Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/71004
Title: An integrative approach to the regulation of mitochondrial respiration during exercise: Focus on high-intensity exercise
Authors: Calbet, José A. 
Martín Rodríguez, Saúl 
Martín Rincón, Marcos 
Morales Álamo, David 
UNESCO Clasification: 2411 Fisiología humana
241106 Fisiología del ejercicio
Keywords: Fatigue
High-Intensity Exercise
Mitochondrial Respiration
Oxidative Stress
Sprint Performance
Issue Date: 2020
Project: Viabilidad y Sostenibilidad Del Adelgazamiento Mediante Tratamiento Intensificado en Pacientes Con Sobrepeso U Obesidad: Mecanismos Neuroendocrinos y Moleculares 
Identificacion E Integracion de Nuevos Factores Moleculares, Fisiologicos y Bioelectricos Determinantes Del Rendimiento en El Ejercicio de Sprint 
Desarrollo y Caracterización Molecular de Un Nuevo Modelo de Precondicionamiento Remoto 
Estudio Longitudinal de Los Efectos de Una Modificación Intensiva Del Estilo de Vida en la Composición Corporal E Indicadores Bioquímicos y Moleculares de Salud en Pacientes Con Sobrepeso y Obesidad: Aplicación Para la Evaluación Fisiológica de Rutas y Sistemas de Monitorización Del Esfuerzo 
Journal: Redox Biology 
Abstract: During exercise, muscle ATP demand increases with intensity, and at the highest power output, ATP consumption may increase more than 100-fold above the resting level. The rate of mitochondrial ATP production during exercise depends on the availability of O2, carbon substrates, reducing equivalents, ADP, Pi, free creatine, and Ca2+. It may also be modulated by acidosis, nitric oxide and reactive oxygen and nitrogen species (RONS). During fatiguing and repeated sprint exercise, RONS production may cause oxidative stress and damage to cellular structures and may reduce mitochondrial efficiency. Human studies indicate that the relatively low mitochondrial respiratory rates observed during sprint exercise are not due to lack of O2, or insufficient provision of Ca2+, reduced equivalents or carbon substrates, being a suboptimal stimulation by ADP the most plausible explanation. Recent in vitro studies with isolated skeletal muscle mitochondria, studied in conditions mimicking different exercise intensities, indicate that ROS production during aerobic exercise amounts to 1-2 orders of magnitude lower than previously thought. In this review, we will focus on the mechanisms regulating mitochondrial respiration, particularly during high-intensity exercise. We will analyze the factors that limit mitochondrial respiration and those that determine mitochondrial efficiency during exercise. Lastly, the differences in mitochondrial respiration between men and women will be addressed.
URI: http://hdl.handle.net/10553/71004
ISSN: 2213-2317
DOI: 10.1016/j.redox.2020.101478
Source: Redox Biology [ISSN 2213-2317], v. 35, 101478, (Agosto 2020)
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