The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Interaction among Skeletal Muscle Metabolic Energy Systems during Intense Exercise
Open accessAbstract
High-intensity exercise can result in up to a 1,000-fold increase in the rate of ATP demand compared to that at rest (Newsholme et al., 1983). To sustain muscle contraction, ATP needs to be regenerated at a rate complementary to ATP demand. Three energy systems function to replenish ATP in muscle: (1) Phosphagen, (2) Glycolytic, and (3) Mitochondrial Respiration. The three systems differ in the substrates used, products, maximal rate of ATP regeneration, capacity of ATP regeneration, and their associated contributions to fatigue. In this exercise context, fatigue is best defined as a decreasing force production during muscle contraction despite constant or increasing effort. The replenishment of ATP during intense exercise is the result of a coordinated metabolic response in which all energy systems contribute to different degrees based on an interaction between the intensity and duration of the exercise, and consequently the proportional contribution of the different skeletal muscle motor units. Such relative contributions also determine to a large extent the involvement of specific metabolic and central nervous system events that contribute to fatigue. The purpose of this paper is to provide a contemporary explanation of the muscle metabolic response to different exercise intensities and durations, with emphasis given to recent improvements in understanding and research methodology.
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Cites
Biochemistry of exercise-induced metabolic acidosis
Robergs, R. A., Ghiasvand, F., & Parker, D. (2004) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00114.2004 · Cited by 1,304
Self-citationRecovery of power output and muscle metabolites following 30 s of maximal sprint cycling in man
Bogdanis, G. C., Nevill, M. E., Boobis, L. H., Lakomy, H. K., & Nevill, A. M. (1995) · The Journal of Physiology · doi:10.1113/jphysiol.1995.sp020533 · Cited by 431
Sahlin, K., Harris, R. C., & Hultman, E. (1979) · Scandinavian Journal of Clinical and Laboratory Investigation · doi:10.3109/00365517909108833 · Cited by 180
Changes in muscle metabolites in females with 30-s exhaustive exercise.
JACOBS, I., BAR-OR, O., KARLSSON, J., DOTAN, R., TESCH, P., KAISER, P., & INBAR, O. (1982) · Medicine & Science in Sports & Exercise · doi:10.1249/00005768-198206000-00009 · Cited by 74 · cited 1×
“Thus, cells rely on other mechanisms to supply ATP to support cell work, which involves the store of energy in more complex molecules such as glycogen and triacylglycerols, and more importantly, having a sensitive control system to rapidly increase metabolism during times of energy (ATP) demand.”
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Cited by
Buizza, C., Bazzoli, L., & Ghilardi, A. (2022) · Adolescent Research Review · doi:10.1007/s40894-022-00192-7 · Cited by 149
Mielgo-Ayuso, J., Calleja-Gonzalez, J., Marqués-Jiménez, D., Caballero-García, A., Córdova, A., & Fernández-Lázaro, D. (2019) · Nutrients · doi:10.3390/nu11040757 · Cited by 91
Wang, D., Yang, Y., Zou, X., Zhang, J., Zheng, Z., & Wang, Z. (2020) · The Journals of Gerontology Series A · doi:10.1093/gerona/glaa214 · Cited by 87
Mills, S., Candow, D. G., Forbes, S. C., Neary, J. P., Ormsbee, M. J., & Antonio, J. (2020) · Nutrients · doi:10.3390/nu12061880 · Cited by 63
Weigt, C., Hertrampf, T., Zoth, N., Fritzemeier, K. H., & Diel, P. (2012) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2011.12.013 · Cited by 56
Metadata
- Authors
- Baker, J. S., McCormick, M. C., & Robergs, R. A.
- Venue
- Journal of Nutrition and Metabolism
- Publisher
- Hindawi Limited
- Published
- 2010
- Volume
- 2010
- Pages
- 1-13
- ISSN
- 2090-0724 (ISSN-L)
- 2090-0732
- OpenAlex
- W2065156666
- Cited by
- 392
- References
- 4
- FWCI
- 11.01
- Type
- journal article
- Language
- en
- Open access
- gold
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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