Another potential mechanism of hypoxia-induced hypertrophy
is its effect on the activity of reactive oxygen species
(ROS). Reactive oxygen species production has been shown
to promote growth in both smooth muscle and cardiac
muscle (170), and it is theorized to have similar hypertrophic
effects on skeletal muscle (171). Nitric oxide, an ROS produced
during exercise, has been shown to mediate the proliferation
of satellite cells, which would presumably lead to
greater skeletal muscle growth (81,174). Reactive oxygen
species generated during resistance training also has been
shown to activate MAPK signaling in skeletal myoblasts (83),
potentially modulating a hypertrophic response.
Hypoxia also may promote hypertrophic effects from
reactive hyperemia (i.e., increased blood flow) after ischemic
exercise (173). Hyperemia within damaged muscle would
conceivably allow for the delivery of anabolic endocrine
agents and growth factors to satellite cells, thereby regulating
their proliferation and subsequent fusion into myotubes