COMMENTARY TO ACCOMPANY

Adipose Tissue Remodeling During

Endurance Training
The role of brown adipose tissue (BAT) in defending body
temperature was demonstrated initially by Foster and Frydman
(1) who showed that BAT was the site of cold-induced thermogenesis. This was followed by the identification that heat
production occurred via the uncoupling of BAT mitochondria
through uncoupling protein 1 (UCP1) (5). Finally, work from
Flier and colleagues demonstrated that BAT protected mice
against the development of obesity and diabetes (2) and firmly
established BAT as a thermoregulatory organ that could be targeted to reduce the risk of obesity and diabetes. Around the
same time it was suggested that BAT could actively defend body
weight through diet-induced thermogenesis (DIT). More recently, the discovery of BAT in adult humans has renewed
interest in brown fat research and in understanding ways to
remodel white adipose tissue (WAT) to a phenotype more
similar to BAT. This process, termed browning, is marked
by the appearance of beige adipocytes in WAT that are
functionally similar to brown adipocytes. Exercise had been
postulated for a while to reduce BAT thermogenesis, but, somewhat surprisingly, recent work has demonstrated that endurance training promotes the browning of WAT in rodents. At
first glance, exercise-induced browning of WAT seems somewhat counterintuitive; however, in the current issue of the
Journal, Sepa-Kishi and Ceddia (6) discuss novel findings
that might explain the opposing effects of exercise on BAT
and subcutaneous WAT (scWAT) thermogenesis.
Sepa-Kishi and Ceddia (6) put forth the hypothesis that
remodeling of adipose tissue during exercise training functions
to shift thermogenesis away from classical BAT toward scWAT,
where it would not necessarily affect core body temperature.
In effect, this would allow the animal to deal with greater heat
production during exercise. These ideas stem from their recent
study in which endurance training reduced UCP1 content and
lipid oxidation in classical BAT. In contrast, exercise promoted
beige adipocytes, UCP1 content, and fatty acid oxidation in
scWAT. An interesting observation was that energy expenditure
after exercise remained elevated despite a reduction in BAT

thermogenesis, leading the authors to suggest that exerciseinduced scWAT browning can compensate partially for the
reduction in BAT. Similarly, scWAT browning could limit
adiposity during high-fat feeding by promoting DIT.
The beneficial effects of exercise on whole-body energy
homeostasis are undoubtable, but the exact contribution of
scWAT browning and the reality of DIT are a matter of debate
(3). Indeed, exercise does suppress BAT activity in humans;
however, the evidence for browning is less apparent (7). Alternatively, the reduction in BAT activity could be a means of
shifting energy away from uncoupling and toward working
muscle, whereas the increase in WAT fatty acid oxidation
might partly support adenosine triphosphate synthesis required
for greater in situ de novo lipogenesis (4). Exercise training at
thermoneutrality or in UCP1 knockout mice could be useful
in teasing apart UCP1-dependent versus -independent effects
on whole-body energy expenditure. In addition, as stated by
the authors, understanding the cellular source of beige cells and
the neural circuitry involved in the downregulation of BAT
and upregulation of scWAT browning could prove useful in
discovering novel therapies to combat obesity and diabetes.

Emilio P. Mottillo
Department of Medicine
McMaster University
Hamilton, Ontario, Canada

References
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Disclosure of funding: E.P. Mottillo is supported by a postdoctoral fellowship from the

Canadian Diabetes Association.
Authors for this section are recruited by Commentary Editor: Russell R. Pate, Ph.D.,
FACSM, Department of Exercise Science, University of South Carolina, Columbia, SC
29208 (E-mail: rpate@mailbox.sc.edu).
0091-6331/4401/3
Exercise and Sport Sciences Reviews
DOI: 10.1249/JES.0000000000000072
Copyright 2015 by the American College of Sports Medicine

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