Double muscling is a trait previously described in several mammalian species including cattle and sheep and is caused by mutations in the myostatin (MSTN) gene (previously referred to as GDF8). Here we describe a new mutation in MSTN found in the whippet dog breed that results in a double-muscled phenotype known as the “bully” whippet. Individuals with this phenotype carry two copies of a two-base-pair deletion in the third exon of MSTN leading to a premature stop codon at amino acid 313. Individuals carrying only one copy of the mutation are, on average, more muscular than wild-type individuals (p = 7.43 × 10−6; Kruskal-Wallis Test) and are significantly faster than individuals carrying the wild-type genotype in competitive racing events (Kendall's nonparametric measure, τ = 0.3619; p ≈ 0.00028). These results highlight the utility of performance-enhancing polymorphisms, marking the first time a mutation in MSTN has been quantitatively linked to increased athletic performance.
What I thought as I read about this dog muscle gene deletion mutation: Future genetic engineers looking to enhance human function will search through animal genetic variations and choose ones that provide desired enhancements. Take this myostatin mutation for example. Humans also have myostatin genes. A similar mutation introduced into human myostatin might yield the same enhancement to human musculature.
Other species of mammals are adapted to a large variety of conditions and ecological niches. They have many of the same genes but in different variations. We are going to find variations such as the one above that does something special for other species. These variations and their functional purposes are going to serve as a grab bag of pre-tested genetic variations that can allow humans to endow themselves with a large variety of special abilities that humans now lack.
No need to meekly accept the disapproving moral sanction of others when you do not exercise enough. If you do not like to exercise blame it on your genes.
Background
A sedentary lifestyle remains a major threat to health in contemporary societies. To get more insight in the relative contribution of genetic and environmental influences on individual differences in exercise participation, twin samples from seven countries participating in the GenomEUtwin project were used.
Methodology
Self-reported data on leisure time exercise behavior from Australia, Denmark, Finland, Norway, the Netherlands, Sweden and United Kingdom were used to create a comparable index of exercise participation in each country (60 minutes weekly at a minimum intensity of four metabolic equivalents).
Principal Findings
Modest geographical variation in exercise participation was revealed in 85,198 subjects, aged 19–40 years. Modeling of monozygotic and dizygotic twin resemblance showed that genetic effects play an important role in explaining individual differences in exercise participation in each country. Shared environmental effects played no role except for Norwegian males. Heritability of exercise participation in males and females was similar and ranged from 48% to 71% (excluding Norwegian males).
This result suggests one potential solution for the tendency of people in modern societies to get insufficient exercise: Genetically engineer offspring to get more joy from exercise. Also, identification of the genetic variations that contribute to the urge to exercise could lead to development of drugs that make exercise more enjoyable.
But genetic engineering will likely lead to the development of methods to reduce the need for exercise. Look at how anabolic steriods increase muscle mass build-up in response to exercise. We'll eventually have safer ways to control extent of muscle mass. We'll also gain complete control of appetite and find ways to cause the body to burn off excess fat. We'll also find lower exercise ways to produce other physiological benefits that we now gain from exercise.
Since an increasing fraction of all physical labor is automated we really need to find ways to adapt our metabolisms to the changes in our environment which are the results of our technology. This problem is only going to get worse as robots take over cleaning the house, mowing the lawn, and other physical chores us desk jockeys and drivers still do. Biotechnology will provide the solutions.
Dartmouth researchers have found yet another way to make mice have big muscles without exercise.
A team of researchers, led by scientists at Dartmouth Medical School and Dartmouth College, have identified and tested a gene that dramatically alters both muscle metabolism and performance. The researchers say that this finding could someday lead to treatment for muscle diseases, including helping the elderly who suffer from muscle deterioration and improving muscle performance in endurance athletes.
The ban on so-called "gene doping" or gene therapy by many athletic associations slows the rate of progress for the development of gene therapies that increase musculature. Eventually the athletic associations are going to split over this issue. New athletic associations will form that allow genetic engineering. Those associations and companies will put on competitions between the genetically enhanced that eclipse the competitions between natural humans.
Want big muscles without all the hard work? Genetic engineering of an enzyme is the ticket.
The researchers report that the enzyme called AMP-activated protein kinase (or AMPK) is directly involved in optimizing muscle activity. The team bred a mouse that genetically expressed AMPK in an activated state. Like a trained athlete, this mouse enjoyed increased capacity to exercise, manifested by its ability to run three times longer than a normal mouse before exhaustion. One particularly striking feature of the finding was the accumulation of muscle glycogen, the stored form of carbohydrates, a condition that many athletes seek by "carbo-loading" before an event or game. The study appears in the Nov. 14 online issue of the American Journal of Physiology: Endocrinology and Metabolism.
"Our genetically altered mouse appears to have already been an exercise program," says Lee Witters, the Eugene W. Leonard 1921 Professor of Medicine and Biochemistry at Dartmouth Medical School and professor of biological sciences at Dartmouth College. "In other words, without a prior exercise regimen, the mouse developed many of the muscle features that would only be observed after a period of exercise training."
Even if you were genetically engineered to grow big muscles naturally there might still be health benefits to exercise such as development of better arteries and veins. But then that just calls out for gene therapy the circulatory system to compensate for the lack of exercise there too.
The ability to stimulate muscle growth would bring great benefits to elderly people with shrivelled muscles. Okay scientists, figure this out before we get much older.
Witters, whose lab led the study, explains that this finding has implication for anyone with a muscle disease and especially for the growing proportion of the population that is aging. Deteriorating muscles often make the elderly much more prone to fall, leading to hip and other fractures. According to Witters, there is tremendous interest in the geriatric field to find ways to improve muscle performance.
Of course athletes will use gene therapy to enhance muscle strength as soon as it becomes possible.
"We now wonder if it's possible to achieve elements of muscular fitness without having to exercise, which in turn, raises many questions about possible modes of exercise performance enhancement, including the development of drugs that could do the same thing as we have done genetically," he says. "This also might raise to some the specter of 'gene doping,' something seriously being talked about in the future of high-performance athletes."
Gene doping will take off long before it becomes safe to use. Old folks will benefit from the willingness of athletes to take risks with new biotechnologies. The athletes will serve as very willing guinea pigs.