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An acute bout of high-intensity interval training increases the nuclear abundance of PGC-1α and activates mitochondrial biogenesis in human skeletal muscle.

Abstract

Low-volume, high-intensity interval training (HIT) increases skeletal muscle mitochondrial capacity, yet little is known regarding potential mechanisms promoting this adaptive response. Our purpose was to examine molecular processes involved in mitochondrial biogenesis in human skeletal muscle in response to an acute bout of HIT. Eight healthy men performed 4 × 30-s bursts of all-out maximal intensity cycling interspersed with 4 min of rest. Muscle biopsy samples (vastus lateralis) were obtained immediately before and after exercise, and after 3 and 24 h of recovery. At rest, the majority of peroxisome proliferator-activated receptor γ coactivator (PGC)-1α, a master regulator of mitochondrial biogenesis, was detected in cytosolic fractions. Exercise activated p38 MAPK and AMPK in the cytosol. Nuclear PGC-1α protein increased 3 h into recovery from exercise, a time point that coincided with increased mRNA expression of mitochondrial genes. This was followed by an increase in mitochondrial protein content and enzyme activity after 24 h of recovery. These findings support the hypothesis that an acute bout of low-volume HIT activates mitochondrial biogenesis through a mechanism involving increased nuclear abundance of PGC-1α.

Authors+Show Affiliations

Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21451146

Citation

Little, Jonathan P., et al. "An Acute Bout of High-intensity Interval Training Increases the Nuclear Abundance of PGC-1α and Activates Mitochondrial Biogenesis in Human Skeletal Muscle." American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, vol. 300, no. 6, 2011, pp. R1303-10.
Little JP, Safdar A, Bishop D, et al. An acute bout of high-intensity interval training increases the nuclear abundance of PGC-1α and activates mitochondrial biogenesis in human skeletal muscle. Am J Physiol Regul Integr Comp Physiol. 2011;300(6):R1303-10.
Little, J. P., Safdar, A., Bishop, D., Tarnopolsky, M. A., & Gibala, M. J. (2011). An acute bout of high-intensity interval training increases the nuclear abundance of PGC-1α and activates mitochondrial biogenesis in human skeletal muscle. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, 300(6), pp. R1303-10. doi:10.1152/ajpregu.00538.2010.
Little JP, et al. An Acute Bout of High-intensity Interval Training Increases the Nuclear Abundance of PGC-1α and Activates Mitochondrial Biogenesis in Human Skeletal Muscle. Am J Physiol Regul Integr Comp Physiol. 2011;300(6):R1303-10. PubMed PMID: 21451146.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - An acute bout of high-intensity interval training increases the nuclear abundance of PGC-1α and activates mitochondrial biogenesis in human skeletal muscle. AU - Little,Jonathan P, AU - Safdar,Adeel, AU - Bishop,David, AU - Tarnopolsky,Mark A, AU - Gibala,Martin J, Y1 - 2011/03/30/ PY - 2011/4/1/entrez PY - 2011/4/1/pubmed PY - 2011/9/17/medline SP - R1303 EP - 10 JF - American journal of physiology. Regulatory, integrative and comparative physiology JO - Am. J. Physiol. Regul. Integr. Comp. Physiol. VL - 300 IS - 6 N2 - Low-volume, high-intensity interval training (HIT) increases skeletal muscle mitochondrial capacity, yet little is known regarding potential mechanisms promoting this adaptive response. Our purpose was to examine molecular processes involved in mitochondrial biogenesis in human skeletal muscle in response to an acute bout of HIT. Eight healthy men performed 4 × 30-s bursts of all-out maximal intensity cycling interspersed with 4 min of rest. Muscle biopsy samples (vastus lateralis) were obtained immediately before and after exercise, and after 3 and 24 h of recovery. At rest, the majority of peroxisome proliferator-activated receptor γ coactivator (PGC)-1α, a master regulator of mitochondrial biogenesis, was detected in cytosolic fractions. Exercise activated p38 MAPK and AMPK in the cytosol. Nuclear PGC-1α protein increased 3 h into recovery from exercise, a time point that coincided with increased mRNA expression of mitochondrial genes. This was followed by an increase in mitochondrial protein content and enzyme activity after 24 h of recovery. These findings support the hypothesis that an acute bout of low-volume HIT activates mitochondrial biogenesis through a mechanism involving increased nuclear abundance of PGC-1α. SN - 1522-1490 UR - https://www.unboundmedicine.com/medline/citation/21451146/An_acute_bout_of_high_intensity_interval_training_increases_the_nuclear_abundance_of_PGC_1α_and_activates_mitochondrial_biogenesis_in_human_skeletal_muscle_ L2 - http://www.physiology.org/doi/full/10.1152/ajpregu.00538.2010?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -