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J Appl Physiol 103: 1102, 2007; doi:10.1152/japplphysiol.00101.2007b
8750-7587/07 $8.00
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POINT-COUNTERPOINT

Rebuttal from Drs. O'Connor and Pavlath

We believe to critically evaluate the contribution of satellite cells to hypertrophy, the following conditions need to be fulfilled: 1) analysis of a complete spectrum of time points (early and late) after application of a hypertrophic stimulus; 2) sufficiently large increases in myofiber cross-sectional area or diameter; 3) enumeration of myonuclear number using a method to clearly delineate the sarcolemma; and 4) to show cause and effect rather than correlation, ablation of satellite cell activity. The papers cited by McCarthy and Esser in various models of hypertrophy fail to satisfy one or more of these criteria and, therefore, do not provide conclusive evidence against the necessity for satellite cells in hypertrophy. For example, the vast majority of the clenbuterol literature only analyzes muscle weight and content of total protein, RNA, and DNA. Muscle weight and total protein are non-specific measures including both muscle and non-muscle components of the tissue. Total DNA is an inaccurate measure of myonuclei, including fibroblasts, inflammatory cells, etc. Kim et al. (3) analyzed myonuclear number in response to clenbuterol but only at 14 days using inappropriate methods. In contrast, myonuclear number was appropriately analyzed in some studies (5, 6) but only at early time points before the myonuclear domain ceiling of the existing myonuclei was likely to be exceeded. The time points chosen for study in the synergist ablation (2) and stretch overload (4) studies were too early in the hypertrophic process for appropriate interpretations on the role of satellite cells. Not commented on by McCarthy and Esser is that one of their cited studies (1) demonstrated preferential increments in DNA content rather than RNA or protein accretion during the later stages of cimaterol-induced hypertrophy, thus suggesting a role for satellite cells. The limitations inherent in using DNA content as a measure of satellite cells must be kept in mind though.

In summary, we believe the evidence generated from various models of muscle growth in multiple species support our contention that muscle growth may be viewed as a continuum of temporally regulated responses. We believe that muscle growth consists of multiple phases, including accelerated transcriptional and translational responses followed by satellite cell addition during the later stages of hypertrophy. Satellite cell addition is necessary only if a certain threshold myofiber size is reached.

REFERENCES

  1. Beermann DH, Butler WR, Hogue DE, Fishell VK, Dalrymple RH, Ricks CA, Scanes CG. Cimaterol-induced muscle hypertrophy and altered endocrine status in lambs. J Anim Sci 65: 1514–1524, 1987.[Abstract/Free Full Text]
  2. Fleckman P, Bailyn RS, Kaufman S. Effects of the inhibition of DNA synthesis on hypertrophying skeletal muscle. J Biol Chem 253: 3220–3227, 1978.[Medline]
  3. Kim YS, Lee YB, Ashmore CR. Cimaterol-induced growth in rats: growth pattern and biochemical characteristics. Growth Dev Aging 52: 41–45, 1988.[ISI][Medline]
  4. Lowe DA, Alway SE. Stretch-induced myogenin, MyoD, and MRF4 expression and acute hypertrophy in quail slow-tonic muscle are not dependent upon satellite cell proliferation. Cell Tissue Res 296: 531–539, 1999.[CrossRef][ISI][Medline]
  5. Maltin CA, Delday MI. Satellite cells in innervated and denervated muscles treated with clenbuterol. Muscle Nerve 15: 919–925, 1992.[CrossRef][ISI][Medline]
  6. Rehfeldt C, Weikard R, Reichel K. [The effect of the beta-adrenergic agonist clenbuterol on the growth of skeletal muscles of rats]. Arch Tierernahr 45: 333–344, 1994.[Medline]




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