Substrate metabolism in seasonally acclimatized American goldfinches

The ability to restrict carbohydrate use under cold stress is a component of the winter acclimatization process in the American goldfinch, and one mechanism which might foster this ability in the increase in beta-oxidative capacity of the flight muscles, permitting a greater reliance on fatty acids by winter animals during cold-induced thermogenesis.

Abstract

Concentration of ([Glc]) and turnover (Ro) of plasma glucose, concentration of free fatty acids in plasma ([FFA]), and concentration of glycogen in muscle and liver were measured in freshly captured summer- and winter-acclimatized American goldfinches (Carduelis tristis). These birds were acutely exposed to one of three thermal regimes: 1) "thermoneutral," 30 degrees C in air, 2) "cold," -15 degrees C in air, and 3) "severe cold," 0 degrees C in 79% He and 21% O2. Additionally, the activities of citrate synthase (CS), phosphofructokinase (PFK), and beta-hydroxyacyl-CoA dehydrogenase (HOAD) were measured in pectoralis and leg muscles of winter and summer birds. Ro for goldfinches at 30 degrees C is unchanged between winter and summer, whereas it is 25% lower at -15 degrees C in winter than in summer birds, even though rates of heat production are similar. Additionally, winter animals depleted muscle glycogen at slower rates than summer individuals when exposed to "cold" or "severe cold." [Glc] and [FFA] for each test regime did not vary between seasons. The activity of the beta-oxidative enzyme HOAD is the pectoralis muscle (the main thermogenic tissue) increases by 50% from summer to winter, but the activities of PFK and CS remain essentially constant. We conclude that the ability to restrict carbohydrate use under cold stress is a component of the winter acclimatization process in the American goldfinch. One mechanism which might foster this ability in the increase in beta-oxidative capacity of the flight muscles, permitting a greater reliance on fatty acids by winter animals during cold-induced thermogenesis.