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Received March 31, 2008
Revised April 25, 2008
Accepted after revision April 25, 2008
1 Università degli Studi di Verona
2 Institute of Clinical Pathology and Medical Research (ICPMR), Westmead Hospital
* To whom correspondence should be addressed. E-mail: ulippi{at}tin.it.
We have read with interest the recent article by Williams and Folland., who concluded that human physical performance is essentially multifactorial and determined by a range of environmental (physical training, nutrition and technological aids) and genetic factors (Williams & Folland, 2008). Identifying the genes relevant to human athletic performance has been difficult in the past, because each causal gene makes only a small contribution to overall heritability. Accordingly, the adoption of a "single-gene-as-magic-bullet" philosophy is questionable, especially considering that the 2005 human gene map for physical performance and health-related phenotypes already includes 165 autosomal gene entries and quantitative trait loci, plus five others on the X chromosome (Lippi, 2008). All these genes contribute, however, to generate a cluster of phenotypes. William and Folland highlighted that in addition to well-established maximal rate of oxygen uptake, at least three other endurance phenotypes (economy of movement, lactate/ventilatory threshold and, potentially, oxygen uptake kinetics) contribute to the endurance performance phenotype (time taken to travel a given distance) seen in elite competition (Williams & Folland, 2008).
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