Journal
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
Volume 321, Issue 3, Pages R352-R363Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpregu.00342.2020
Keywords
fetal growth; fetal hypoxemia; fetal protein accretion; myogenesis; skeletal muscle
Categories
Funding
- National Institute of Health (NIH) [R01DK108910, R01HD071068, R01HL142483, R01HD079404, R01DK088139, R01HD093701, S10OD023553]
- University of Colorado Anschutz Medical Campus Diabetes Research Center Core Services - NIH [P30-DK116073]
- Ludeman Family Center for Women's Health Research
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Fetal anemic hypoxemia was found to reduce muscle growth, leading to decreased muscle weight and fiber area, as well as reduced myoblast proliferation and differentiation. However, overall protein kinetic rates did not differ significantly between anemic and control fetuses.
Fetal skeletal muscle growth requires myoblast proliferation, differentiation, and fusion into myofibers in addition to protein accretion for fiber hypertrophy. Oxygen is an important regulator of this process. Therefore, we hypothesized that fetal anemic hypoxemia would inhibit skeletal muscle growth. Studies were performed in late-gestation fetal sheep that were bled to anemic and therefore hypoxemic conditions beginning at -125 days of gestation (term =148 days) for 9 +/- 0 days (n = 19) and compared with control fetuses (n = 16). A metabolic study was performed on gestational day -134 to measure fetal protein kinetic rates. Myoblast proliferation and myofiber area were determined in biceps femoris (BF), tibialis anterior (TA), and flexor digitorum superficialis (FDS) muscles. mRNA expression of muscle regulatory factors was determined in BF. Fetal arterial hematocrit and oxygen content were 28% and 52% lower, respectively, in anemic fetuses. Fetal weight and whole body protein synthesis, breakdown, and accretion rates were not different between groups. Hindlimb length, however, was 7% shorter in anemic fetuses. TA and FDS muscles weighed less, and FDS myofiber area was smaller in anemic fetuses compared with controls. The percentage of Pax7+ myoblasts that expressed Ki67 was lower in BF and tended to be lower in FDS from anemic fetuses indicating reduced myoblast proliferation. There was less MYOD and MYF6 mRNA expression in anemic versus control BF consistent with reduced myoblast differentiation. These results indicate that fetal anemic hypoxemia reduced muscle growth. We speculate that fetal muscle growth may be improved by strategies that increase oxygen availability.
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