Rapid Atrophy and Hypertrophy of an Avian Flight Muscle

Abstract

Eared Grebes (Podiceps nigricollis) use Mono Lake in eastern California as a rest stop during spring migration. Some nonbreeders remain for the summer, and in the autumn the lake becomes a staging area that may accommodate 750,000 returning breeders and young of the year. There the birds become obese by feeding on invertebrates and, if they have not already done so, molt. Most grebes remain several months until a decline in prey populations stimulates further migration. During this period the birds become flightless, and the flight muscles may lose up to 50% of their mass. Myofibers from atrophic birds show evidence of mitochondrial division (or fusion). Even severely atrophic fibers retain a high mitochondrial density (27% vs. 33% in migratory condition), so that relative volume remains stable although absolute volume is reduced. In contrast, intracellular triglyceride droplets are extremely sparse in atrophic fibers, even though most of the birds are carrying >200 g of subcutaneous fat. Mean myofiber diameter increases and decreases with atrophy and hypertrophy. In late autumn, as food availability declines, the birds engage in conspicuous flapping exercises. In the same period, intracellular lipid reappears in the muscles. Within several weeks the muscles are rebuilt to full size and the grebes emigrate. The benefits, if any, of this cycle of muscle atrophy and concomitant obesity, followed by muscle hypertrophy and weight loss, remain obscure.