High-power resistance exercise induces MAPK phosphorylation in weightlifting trained men

Andrew J. Galpin, Andrew C. Fry, Loren Z.F. Chiu, Donald Thomason, Brian K. Schilling

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Power is critical to muscle performance, specifically in athletic populations. Mitogen-activated protein kinase (MAPK) pathways (extracellular signal-regulated protein kinase (ERK 1/2), p38, and c-Jun NH2-terminal kinase (JNK)) are intracellular signal transduction mechanisms that partially regulate exercise-induced skeletal muscle alterations. These pathways are highly responsive to exercise, but their reaction to high power, multi-joint resistance exercise is yet to be examined. Nine weightlifting-trained men performed 15 sets of three repetitions of a dynamic clean pull exercise at 85% of their one repetition maximum. Vastus lateralis biopsies were obtained prior to (pre) and after the 8th (mid) and 15th set (post) of exercise. Three subjects returned to serve as non-exercising controls for a similar sequence of biopsies (CON). The ratio of phosphorylated MAPK to total MAPK increased significantly for p38 (3.0 fold, p < 0.05) and JNK (2.4 fold, p < 0.05) by the mid biopsy. ERK 1/2 phosphorylation followed a similar trend (2.3 fold) (p = 0.052). The ratio of phosphorylation to total MAPK did not differ from mid to post biopsy. None of the pathways were phosphorylated above resting in the CON condition (p > 0.05), and thus the biopsy procedure itself did not account for the entire increase in MAPK phosphorylation during EX. These data indicate MAPK pathways are activated early and remain elevated throughout the duration of high power resistance exercise. These findings help describe the mechanisms partially responsible for chronic adaptations in response to high intensity, high power resistance training in humans.

Original languageEnglish (US)
Pages (from-to)80-87
Number of pages8
JournalApplied Physiology, Nutrition and Metabolism
Volume37
Issue number1
DOIs
StatePublished - Feb 1 2012

Fingerprint

Mitogen-Activated Protein Kinases
Phosphorylation
Exercise
Biopsy
Resistance Training
JNK Mitogen-Activated Protein Kinases
Extracellular Signal-Regulated MAP Kinases
Quadriceps Muscle
Protein Kinases
Sports
Signal Transduction
Skeletal Muscle
Joints
Muscles
Population

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Nutrition and Dietetics
  • Physiology (medical)

Cite this

High-power resistance exercise induces MAPK phosphorylation in weightlifting trained men. / Galpin, Andrew J.; Fry, Andrew C.; Chiu, Loren Z.F.; Thomason, Donald; Schilling, Brian K.

In: Applied Physiology, Nutrition and Metabolism, Vol. 37, No. 1, 01.02.2012, p. 80-87.

Research output: Contribution to journalArticle

Galpin, Andrew J. ; Fry, Andrew C. ; Chiu, Loren Z.F. ; Thomason, Donald ; Schilling, Brian K. / High-power resistance exercise induces MAPK phosphorylation in weightlifting trained men. In: Applied Physiology, Nutrition and Metabolism. 2012 ; Vol. 37, No. 1. pp. 80-87.
@article{492ae405a56a4716918ba492390af85b,
title = "High-power resistance exercise induces MAPK phosphorylation in weightlifting trained men",
abstract = "Power is critical to muscle performance, specifically in athletic populations. Mitogen-activated protein kinase (MAPK) pathways (extracellular signal-regulated protein kinase (ERK 1/2), p38, and c-Jun NH2-terminal kinase (JNK)) are intracellular signal transduction mechanisms that partially regulate exercise-induced skeletal muscle alterations. These pathways are highly responsive to exercise, but their reaction to high power, multi-joint resistance exercise is yet to be examined. Nine weightlifting-trained men performed 15 sets of three repetitions of a dynamic clean pull exercise at 85{\%} of their one repetition maximum. Vastus lateralis biopsies were obtained prior to (pre) and after the 8th (mid) and 15th set (post) of exercise. Three subjects returned to serve as non-exercising controls for a similar sequence of biopsies (CON). The ratio of phosphorylated MAPK to total MAPK increased significantly for p38 (3.0 fold, p < 0.05) and JNK (2.4 fold, p < 0.05) by the mid biopsy. ERK 1/2 phosphorylation followed a similar trend (2.3 fold) (p = 0.052). The ratio of phosphorylation to total MAPK did not differ from mid to post biopsy. None of the pathways were phosphorylated above resting in the CON condition (p > 0.05), and thus the biopsy procedure itself did not account for the entire increase in MAPK phosphorylation during EX. These data indicate MAPK pathways are activated early and remain elevated throughout the duration of high power resistance exercise. These findings help describe the mechanisms partially responsible for chronic adaptations in response to high intensity, high power resistance training in humans.",
author = "Galpin, {Andrew J.} and Fry, {Andrew C.} and Chiu, {Loren Z.F.} and Donald Thomason and Schilling, {Brian K.}",
year = "2012",
month = "2",
day = "1",
doi = "10.1139/H11-131",
language = "English (US)",
volume = "37",
pages = "80--87",
journal = "Applied Physiology, Nutrition and Metabolism",
issn = "1715-5312",
publisher = "National Research Council of Canada",
number = "1",

}

TY - JOUR

T1 - High-power resistance exercise induces MAPK phosphorylation in weightlifting trained men

AU - Galpin, Andrew J.

AU - Fry, Andrew C.

AU - Chiu, Loren Z.F.

AU - Thomason, Donald

AU - Schilling, Brian K.

PY - 2012/2/1

Y1 - 2012/2/1

N2 - Power is critical to muscle performance, specifically in athletic populations. Mitogen-activated protein kinase (MAPK) pathways (extracellular signal-regulated protein kinase (ERK 1/2), p38, and c-Jun NH2-terminal kinase (JNK)) are intracellular signal transduction mechanisms that partially regulate exercise-induced skeletal muscle alterations. These pathways are highly responsive to exercise, but their reaction to high power, multi-joint resistance exercise is yet to be examined. Nine weightlifting-trained men performed 15 sets of three repetitions of a dynamic clean pull exercise at 85% of their one repetition maximum. Vastus lateralis biopsies were obtained prior to (pre) and after the 8th (mid) and 15th set (post) of exercise. Three subjects returned to serve as non-exercising controls for a similar sequence of biopsies (CON). The ratio of phosphorylated MAPK to total MAPK increased significantly for p38 (3.0 fold, p < 0.05) and JNK (2.4 fold, p < 0.05) by the mid biopsy. ERK 1/2 phosphorylation followed a similar trend (2.3 fold) (p = 0.052). The ratio of phosphorylation to total MAPK did not differ from mid to post biopsy. None of the pathways were phosphorylated above resting in the CON condition (p > 0.05), and thus the biopsy procedure itself did not account for the entire increase in MAPK phosphorylation during EX. These data indicate MAPK pathways are activated early and remain elevated throughout the duration of high power resistance exercise. These findings help describe the mechanisms partially responsible for chronic adaptations in response to high intensity, high power resistance training in humans.

AB - Power is critical to muscle performance, specifically in athletic populations. Mitogen-activated protein kinase (MAPK) pathways (extracellular signal-regulated protein kinase (ERK 1/2), p38, and c-Jun NH2-terminal kinase (JNK)) are intracellular signal transduction mechanisms that partially regulate exercise-induced skeletal muscle alterations. These pathways are highly responsive to exercise, but their reaction to high power, multi-joint resistance exercise is yet to be examined. Nine weightlifting-trained men performed 15 sets of three repetitions of a dynamic clean pull exercise at 85% of their one repetition maximum. Vastus lateralis biopsies were obtained prior to (pre) and after the 8th (mid) and 15th set (post) of exercise. Three subjects returned to serve as non-exercising controls for a similar sequence of biopsies (CON). The ratio of phosphorylated MAPK to total MAPK increased significantly for p38 (3.0 fold, p < 0.05) and JNK (2.4 fold, p < 0.05) by the mid biopsy. ERK 1/2 phosphorylation followed a similar trend (2.3 fold) (p = 0.052). The ratio of phosphorylation to total MAPK did not differ from mid to post biopsy. None of the pathways were phosphorylated above resting in the CON condition (p > 0.05), and thus the biopsy procedure itself did not account for the entire increase in MAPK phosphorylation during EX. These data indicate MAPK pathways are activated early and remain elevated throughout the duration of high power resistance exercise. These findings help describe the mechanisms partially responsible for chronic adaptations in response to high intensity, high power resistance training in humans.

UR - http://www.scopus.com/inward/record.url?scp=84856565353&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84856565353&partnerID=8YFLogxK

U2 - 10.1139/H11-131

DO - 10.1139/H11-131

M3 - Article

VL - 37

SP - 80

EP - 87

JO - Applied Physiology, Nutrition and Metabolism

JF - Applied Physiology, Nutrition and Metabolism

SN - 1715-5312

IS - 1

ER -