genes (8, 9). Thus, ROS can exert favorable effects and can be
involved in the process of training adaptation. Up-regulation of
endogenous antioxidant systems in response to regular training
exerts beneficial effects in the prevention of chronic disease
processes (10) and has also been related to longevity in flies (11)
and mice (12).
The maximal capacity to take up, transport and utilize oxygen
during exercise is V˙O2max (13). Endurance is defined as the time
limit of a person’s or animal’s ability to maintain a specific power
level during a running protocol (14). Large-scale epidemiologic
studies of humans with and without cardiovascular disease show
that low aerobic exercise capacity is an stronger predictor of
mortality than are other established risk factors, such as diabetes,
smoking, hypertension, or chronic obstructive pulmonary disease
(15–18). These observations are consistent with the role of
impaired regulation of mitochondrial function as an important
mechanism for low aerobic capacity (19). The relations among
V˙O2max, muscle oxidative capacity, endurance capacity, and
maximal aerobic workload capacity have been discussed for
years (20). Davies et al (21) concluded that muscle oxidative
capacity (ie, the mitochondrial content of muscle) was a major
determinant of endurance capacity, whereas V˙O2max was only
indirectly related to endurance capacity but was directly related
to exercise intensity. In eukaryotic cells, mitochondrial biogenesis
requires gene products from 2 physically separated genomes—
one contained within the organelle and the other contained
within the nucleus. Peroxisome proliferator–activated
receptor co-activator 1 (PGC-1) is a recently identified coactivator
of nuclear receptors. It powerfully induces mRNA expression
for important nuclear transcription factors such as nuclear
respiratory factor 1 (NRF-1) and mitochondrial transcription