitch, glycolytic, and fatiguable. According to Anderson, Schjerling, & Saltin (2000), to produce a protein, a muscle cell must have a "blueprint" to specify the order in which amino acids should be put together to make the protein. The nucleus copies the DNA into a molecule called messenger RNA (mRNA). When information leaves the nucleus and enters into the cytoplasm, where the protein will be made, this action starts the transcription process. The last step in the assembly of amino acid is the translation, where expression of the gene is made. This literature review will focus on studies using aerobic training to produce more oxidative muscle fiber. A few studies have tried to convert type I fibers to type II, but studies have been unable to see any consistent data of fast type IIa fibers being converted to type I (Anderson et al. 2000). The time required for this type of conversion is quite lengthy in comparison to the time it takes to shift from IIx and IIa.

The seven articles used in this literature review studied different subjects, different protocols determining lower body muscle type, and found similar result. The bulk of the studies used the gastronomies as the fast twitch muscle fiber and the soleus as the slow twitch muscle fiber. Five studies by Termin, Staron, & Pette (1989), Bigard et al. (1999), Wang et al, (2004), Handschin et al. (2007) and Tikikita et al. (2010), used rats to look at two types of genes PGC-Ia and PPARS. The other two studies used humans as there subjects. Anderson et al. (2000) looked at elite athletes and Dalgas et al. (2010) looked at patients with multiple sclerosis.

Termin, Staron, and Pette (1989), investigated properties and distribution of HCIId and fiber type IID in view of its intermediate characteristics in adult male Wistar rats. The results found that chronic low-frequency stimulation gradually decreased the HCIIb content. Interestingly, large variation existed in the HCIIa and HCIId distribution between different animals stimulated for equal time periods. For example, unlike rabbits, fast-twitch muscle in rats does not respond to increase contractile activity with appreciable increases in slow myosin light or heavy chain isoforms. A rapid decrease in HCIIb mRNA was observed and an increase in HCIIa mRNA in chronically stimulated rat fast twitch muscles. It appears that the stimulation induced transitions follow the order HCIIb→HCIId → HCIIa.

In 1999, Bigard and collegues examined the impact of endurance training on MHC distribution in the fast-twitch muscle a long time after damage, when the muscle has had time to fully regenerate. The study used male Wistar rats that were given a toxin injection and put through a 5 week treadmill running program (T-Trained) or nothing (S-Sedentary). Oddly enough, trained and sedentary rats had no significant differences for body weight. The trained rats had increased type IIa and type IIx, while typeIIb decreased. This study illustrated that endurance training alters the pattern of MHC expression in EDL muscle during regeneration. The speed at which myosin transitions occurred as a result of endurance training was not affected by the immaturity of the growing fibers. Unfortunately, Bigard et al. (1999) was unable to explain why regenerated myofibers are more sensitive to exercise training than regenerating one.

In obese and diabetic patients, skeletal muscle has been observed to have a reduced oxidative capacity and a decreased percentage of type I fibers. Wang and colleagues (2004) believe an increase in oxidative fibers can lead to improved insulin action and reduced adipocyte size. This study uncovers the possibility that PPARS, as the first transcription factor able to drive the formation of function type I muscle fibers, can cause an activation through a complex pathways both enhancing physical performance and creating a state of obesity resistance. The results found that activation of PPARS leads to muscle fiber transformation similar to PGC-Ia, and higher levels of PPARS revealed higher levels of type I fibers. Another observation found muscle fiber switch by PPARS protects against obesity. Transgenic or mice with PPARS and control mice were both fed high fat diets. The control mice became obese, whereas the transgenic mice still maintained a normal body weight and fat mass composition. This article shows that mice with increased oxidative fibers are resistant to high-fat induced obesity and glucose intolerance. Lastly, this research article found activation of PPARS enhances physical performance. Transgenic mice were able to sustain a higher running distance, and ran about 1 hour longer than the control mice. The PPARS mediated transcription gene was considered the "long-distance running" phenotype (Wang et al., 2004). Overall this article indicates that exercise may increase endogenous ligands for PPARS as tissues are undergoing substantial increases in fatty-acid internalization and burning. Exercise can also induce expression of PGC-Ia and thereby activate PPARS.

Handschin and colleagues (2007) used