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1.
Adv Exp Med Biol ; 1072: 103-109, 2018.
Artículo en Inglés | MEDLINE | ID: mdl-30178331

RESUMEN

Low back pain (LBP) is suggested to be related to deconditioning of back muscles by a decreased capacity for hyperemia in exercising muscles. However, only inconsistent evidence exists regarding back muscle perfusion and oxygen saturation in healthy subjects and patients suffering from (chronic) LBP. AIM: We measured muscle perfusion in healthy subjects during the Biering-Sørensen (BS) test (the gold standard for evaluating back muscle endurance) using a commercial near-infrared spectroscopy (NIRS) device. We analysed data sets of five female healthy subjects (age: 34 ± 15 years) who reached the maximum of 4 min during the BS test. Muscle oxygenation (SmO2) and perfusion ([tHb]) were measured using the Moxy NIRS device (Fortiori Design LLC, Hutchinson, USA). Probes were set unilaterally on M. longissimus, M. iliocostalis and M. multifidus. Additionally, mean arterial blood pressure (MAP), pulse pressure (PP), heart rate (HR), arterial oxygen saturation (SpO2) and lactate (pre, task, post) were measured. We observed (i) a large inter-subject variability in the SmO2 and [tHb] responses in the three muscles (i.e., SmO2 desaturations in the in M. longissimus across subjects during the task ranging from 1.1% to -56.6%), and (ii) a consistent response of the systemic signals in all subjects (i.e., increase in MAP, PP and HR). Lactate changes (post task minus task period) correlated with changes in PP and SmO2 of the multifidus muscle. Our preliminary results showed that during the BS test the response in the peripheral muscles was more variable than the central systemic response. A goal for future investigations is to explain this variability in the periphery by considering, for example, subject-specific changes in systemic cardiovascular activity, lactate and in the microvascular perfusion of muscle tissue.


Asunto(s)
Músculos de la Espalda/irrigación sanguínea , Músculos de la Espalda/metabolismo , Oximetría/métodos , Resistencia Física/fisiología , Espectroscopía Infrarroja Corta/métodos , Adulto , Presión Sanguínea/fisiología , Prueba de Esfuerzo/métodos , Femenino , Frecuencia Cardíaca/fisiología , Humanos , Consumo de Oxígeno/fisiología
2.
Eur J Appl Physiol ; 112(4): 1527-36, 2012 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-21847575

RESUMEN

The non-therapeutic use of genes to enhance athletic performance (gene doping) is a novel threat to the world of sports. Skeletal muscle is a prime target of gene therapy and we asked whether we can develop a test system to produce and detect gene doping. Towards this end, we introduced a plasmid (pCMV-FAK, 3.8 kb, 50 µg) for constitutive expression of the chicken homologue for the regulator of muscle growth, focal adhesion kinase (FAK), via gene electro transfer in the anti-gravitational muscle, m. soleus, or gastrocnemius medialis of rats. Activation of hypertrophy signalling was monitored by assessing the ribosomal kinase p70S6K and muscle fibre cross section. Detectability of the introduced plasmid was monitored with polymerase chain reaction in deoxyribonucleic acids (DNA) from transfected muscle and serum. Muscle transfection with pCMV-FAK elevated FAK expression 7- and 73-fold, respectively, and increased mean cross section by 52 and 16% in targeted muscle fibres of soleus and gastrocnemius muscle 7 days after gene electro transfer. Concomitantly p70S6K content was increased in transfected soleus muscle (+110%). Detection of the exogenous plasmid sequence was possible in DNA and cDNA of muscle until 7 days after transfection, but not in serum except close to the site of plasmid deposition, 1 h after injection and surgery. The findings suggest that the reliable detection of gene doping in the immoral athlete is not possible unless a change in the current practice of tissue sampling is applied involving the collection of muscle biopsy close to the site of gene injection.


Asunto(s)
Doping en los Deportes , Quinasa 1 de Adhesión Focal/biosíntesis , Quinasa 1 de Adhesión Focal/genética , Músculo Esquelético/enzimología , Reacción en Cadena de la Polimerasa , Transfección , Animales , Secuencia de Bases , Biopsia , Pollos , ADN/sangre , Electroporación , Inducción Enzimática , Hipertrofia , Masculino , Datos de Secuencia Molecular , Músculo Esquelético/patología , Ratas , Ratas Wistar , Reproducibilidad de los Resultados , Proteínas Quinasas S6 Ribosómicas 70-kDa/metabolismo , Transducción de Señal , Factores de Tiempo
3.
Sci Rep ; 12(1): 8306, 2022 05 18.
Artículo en Inglés | MEDLINE | ID: mdl-35585081

RESUMEN

The aim of our study was (I) To compare back muscle oxygenation and perfusion as well as Biering-Sorensen muscle endurance (BSME) test holding times between chronic non-specific low back pain (CNSLBP) patients and asymptomatic controls matched for age, body mass index (BMI), sex and physical activity, and (II) to investigate factors associated with BSME holding times. Muscle perfusion (tHb) and oxygenation (SmO2) were measured by near-infrared spectroscopy (NIRS) based oximetry in three back muscles during the BSME. Reliability of tHb and SmO2 was assessed in a separate sample. BSME holding time and SmO2 were compared between patients (n = 45) and controls (n = 45) and factors associated with BSME holding time were assessed using multiple linear regression. Reliability for SmO2 was excellent (ICC = 0.87-0.99). THb showed poor to moderate reliability and was not further used. Groups differed for BSME holding time (P = 0.03), pain intensity (P ≤ 0.0005) and subcutaneous tissue thickness (P = 0.01) but not for NIRS measures. Physical activity and BMI were associated with BSME holding times. Insufficient muscle oxygenation does not seem to be a major factor contributing to CNSLBP. Future investigation should evaluate other determinants of BSME holding times, such as motivation and recruitment of auxiliary muscles.


Asunto(s)
Músculos de la Espalda , Dolor de la Región Lumbar , Ejercicio Físico , Prueba de Esfuerzo/métodos , Humanos , Músculo Esquelético/fisiología , Resistencia Física/fisiología , Reproducibilidad de los Resultados
4.
Exp Physiol ; 95(3): 451-62, 2010 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-19897567

RESUMEN

Human muscle operates along a continuum of power output, which is set through bioenergetic and anatomical principles. In turn, environmental and intrinsic factors during contractile work exert pronounced control over muscle performance by instructing muscle remodelling. This phenotypic control is specifically indicated with intense exercise at altitude, when extra strain is put on energy supply and the temperature-dependent mechanical efficiency of contraction. While it is classically thought that chronic exposure to hypoxia is maladaptive, repeated short episodes of reduced oxygenation alone or in combination with intense endurance work is now understood to preserve exercise performance when atmospheric oxygen levels are low. Endurance training at moderate altitude exploits the temperature-dependent malleability of energy supply that may maximize metabolic flux at altitude. The contribution of genomic mechanisms is important to the plasticity of metabolic pathways in exercised muscle. This is highlighted by the association of distinct gene polymorphisms in master governors of mitochondrial and vascular growth with exercise phenotypes. Feedforward control of human locomoter muscle by exercise involves the transient upregulation of transcript expression for metabolic processes. The response of the mitochondrial transcriptome to intense exercise is graded with respect to mitochondrial content and deoxygenation during muscle work and reflects exercise-induced mitochondrial biogenesis. This supports the notion that genome-mediated muscle malleability is under feedback control by design constraints of the pathway of oxygen. Thus, activity-dependent and genetic mechanisms contribute to the interindividual difference in the metabolic bottlenecks in athletes performing in exceptional environmental conditions.


Asunto(s)
Adaptación Fisiológica/fisiología , Altitud , Rendimiento Atlético/fisiología , Músculo Esquelético/fisiología , Consumo de Oxígeno/fisiología , Regulación de la Expresión Génica/fisiología , Genómica , Humanos , Hipoxia/fisiopatología
5.
Eur J Appl Physiol ; 110(6): 1095-8, 2010 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-20941629

RESUMEN

Studies on gene-phenotype associations are a popular theme in exercise physiology. This editorial follows up on the current limitations in this quest with regard to the identification of mechanistically important relationships.


Asunto(s)
Tolerancia al Ejercicio/genética , Ejercicio Físico/fisiología , Genes/fisiología , Estudios de Asociación Genética/normas , Ligamiento Genético , Adulto , Femenino , Humanos , Masculino , Persona de Mediana Edad , Fenotipo , Polimorfismo Genético/fisiología , Estándares de Referencia , Adulto Joven
6.
Eur J Appl Physiol ; 106(3): 389-98, 2009 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-19294408

RESUMEN

We examined the involvement of focal adhesion kinase (FAK) in mechano-regulated signalling to protein synthesis by combining muscle-targeted transgenesis with a physiological model for un- and reloading of hindlimbs. Transfections of mouse tibialis anterior muscle with a FAK expression construct increased FAK protein 1.6-fold versus empty transfection in the contralateral leg and elevated FAK concentration at the sarcolemma. Altered activation status of phosphotransfer enzymes and downstream translation factors showed that FAK overexpression was functionally important. FAK auto-phosphorylation on Y397 was enhanced between 1 and 6 h of reloading and preceded the activation of p70S6K after 24 h of reloading. Akt and translation initiation factors 4E-BP1 and 2A, which reside up- or downstream of p70S6K, respectively, showed no FAK-modulated regulation. The findings identify FAK as an upstream element of the mechano-sensory pathway of p70S6K activation whose Akt-independent regulation intervenes in control of muscle mass by mechanical stimuli in humans.


Asunto(s)
Proteína-Tirosina Quinasas de Adhesión Focal/fisiología , Mecanotransducción Celular/fisiología , Proteínas Musculares/biosíntesis , Transducción de Señal/fisiología , Animales , Quinasa 1 de Adhesión Focal/fisiología , Proteína-Tirosina Quinasas de Adhesión Focal/metabolismo , Masculino , Ratones , Proteína Quinasa 3 Activada por Mitógenos/fisiología , FN-kappa B/fisiología , Fosforilación/fisiología , Proteínas Quinasas S6 Ribosómicas 70-kDa/fisiología
7.
Endocrinol Metab Clin North Am ; 39(1): 183-200, xi, 2010 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-20122458

RESUMEN

Endurance athletes demonstrate an exceptional resistance to fatigue when exercising at high intensity. Much research has been devoted to the contribution of aerobic capacity for the economy of endurance performance. Important aspects of the fine-tuning of metabolic processes and power output in the endurance athlete have been overlooked. This review addresses how training paradigms exploit bioenergetic pathways in recruited muscle groups to promote the endurance phenotype. A special focus is laid on the genome-mediated mechanisms that underlie the conditioning of fatigue resistance and aerobic performance by training macrocycles and complements. The available data on work-induced muscle plasticity implies that different biologic strategies are exploited in athletic and untrained populations to boost endurance capacity. Olympic champions are probably endowed with a unique constitution that renders the conditioning of endurance capacity for competition particularly efficient.


Asunto(s)
Ejercicio Físico/fisiología , Resistencia Física/fisiología , Adenosina Trifosfato , Rendimiento Atlético/fisiología , Dieta , Metabolismo Energético , Fatiga/clasificación , Ácidos Grasos/metabolismo , Expresión Génica , Humanos , Proteínas Musculares/biosíntesis , Proteínas Musculares/genética , Proteínas Musculares/metabolismo , Músculo Esquelético/fisiología , Consumo de Oxígeno , Resistencia Física/genética , Aptitud Física/fisiología
8.
Appl Physiol Nutr Metab ; 34(3): 447-53, 2009 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-19448713

RESUMEN

Performance of striated muscle relies on the nerve-driven activation of the sarcomeric motor and coupled energy supply lines. This biological engine is unique; its mechanical and metabolic characteristics are not fixed, but are tailored by functional demand with exercise. This remodelling is specific for the imposed muscle stimulus. This is illustrated by the increase in local oxidative capacity with highly repetitive endurance training vs. the preferential initiation of sarcomerogenesis with strength training regimes, where high-loading increments are imposed. The application of molecular biology has provided unprecedented insight into the pathways that govern muscle plasticity. Time-course analysis indicates that the adjustments to muscle work involve a broad regulation of transcript expression during the recovery phase from a single bout of exercise. Highly resolving microarray analysis demonstrates that the specificity of an endurance-exercise stimulus is reflected by the signature of the transcriptome response after muscle work. A quantitative match in mitochondrial transcript adjustments and mitochondrial volume density after endurance training suggests that the gradual accumulation of expressional microadaptations underlies the promotion of fatigue resistance with training. This regulation is distinguished from control of muscle growth via the load-dependent activation of sarcomerogenesis. Discrete biochemical signalling systems have evolved that sense metabolic perturbations during exercise and trigger a specific expression program, which instructs the remodelling of muscle makeup. A drop in muscle oxygen tension and metabolite perturbations with exercise are recognized as important signals in the genome-mediated remodelling of the metabolic muscle phenotype in humans.


Asunto(s)
Adaptación Fisiológica/fisiología , Regulación de la Expresión Génica/fisiología , Mitocondrias/metabolismo , Músculo Esquelético/fisiología , Ejercicio Físico , Humanos , Proteínas Musculares/genética , Proteínas Musculares/metabolismo
9.
High Alt Med Biol ; 10(2): 183-93, 2009.
Artículo en Inglés | MEDLINE | ID: mdl-19519225

RESUMEN

The ascent of humans to the summits of the highest peaks on Earth initiated a spurt of explorations into the physiological consequences of physical activity at altitude. The past three decades have demonstrated that the resetting of respiratory and cardiovascular control with chronic exposure to altitudes above 4000 m is accompanied by important structural-functional adjustments of skeletal muscle. The fully altitude-adapted phenotype preserves energy charge at reduced aerobic capacity through the promotion of anaerobic substrate flux and tighter metabolic control, often at the expense of muscle mass. In seeming contrast, intense physical activity at moderate hypoxia (2500 to 4000 m) modifies this response in both low and high altitude natives through metabolic compensation by elevating local aerobic capacity and possibly preventing muscle fiber atrophy. The combined use of classical morphometry and contemporary proteomic technology provides a highly resolved picture of the temporal control of hypoxia-induced muscular adaptations. The muscle proteome signature identifies mitochondrial autophagy and protein degradation as prime adaptive mechanisms to passive altitude exposure and ascent to extreme altitude. Protein measures also explain the lactate paradox by a sparing of glycolytic enzymes from general muscle wasting. Enhanced mitochondrial and angiogenic protein expression in human muscle with exercise up to 4000 m is related to the reduction in intramuscular oxygen content below 1% (8 torr), when the master regulator of hypoxia-dependent gene expression, HIF-1alpha, is stabilized. Accordingly, it is proposed here that the catabolic consequences of chronic hypoxia exposure reflect the insufficient activation of hypoxia-sensitive signaling and the suppression of energy-consuming protein translation.


Asunto(s)
Altitud , Ejercicio Físico/fisiología , Proteínas Musculares/metabolismo , Músculo Esquelético/metabolismo , Adaptación Fisiológica , Humanos , Factor 1 Inducible por Hipoxia/genética , Factor 1 Inducible por Hipoxia/metabolismo , Mitocondrias Musculares/metabolismo , Fibras Musculares Esqueléticas/metabolismo
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