Financiado en parte por ZOLL Medical Corporation
Modelling in vivo creatine/phosphocreatine in vitro reveals divergent adaptations in human muscle mitochondrial respiratory control by ADP after acute and chronic exercise
Ydfors M, Hughes MC, Laham R, Schlattner U, Norrbom J, Perry CG
The Journal of physiology · 45 citas
Etiquetas de revisión
Financiado por la industriaSolo mecanismosDatos neutrales que nuestra revisión registró sobre cómo se hizo este estudio. Describen el método, nunca si nos gusta el resultado.
Cómo se estudió
- Diseño
- Estudio in vitro o de mecanismos (clasificado por nuestro filtro de IA)
- Estudiado en
- Personas
- Resultado principal
- Solo mecanismos
Quién lo pagó
- Financiación
- Financiado por la industria
- Empresa
- ZOLL Medical Corporation
- Universidad u hospital
- York University
- Universidad u hospital
- University College Dublin
- Gobierno
- Canadian Institutes of Health Research
- Gobierno
- CIHR
Según 5 financiadores declarados.
Publicación
- Publicado
- 2015-12-03 · J Physiol · vol. 594 · número 11 · págs. 3127–3140
- Editorial
- Wiley
- Citado
- 56 citas · más que el 96% de estudios similares · 7.4× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 63 trabajos
- Acceso
- Acceso abierto (copia en repositorio)
- Áreas de investigación
- Cardiovascular and exercise physiology · Muscle metabolism and nutrition · Adipose Tissue and Metabolism
- Palabras clave
- Phosphocreatine, Creatine, In vivo, Respiratory system, Human muscle, In vitro, Mitochondrion, Fast twitch muscle, Biology, Internal medicine, Medicine, Skeletal muscle, Cell biology, Energy metabolism, Biochemistry
- MeSH
- muscle, skeletal, mitochondria, humans, creatine, phosphocreatine, adenosine diphosphate, exercise, adaptation, physiological, time factors, adult, male, creatine kinase, mitochondrial form, young adult
6 autores
- Mia Ydfors🇸🇪Karolinska Institutet
- Meghan C. Hughes🇨🇦York University
- Robert Laham🇨🇦York University
- Uwe Schlattner🇫🇷Laboratory of Fundamental and Applied Bioenergetics; Université Grenoble Alpes
- Jessica Norrbom🇸🇪Karolinska Institutet
- Christopher G. R. Perry🇨🇦 · autor de correspondenciaYork University
Resumen
El texto original del estudio, en el idioma en que se publicó.
Key points
Mitochondrial respiratory sensitivity to ADP is thought to influence muscle fitness and is partly regulated by cytosolic-mitochondrial diffusion of ADP or phosphate shuttling via creatine/phosphocreatine (Cr/PCr) through mitochondrial creatine kinase (mtCK). Previous measurements of respiration in vitro with Cr (saturate mtCK) or without (ADP/ATP diffusion) show mixed responses of ADP sensitivity following acute exercise vs. less sensitivity after chronic exercise. In human muscle, modelling in vivo 'exercising' [Cr:PCr] during in vitro assessments revealed novel responses to exercise that differ from detections with or without Cr (±Cr). Acute exercise increased ADP sensitivity when measured without Cr but had no effect ±Cr or with +Cr:PCr, whereas chronic exercise increased sensitivity ±Cr but lowered sensitivity with +Cr:PCr despite increased markers of mitochondrial oxidative capacity. Controlling in vivo conditions during in vitro respiratory assessments reveals responses to exercise that differ from typical ±Cr comparisons and challenges our understanding of how exercise improves metabolic control in human muscle.
Abstract
Mitochondrial respiratory control by ADP (Kmapp ) is viewed as a critical regulator of muscle energy homeostasis. However, acute exercise increases, decreases or has no effect on Kmapp in human muscle, whereas chronic exercise surprisingly decreases sensitivity despite greater mitochondrial content. We hypothesized that modelling in vivo mitochondrial creatine kinase (mtCK)-dependent phosphate-shuttling conditions in vitro would reveal increased sensitivity (lower Kmapp ) after acute and chronic exercise. The Kmapp was determined in vitro with 20 mm Cr (+Cr), 0 mm Cr (-Cr) or 'in vivo exercising' 20 mm Cr/2.4 mm PCr (Cr:PCr) on vastus lateralis biopsies sampled from 11 men before, immediately after and 3 h after exercise on the first, fifth and ninth sessions over 3 weeks. Dynamic responses to acute exercise occurred throughout training, whereby the first session did not change Kmapp with in vivo Cr:PCr despite increases in -Cr. The fifth session decreased sensitivity with Cr:PCr or +Cr despite no change in -Cr. Chronic exercise increased sensitivity ±Cr in association with increased electron transport chain content (+33-62% complexes I-V), supporting classic proposals that link increased sensitivity to oxidative capacity. However, in vivo Cr:PCr reveals a perplexing decreased sensitivity, contrasting the increases seen ±Cr. Functional responses occurred without changes in fibre type or proteins regulating mitochondrial-cytosolic energy exchange (mtCK, VDAC and ANT). Despite the dynamic responses seen with ±Cr, modelling in vivo phosphate-shuttling conditions in vitro reveals that ADP sensitivity is unchanged after high-intensity exercise and is decreased after training. These findings challenge our understanding of how exercise regulates skeletal muscle energy homeostasis.
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