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Review
. 2020 Jul 14:11:816.
doi: 10.3389/fphys.2020.00816. eCollection 2020.

Sarcoplasmic Hypertrophy in Skeletal Muscle: A Scientific "Unicorn" or Resistance Training Adaptation?

Affiliations
Review

Sarcoplasmic Hypertrophy in Skeletal Muscle: A Scientific "Unicorn" or Resistance Training Adaptation?

Michael D Roberts et al. Front Physiol. .

Abstract

Skeletal muscle fibers are multinucleated cells that contain mostly myofibrils suspended in an aqueous media termed the sarcoplasm. Select evidence suggests sarcoplasmic hypertrophy, or a disproportionate expansion of the sarcoplasm relative to myofibril protein accretion, coincides with muscle fiber or tissue growth during resistance training. There is also evidence to support other modes of hypertrophy occur during periods of resistance training including a proportional accretion of myofibril protein with fiber or tissue growth (i.e., conventional hypertrophy), or myofibril protein accretion preceding fiber or tissue growth (i.e., myofibril packing). In this review, we discuss methods that have been used to investigate these modes of hypertrophy. Particular attention is given to sarcoplasmic hypertrophy throughout. Thus, descriptions depicting this process as well as the broader implications of this phenomenon will be posited. Finally, we propose future human and rodent research that can further our understanding in this area of muscle physiology.

Keywords: muscle hypertrophy; myofiber; myofibril; resistance training; sarcoplasm.

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Figures

FIGURE 1
FIGURE 1
A simplified schematic of muscle fiber morphology. The left inset is a recreated figure of what would be observed under a TEM if tissue were prepared for cross-sectional imaging. The right inset image is a pseudocolored cross-sectional TEM image within the skeletal muscle fiber of a Wistar rat showing different cellular components (15,000×). Notably, much of the attention in this figure is devoted to myofibrils. However, it is also important to note that mitochondria make up ∼5% of the muscle cell area in cross section. The image was licensed from sciencesource.com (courtesy of Jose Luis Calvo) by the authors for scientific publication purposes.
FIGURE 2
FIGURE 2
A pseudocolored cross-sectional TEM image from a Wistar rat (8,000×) demonstrating morphological differences between different muscle fiber types. The image was licensed from sciencesource.com (courtesy of Jose Luis Calvo) by the authors for scientific publication purposes.
FIGURE 3
FIGURE 3
Conceptualization of conventional versus sarcoplasmic hypertrophy, and how these phenomena would manifest with the electrophoresis technique discussed. The left inset demonstrates various modes of muscle fiber hypertrophy. The small blue circles within the fiber represent mitochondria, the smaller gray circles occupying most of the intracellular space represent myofibrils, and the remainder of the space represents the sarcoplasm. In situations where hypertrophy occurs due to the proportional accretion of myofibrillar protein (i.e., conventional hypertrophy), there could either be the addition of new myofibrils to the periphery which “push” the cell outward (indicated as new yellow dots), or there could be the thickening of pre-existing myofibrils (indicated by the haloing of gray circles). Alternatively, sarcoplasmic hypertrophy occurs through the disproportionate expansion of the sarcoplasm relative to myofibril addition. Select studies have shown this process may occur in response to resistance training, although some studies refute this model of hypertrophy. This process could potentially be shown through TEM imaging, phalloidin staining, or the determination of specific tension in isolated fibers (not depicted in figure). This process could also be reflected when analyzing pre- and post-training biopsy specimens through SDS-PAGE and Coomassie staining, and analyzing the changes in myosin heavy chain (MHC) and actin protein band densities (illustrated on the right inset of the figure).
FIGURE 4
FIGURE 4
Two hypothetical mechanisms of muscle fiber hypertrophy. In our proposed sarcoplasm expansion hypothesis of hypertrophy model, muscle fibers first grow through sarcoplasmic hypertrophy. This allows resident myonuclear domains to spatially, bioenergetically, and biosynthetically prepare for the accretion of additional myofibrils. Although resident domains may synthesize and accumulate some myofibril protein during this phase of hypertrophy, we hypothesize the predominance of sarcoplasmic hypertrophy reduces the transcriptional burden on resident domains. Once sarcoplasmic hypertrophy leads to appreciable cell growth, an additional myonuclear domain is acquired via satellite cell fusion. This new myonuclear domain can then appreciably contribute to myofibril protein accretion by “backfilling” space created through sarcoplasm expansion. In the myofibril expansion hypothesis of hypertrophy model, muscle fibers rapidly synthesize and accrue myofibril protein. This phenomenon leads to myofibril packing which acts to push the sarcolemma outward. Fibers eventually reach a size threshold, which leads to an additional myonuclear domain being acquired via satellite cell fusion. At this point both domains can operate to maintain and further synthesize new myofibrils.
FIGURE 5
FIGURE 5
This figure puts forth the hypothesis that sarcoplasmic hypertrophy with years of resistance training may be due to large muscle fibers exceeding a myofibril accretion threshold. This phenomenon is similar to the transcriptional stress theory posited in Figure 3. Specifically, we propose muscle cells grow via myofibril accretion due to a certain threshold size. Thereafter, fibers can no longer add myofibrils due to significant stress to resident myonuclear domains. Based on limited evidence cited in-text, we propose this mechanism may be evident in individuals who engage in higher volume training for years (e.g., bodybuilders).

References

    1. Ahtiainen J. P., Walker S., Peltonen H., Holviala J., Sillanpaa E., Karavirta L., et al. (2016). Heterogeneity in resistance training-induced muscle strength and mass responses in men and women of different ages. Age 38:10. - PMC - PubMed
    1. Allen D. L., Roy R. R., Edgerton V. R. (1999). Myonuclear domains in muscle adaptation and disease. Muscle Nerve 22 1350–1360. 10.1002/(sici)1097-4598(199910)22:10<1350::aid-mus3>3.0.co;2-8 - DOI - PubMed
    1. Alway S. E., Macdougall J. D., Sale D. G., Sutton J. R., Mccomas A. J. (1988). Functional and structural adaptations in skeletal muscle of trained athletes. J. Appl. Physiol. 64 1114–1120. 10.1152/jappl.1988.64.3.1114 - DOI - PubMed
    1. Antonio J., Gonyea W. J. (1994). Muscle fiber splitting in stretch-enlarged avian muscle. Med. Sci. Sports Exerc. 26 973–977. - PubMed
    1. Bell K. E., Brook M. S., Snijders T., Kumbhare D., Parise G., Smith K., et al. (2019). Integrated myofibrillar protein synthesis in recovery from unaccustomed and accustomed resistance exercise with and without multi-ingredient supplementation in overweight older men. Front. Nutr. 6:40. 10.3389/fnut.2019.00040 - DOI - PMC - PubMed

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