Moreover, the hypertrophic gains realized were similar
to those experienced by themoderate- to high-intensity group.
There are several theories as to the potential hypertrophic
benefits of muscle hypoxia. For one, hypoxia has been shown
to cause an increased lactate accumulation and reduced acute
lactate clearance rate (173). This may mediate increased cell
swelling, which has been shown to upregulate protein synthesis.
Moreover, the rise in lactate may mediate elevations in
anabolic hormones and cytokines. Takarada et al. (172) noted
a 290% increase in GH levels after low-intensity hypoxic
training and an increase in the concentration of the myogenic
cytokine IL-6, which was sustained for 24 hours postexercise.
Another potential mechanism of hypoxic-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