Genetic influences on the development of grip strength in adolescence

Genetic Influences on the Development of Grip Strength in Adolescence Sexual dimorphism in body size is quite small in humans, especially when viewed within the context of other great apes (Plavcan, 2012; Plavcan & van Schaik, 1997). Although a species-typical mating system cannot appropriately characterize humans, it is apparent that men display a considerable degree of pair bonding, as reflected by the fact that men are merely 7–8% taller and 15–20% heavier than women. These observations have led some authors (e.g., Wood & Eagly, 2002) to dismiss the possibility that male-male competition for mates was a pervasive sexual selection pressure in the Pleistocene environment of evolutionary adaptedness. Total body size, however, is a very crude indicator of a man’s capacity for physical competitiveness. It is likely that reproductive fitness in men was related to fighting success, which, in turn, is more dependent on muscular strength than overall body mass. Indeed, sexual dimorphism in fat-free (muscle) mass far exceeds that for total body mass. Upper-body muscle mass is approximately 75% higher in men than women (Lassek & Gaulin, 2009). As a major secondary sex characteristic, upper-body strength follows a different developmental course in males and females. Boys enjoy minimal advantages in physical strength over their female peers during much of childhood (Butterfield et al., 2009; Molenaar et al., 2010). Sexual dimorphism dramatically increases in middle adolescence – precisely when sexual behaviors and mating opportunities become palpable. From a functional evolutionary perspective, enhanced upper-body strength was likely shaped by recurrent male-male competition for mates in our hominid ancestors (Geary, 2010; Lassek & Gaulin, 2009; Sell, Hone, & Pound, 2012). Hand grip strength (HGS), in particular, is a potent indicator of physical competitiveness. Although it is most directly controlled by muscle fibers in the upper limbs, it is highly correlated with overall body strength (Wind, Takken, Helders & Engelbert, 2010). Furthermore, HGS contributes to proficiency in the use of thrusting tools and clubs – weapons which were highly useful in agonistic encounters during the Pleistocene (Geary, 2010; Young, 2003). Given the differing biological roles of males and females – the latter are specialized for gestation and parenting –the benefit-cost ratio of physical confrontation is much more advantageous in males. Consistent with this behavioral adaptation, large increases in lean body mass accompany secondary sexual development of males but not females (Kirchengast, 2010). The idea that intrasexual competition was responsible for sexual dimorphism in physical strength is supported by the sex-specific pattern of correlations between HGS and various behavioral measures. In males, but not females, HGS is positively associated with a past history of physical aggression and lifetime number of sexual partners (Gallup, White, & Gallup, 2007). These associations implicate testosterone as the mediating variable, given the latter’s role in affecting courtship/mating behaviors and intrasexual competition. Previous literature demonstrates profound sex differences in the HGS of young adults, with scarcely any females exhibiting a grip strength that matches the typical (median) male. In a large community sample of adults aged 20–25, the highest performing female corresponded to the 28th percentile of the male distribution (Leyk et al., 2007). Even when examining a highly select group of female athletes (elite handball and judo players), the top female only exceeded 58% of the unselected male participants. This striking difference between typical males and females strongly suggests that sex-influenced genetic mechanisms underlie the development of HGS. A trait is sex-influenced (or sex-limited) when the processes governing its phenotypic expression differ between males and females.1 Phenotypic expression of a trait might differ due to an interaction of sex hormones with genes (sex-influenced gene expression) or an interaction of gender with environmental exposure (see Isen & Baker, 2008). Sex-influenced genetic mechanisms are typically involved in the development of secondary sex characteristics, in which hormones induce change during and after puberty. Vocal pitch is a prime example; increases in sex hormones during puberty stimulate the lengthening of the pharynx and growth of the vocal cords in the larynx, most prominently in males (Fitch & Giedd, 1999). A classic indicator of sex-influenced processes is a difference in trait variance between males and females. One of the outstanding features of HGS – and indeed, most strength characteristics – is the much higher variability observed in males. The variance in HGS of young men is at least twice that of young women (Hanten et al., 1999; Leyk et al., 2007; Massy-Westropp et al., 2011; Mathiowetz et al., 1985; Mullerpatan, Karnik, & John, 2013; Werle et al., 2009). This suggests that the processes underlying the development of physical strength are different between the sexes. Sex differences in the variance of HGS manifest at puberty, and increasingly diverge as males advance through adolescence (Mathiowetz, Wiemer, & Federman, 1986; Butterfield et al., 2009). Thus, it appears that the masculinizing agent(s) contributing to higher mean HGS also induce greater variability. Sex-influenced processes can also be inferred on the basis of sex differences in the relative magnitude of genetic and environmental influences. It is unclear whether the excess HGS variance in males arises from genetic and/or environmental causes. The classic twin design, by exploiting differences in genetic similarity between monozygotic and dizygotic twins, can help determine the relative importance of genetic and environmental factors in the development of HGS. If individual differences in sensitivity and exposure to androgens are important determinants of HGS, then it is reasonable to assume that the higher phenotypic variance in males is due to novelgenetic effects introduced at puberty. This might lead, not only to more absolute genetic variance, but also to a greater relative role of genetic influences (i.e., higher heritability). On the other hand, it is possible that the greater male variance is due to increased environmental influences. For example, boys are more likely to participate in sports and other extra-curricular activities involving upper-body strength (Thomas, Nelson, & Church, 1991). There are substantial individual differences in physical training during adolescence, perhaps more so in males (given the wider opportunity afforded to them in pursuing their athletic endeavors). Greater variation in physical training could contribute to excess HGS variance via direct environmental effects. This could lead to a situation in which the overall phenotypic variance is higher in adolescent males, yet the proportion due to genetic factors (heritability) is lower. Heritability of HGS Heritability estimates obtained from large, representative studies of adult male twins are typically in the 50–60% range (Frederiksen et al., 2002; Reed, Fabsitz, Selby, & Carmelli, 1991; Silventoinen, Magnusson, Tynelius, Kaprio, & Rasmussen, 2008). However, there is a dearth of large-scale investigations examining the genetic/environmental structure of grip strength in childhood or adolescence (see Beunen & Thomis, 2000, for a review of several studies with small sample sizes). There is also a gap in the literature regarding sex differences in the heritability of HGS. One exception is Fredericksen et al. (2002), who observed a similar pattern of genetic and environmental influences on HGS in older men and women. Although not directly indexing HGS, Peeters et al. (2005) found that genetic influences on the stability of upper-body strength during adolescence were of greater importance in males than females. Present Study To our knowledge, no study has yet examined genetic influences on the development of HGS in adolescence. Although a prior study examined familial influences on change in HGS over a 7-year period, the sample design (use of nuclear families) precluded a disentangling of shared environmental and genetic influences (Katzmarzyk, Gledhill, Perusse, & Bouchard, 2001). Moreover, the authors did not focus on any particular developmental period. Adolescence is a period in which physical strength characteristics begin to dramatically diverge between the sexes. As such, it provides the ideal window to delineate the genetic/environmental causes of sexual dimorphismin HGS. We used a latent growth design to model the development of HGS across a six-year period spanning from early to late adolescence. By using a large representative sample of twins from approximately age 11 to 17, we sought to determine whether the genetic and/or environmental sources of HGS growth are similar between males and females.