Related Experiment Video
Updated: May 26, 2026
07:20
Human Skeletal Muscle Biopsy Procedures Using the Modified Bergström Technique
Published on: September 10, 2014
High-power resistance exercise induces MAPK phosphorylation in weightlifting trained men
Andrew J Galpin1, Andrew C Fry, Loren Z F Chiu
1University of Memphis, Department of Exercise and Sport Sciences, Memphis, TN 38152, USA. agalpin@fullerton.edu
Summary
Mitogen-activated protein kinase (MAPK) pathways, including p38 and c-Jun NH(2)-terminal kinase (JNK), activate early during high-power resistance exercise. These pathways remain elevated throughout the workout, contributing to skeletal muscle adaptations in athletes.
Area of Science:
- Exercise Physiology
- Molecular Biology
- Sports Science
Background:
- Muscle power is crucial for athletic performance.
- Mitogen-activated protein kinase (MAPK) pathways regulate exercise-induced skeletal muscle changes.
- The response of MAPK pathways to high-power, multi-joint resistance exercise is not well understood.
Purpose of the Study:
- To investigate the activation patterns of MAPK pathways (ERK 1/2, p38, JNK) during high-power resistance exercise.
- To determine if MAPK pathway activation occurs early and persists throughout the exercise bout.
- To elucidate the role of MAPK pathways in skeletal muscle adaptations to intense training.
Main Methods:
- Nine weightlifting-trained men performed 15 sets of dynamic clean pulls at 85% of their one-repetition maximum.
- Vastus lateralis muscle biopsies were collected pre-exercise, mid-exercise (after set 8), and post-exercise (after set 15).
- A control group (CON) underwent a similar biopsy sequence without exercise to account for procedural effects.
Main Results:
- Phosphorylation of p38 and JNK significantly increased by the mid-exercise biopsy (3.0-fold and 2.4-fold, respectively; p < 0.05).
- ERK 1/2 phosphorylation showed a similar trend (2.3-fold increase; p = 0.052).
- MAPK pathway phosphorylation levels did not change significantly between mid and post-exercise biopsies, and were not elevated in the control group.
Conclusions:
- MAPK pathways (p38, JNK, and ERK 1/2) are activated early in high-power resistance exercise.
- These pathways remain activated throughout the duration of the exercise bout.
- MAPK pathway activation likely contributes to the chronic adaptations observed in response to high-intensity, high-power resistance training.
Related Concept Videos
01:27Exercise and Muscle Performance
Exercise induces a range of adaptations in muscle tissue, depending on the type and duration of activity. Such physical training can be broadly categorized into two types: endurance exercises and resistance exercises.
Endurance exercises
Endurance exercises involve running, swimming, or cycling, which require repetitive movements with low force output. When a person engages in endurance exercise, a few noticeable changes occur in their skeletal muscles. For instance, the number of capillaries...
Endurance exercises
Endurance exercises involve running, swimming, or cycling, which require repetitive movements with low force output. When a person engages in endurance exercise, a few noticeable changes occur in their skeletal muscles. For instance, the number of capillaries...
01:07MAPK Signaling Cascades
Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
01:26Cellular Adaptation II: Hypertrophy
Hypertrophy is the increase in the size of individual cells, resulting in the enlargement of a tissue or organ. Unlike hyperplasia, which involves an increase in cell number, hypertrophy is characterized by an increase in cell volume. This process often occurs in response to higher functional demand or hormonal stimulation, leading to the production of more structural proteins and organelles, thereby enhancing the cells' work capacity.There are two primary types of hypertrophy: physiological...
01:25cAMP-dependent Protein Kinase Pathways
Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
01:24Muscle Recovery and Fatigue
Muscle fatigue refers to the decline in a muscle's ability to maintain the force of contraction after prolonged activity. It primarily stems from changes within muscle fibers. Even before experiencing muscle fatigue, one may feel tired and have the urge to stop the activity. This response, known as central fatigue, occurs due to changes in the central nervous system, namely the brain and spinal cord. While there is no single mechanism that induces fatigue, it may serve as a protective response...
01:22PI3K/mTOR/AKT Signaling Pathway
The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a rapamycin-insensitive companion...