Estrogen, exercise, and the skeleton

Abstract

Patterns of variation in bone size and shape provide crucial data for reconstructing hominin paleobiology, including ecogeographic adaptation, life history, and functional morphology. Measures of bone strength, including robusticity (diaphyseal thickness relative to length) and cross-sectional geometric properties such as moments of area, are particularly useful for inferring behavior because bone tissue adapts to its mechanical environment. Particularly during skeletal growth, exercise-induced strains can stimulate periosteal modeling so that, to some extent, bone thickness reflects individual behavior. Thus, patterns of skeletal robusticity have been used to identify gender-based activity differences, temporal shifts in mobility, and changing subsistence strategies. Although there is no doubt that mechanical loading leaves its mark on the skeleton, less is known about whether individuals differ in their skeletal responses to exercise. For example, the potential effects of hormones or growth factors on bone-strain interactions are largely unexplored. If the hormonal background can increase or decrease the effects of exercise on skeletal robusticity, then the same mechanical loads might cause different degrees of bone response in different individuals. Here I focus on the role of the hormone estrogen in modulating exercise-induced changes in human bone thickness.

Resistance training and hormone replacement increase MMP-2 activity, quality and quantity of bone in ovariectomized rats

“…On the other hand, it is known that mechanical stress produced by exercise training improves the bone mass 27,28 , mediated by the release of insulin-like growth factor-1 (IGF-1) by osteoblasts, which promotes the proliferation of these cells. The results of our study are corroborated by Pierce, Lee 26 , demonstrating that RT of moderate intensity promotes increases in BMC in rats 1 , Thus, the estrogen replacement has the capacity to increase bone formation concomitant with decreased bone resorption is due to the training load (body mass + training load) and higher concentrations of hormone, favoring greater mineral deposition 29 .…”

“…Estrogen deficiency is related to the occurrence and progression of osteopenia and osteoporosis and regulated by a powerful cytokine TNF-α, which is a primary mediator of bone resorption acting through the osteoprotegerin receptor (OPG) activator of the nuclear factor kB (RANK) system and inhibits a mesenchymal stem cell to become an osteoblast 29 . This activation depends on key factors such as runt-related transcription factor 2 (RUNX-2), bone morphogenetic proteins 2, and transforming growth factor-β (TGF-β) 12 .…”

Developmental evidence for obstetric adaptation of the human female pelvis

“…In humans, direct evidence for hormone-mediated sex-specific bone remodeling patterns of the pelvis is not yet available. Nevertheless, studies on long bone morphology indicate that sexual skeletal dimorphism develops via complex interactions between sex-specific steroid hormone levels, sex-biased gene expression, and gender differences in sensitivity to bone-loading conditions and to hormones such as the growth hormone/insulin-like growth factor 1 (IGF1) axis (42)(43)(44)(45).…”

Size and Shape: Morphology's Impact on Human Speed and Mobility

“…Studies that integrate mobility and reproductive success clearly show that the energetics of daily walking influence interbirth-intervals and offspring survivorship [6][7][8][9]. Studies that applied meta-analyses of ongoing selection in human populations further show a close relationship between locomotor morphology and reproductive success [10] and locomotor stress and drops in ovarian hormones [11]. Furthermore, changes in mobility have consistently been shown to influence weight loss/weight gain, and ovarian function and fecundity have consistently been shown to be particularly sensitive to changes in the metabolic balance/weight, such that an increased imbalance between energy in and energy out decreases fertility [12][13][14][15][16][17].…”