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Author ORCID Identifier



Open Access Dissertation

Document Type


Degree Name

Doctor of Philosophy (PhD)

Degree Program


Year Degree Awarded


Month Degree Awarded


First Advisor

Jason Kamilar

Subject Categories

Biological and Physical Anthropology | Biology


Human eccrine density is highly derived. However, little is known about contemporary variation in this trait, what shapes it, and how it influences heat dissipation. This project explores 3 questions: 1) Is variation in functional eccrine density (FED) explained by childhood climate? 2) Is this variation patterned by geographic ancestry? 3) Is variation in FED associated with differences in heat dissipation capacity? We measured FED and sweat production in 6 body areas via pharmacological stimulation and impressions of sweating skin in 72 participants. Childhood climate variables were taken from the WorldClim database and geographic ancestry was estimated with 23andMe tests. The relationship between FED and heat dissipation capacity was measured in 7 heat-acclimatized endurance runners who cycled in a metabolic chamber at 30°C. Indirect calorimetry was used to calculate heat dissipation quotient (HDQ). Interindividual variation in 6-site FED was more than twofold, ranging from 60.9 to 132.7 glands/cm2. Variation in 6-site FED was best explained by body surface area (negative association, p2=0.004). HDQ was best explained by vO2-peak and whole-body sweat loss and was not related to FED. Our results suggest that variation in per-gland sweat production renders differences in contemporary FED physiologically unimportant, and there is no tradeoff between heat dissipation and water conservation within the range of contemporary FED. In this view, eccrine density did not change via evolutionary adaptation or phenotypic plasticity as humans moved into novel climates; sweating capacity was instead altered via gland-level adaptations. Future research should measure effects of FED in dehydrated states, carefully control for effects of microclimate to rule out phenotypic plasticity in FED, and determine whether gland-level adaptations are sufficient to buffer against increased salt losses potentially incurred by lower FED.