Is the End-Exercise Potentiated-Twitch Decrement a Regulated Variable? A Mechanism-Oriented Review of Muscle Fatigue During High-Intensity Aerobic Exercise.
5 affiliations
- 1Departamento de Ciencias de la Salud, Instituto de Ciencias Biomédicas, Universidad Autónoma de Ciudad Juárez, Ciudad Juárez 32401, Chihuahua, Mexico.
- 2Conahcyt National Laboratory of Body Composition and Energetic Metabolism (LaNCoCoME), Tijuana 22390, Baja California, Mexico.
- 3Facultad de Ciencias de la Cultura Física, Universidad Autónoma de Chihuahua, Chihuahua 31125, Chihuahua, Mexico.
- 4Facultad de Deportes Campus Mexicali, Universidad Autónoma de Baja California, Mexicali 21289, Baja California, Mexico.
- 5Facultad de Medicina y Psicología, Universidad Autónoma de Baja California, Tijuana 22390, Baja California, Mexico.
Abstract
Background
Fatigue in high-intensity exercise is often attributed to a defended ceiling of peripheral fatigue; evidence is mixed.Objectives
We aimed to assess whether the end-exercise potentiated-twitch decrement behaves as a regulated variable across candidate mechanisms.Methods
PubMed/MEDLINE, Scopus, and Web of Science were searched to 12 August 2026. Evidence came from controlled studies in adults, with permeabilized-fiber, rodent, and isolated-actomyosin experiments only where human measurement is impossible.Results
Nine mechanisms met the criteria. Inorganic phosphate and hydrogen ions impair the cross-bridge cycle; reduced sarcolemmal excitability (K⁺) and reduced sarcoplasmic reticulum Ca²⁺ release reverse over minutes and days, respectively. Only the cross-bridge effects are driven by metabolites (protons, ATP, lactate) that are agonists of group III/IV afferents; the afferents do not sense contractile impairment itself. Oxygen delivery, respiratory-muscle work, substrate availability, and perceptual load altered fatigue rate more than the end-exercise value, which varied with duration, prior exercise, muscle mass, and mode.Conclusions
Evidence fits a threshold in the phosphate-force relationship, though this does not demonstrate a defended limit. The decrement is not constant across tasks; we propose, as a testable hypothesis, that the regulated quantity is the summed afferent and effort signal. Selection was purposive, without formal risk-of-bias appraisal.
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BibTeX
@article{ramosjimenez2026endexercise,
title = {{Is the End-Exercise Potentiated-Twitch Decrement a Regulated Variable? A Mechanism-Oriented Review of Muscle Fatigue During High-Intensity Aerobic Exercise.}},
author = {Arnulfo Ramos-Jiménez and Mariazel Rubio-Valles and Marina Trejo-Trejo and Cristhian Emmanuel López-Campos and Jaime Güereca-Arvizuo and Oliver Adán Sollano-Trejo and María Guadalupe Delgadillo-Ramos and Marco Antonio Hernández Lepe},
journal = {Muscles (Basel, Switzerland)},
year = {2026},
month = oct,
doi = {10.3390/muscles5040074},
url = {https://europepmc.org/article/MED/42924646},
note = {CC BY},
}
RIS
TY - JOUR
TI - Is the End-Exercise Potentiated-Twitch Decrement a Regulated Variable? A Mechanism-Oriented Review of Muscle Fatigue During High-Intensity Aerobic Exercise.
AU - Arnulfo Ramos-Jiménez
AU - Mariazel Rubio-Valles
AU - Marina Trejo-Trejo
AU - Cristhian Emmanuel López-Campos
AU - Jaime Güereca-Arvizuo
AU - Oliver Adán Sollano-Trejo
AU - María Guadalupe Delgadillo-Ramos
AU - Marco Antonio Hernández Lepe
PY - 2026
DA - 2026/10/09
JO - Muscles (Basel, Switzerland)
DO - 10.3390/muscles5040074
UR - https://europepmc.org/article/MED/42924646
AB - Background Fatigue in high-intensity exercise is often attributed to a defended ceiling of peripheral fatigue; evidence is mixed.Objectives We aimed to assess whether the end-exercise potentiated-twitch decrement behaves as a regulated variable across candidate mechanisms.Methods PubMed/MEDLINE, Scopus, and Web of Science were searched to 12 August 2026. Evidence came from controlled studies in adults, with permeabilized-fiber, rodent, and isolated-actomyosin experiments only where human measurement is impossible.Results Nine mechanisms met the criteria. Inorganic phosphate and hydrogen ions impair the cross-bridge cycle; reduced sarcolemmal excitability (K⁺) and reduced sarcoplasmic reticulum Ca²⁺ release reverse over minutes and days, respectively. Only the cross-bridge effects are driven by metabolites (protons, ATP, lactate) that are agonists of group III/IV afferents; the afferents do not sense contractile impairment itself. Oxygen delivery, respiratory-muscle work, substrate availability, and perceptual load altered fatigue rate more than the end-exercise value, which varied with duration, prior exercise, muscle mass, and mode.Conclusions Evidence fits a threshold in the phosphate-force relationship, though this does not demonstrate a defended limit. The decrement is not constant across tasks; we propose, as a testable hypothesis, that the regulated quantity is the summed afferent and effort signal. Selection was purposive, without formal risk-of-bias appraisal.
SN - 2813-0413
ER -