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  • 1.
    Axling, U
    et al.
    Department of Experimental Medical Science, Lund University, Lund, Sweden.
    Olsson, C
    Department of Applied Nutrition and Food Chemistry, Section of Food Hygiene, Lund University, Lund, Sweden.
    Xu, J
    Department of Applied Nutrition and Food Chemistry, Section of Food Hygiene, Lund University, Lund, Sweden.
    Fernandez, C
    Department of Experimental Medical Science, Lund University, Lund, Sweden.
    Larsson, S
    Department of Experimental Medical Science, Lund University, Lund, Sweden.
    Ström, Kristoffer
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences. Department of Experimental Medical Science, Lund University, Lund, Sweden.
    Ahrné, S
    Department of Applied Nutrition and Food Chemistry, Section of Food Hygiene, Lund University, Lund, Sweden.
    Holm, C
    Department of Experimental Medical Science, Lund University, Lund, Sweden.
    Molin, G
    Department of Applied Nutrition and Food Chemistry, Section of Food Hygiene, Lund University, Lund, Sweden.
    Berger, K
    Department of Experimental Medical Science, Lund University, Lund, Sweden.
    Green tea powder and Lactobacillus plantarum affect gut microbiota, lipid metabolism and inflammation in high-fat fed C57BL/6J mice2012In: Nutrition and Metabolism, ISSN 1743-7075, Vol. 9, article id 105Article in journal (Refereed)
    Abstract [en]

    Background: Type 2 diabetes is associated with obesity, ectopic lipid accumulation and low-grade inflammation. A dysfunctional gut microbiota has been suggested to participate in the pathogenesis of the disease. Green tea is rich in polyphenols and has previously been shown to exert beneficial metabolic effects. Lactobacillus plantarum has the ability to metabolize phenolic acids. The health promoting effect of whole green tea powder as a prebiotic compound has not been thoroughly investigated previously. Methods. C57BL/6J mice were fed a high-fat diet with or without a supplement of 4% green tea powder (GT), and offered drinking water supplemented with Lactobacillus plantarum DSM 15313 (Lp) or the combination of both (Lp + GT) for 22 weeks. Parameters related to obesity, glucose tolerance, lipid metabolism, hepatic steatosis and inflammation were examined. Small intestinal tissue and caecal content were collected for bacterial analysis. Results: Mice in the Lp + GT group had significantly more Lactobacillus and higher diversity of bacteria in the intestine compared to both mice in the control and the GT group. Green tea strongly reduced the body fat content and hepatic triacylglycerol and cholesterol accumulation. The reduction was negatively correlated to the amount of Akkermansia and/or the total amount of bacteria in the small intestine. Markers of inflammation were reduced in the Lp + GT group compared to control. PLS analysis of correlations between the microbiota and the metabolic variables of the individual mice showed that relatively few components of the microbiota had high impact on the correlation model. Conclusions: Green tea powder in combination with a single strain of Lactobacillus plantarum was able to promote growth of Lactobacillus in the intestine and to attenuate high fat diet-induced inflammation. In addition, a component of the microbiota, Akkermansia, correlated negatively with several metabolic parameters known to be risk factors for the development of type 2 diabetes.

  • 2.
    Azzinnari, M
    et al.
    University of Las Palmas, Spain.
    Martin-Rincon, M
    University of Las Palmas, Spain.
    Juan-Habib, J
    University of Las Palmas, Spain.
    Gelabert-Rebato, M
    University of Las Palmas, Spain.
    Calbet, JAL
    University of Las Palmas, Spain.
    Holmberg, Hans-Christer
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences.
    Morales –Alamo, D
    University of Las Palmas, Spain.
    Efectos del ejercicio en la señalización de NF-kB durante la restricción calórica severa2017Conference paper (Refereed)
    Abstract [es]

    El sobrepeso y la obesidad, en crecimiento en todo el mundo, se asocian con una alta tasa de mortalidad e morbilidad[1,2]. La causa principal que conduce a éstas condiciones patológicas es un balance energético positivo sostenido a largo plazo, debido a la inactividad física y la ingesta calórica excesiva[3]. Por lo tanto, ejercicio físico y restricción calórica podrían ser dos estratégias eficaces para prevenir y contrastar el excesivo acumulo de grasa corporal que caracteriza estas patologías. Sin embargo, durante dietas muy bajas en calorías (<800 Kcal/día) se pierde no solo masa grasa sino también masa muscular, reportando efectos negativos para la salud[4]. En dichas condiciones,  el ejercicio físico permite preservar masa muscular de manera local y dosis-dependiente, mientras la ingestión de proteínas no ejerce particulares efectos protectivos sobre el tejido contráctil[5]. Los mecanismos moleculares implicados en la preservación de la masa muscular inducida por el ejercicio durante este tipo de dietas no han sido definidos claramente. NF-kB es un factor de transcripción cuya activación provoca atrofia muscular, y su bloqueo puede parcialmente limitar este fenomeno[6]. NF-kB se ha mostrado activado de manera aguda por el ejercicio y la restricción calorica, sin embargo no ha sido definida su respuesta a la restricción calórica en conjunción con el ejercicio prolongado de baja intensidad. Además, cuando los niveles basales de NF-kB son altos, el ejercicio no parece aumentar ulteriormente su señalización[7]. Por las razones presentadas, NF-kB podría desempeñar un rol en la preservación de masa magra inducida por el ejercicio durante  la restricción calórica.

    El objetivo del estudio es establecer la respuesta de NF-kB a la restricción calórica severa en conjunción con el ejercicio prolongado de baja intensidad. Las hipótesis fueron las siguientes: 1) la restricción calórica severa activaría la via de NF-kB y 2) dicha activación será atenuada por el ejercicio de manera local y dosis-dependiente.

    15 sujetos con sobrepeso y obesidad fueron sometidos a tres fases experimentales: fase 1, en la que la dieta y el nivel de actividad física de los participantes fue monitorizado durante una semana (PRE); fase 2, caracterizada por cuatro días de ejercicio prolongado y de restricción calórica severa (RCE); fase 3, caracterizada por tres días de ejercicio reducido y una dieta isoenergética (DC). Durante la fase 2, los sujetos ingeriron hidratos de carbono o proteínas (0.8 g/kg peso corporal/día; 320 kcal/día) y hicieron 45 minutos de pedaleo con un solo miembro superior (15% Ppeak) seguidos de 8 horas de caminata (4.5 km/h; 35 km/día). Las biopsias musculares fueron recogidas de ambos los deltoides y del vasto lateral en la fase 1 y después de la fase 2 y 3. Mediante Western blot, se determinó la expresión de NF-κB p105, NF-κB p50, la fosforilación de la Serina 32/36 de IκBα e IκBα total. La composición corporal se midió mediante DXA. Estadística: ANOVA para medidas repetidas.

    Durante los 4 días de restricción calórica severa el deficit energético fue de 5500 Kcal. Después de la fase 2 los sujetos perdieron menos masa magra en los miembros inferiores y en el brazo ejercitado respecto al brazo de control: 57% (P<0.05) y 29% (P=0.05), respectivamente. Tras la fase 2 y 3, el contenido de p105 y de p50 fue menor en los miembros inferiores respecto a los superiores: efecto extremidad P=0.003 y P=0.024 para p105 y p50, respectivamente. Tras la fase 3, la fosforilación de la Serina 32/36 de IkBα aumentó únicamente en las piernas, mientras la expresión total IkBα fue mayor solo en los miembros ejercitados (P<0.05).

    El ejercicio físico atenuó la activación de la señalización de NF-kB durante 4 días de restricción calórica severa, limitando el incremento de la expresión de p50 y p105, que resultó más baja después de la fase 2 y la fase 3 en los miembros inferiores respecto a los miembros superiores, posiblemente debido a la mayor cantidad de ejercicio a la que fueron sometidos. Además, la expresión total de IkBα fue más alta tras la fase 3 solo en los miembros ejercitados, indicando una posible inhibición de la vía de   NF-kB inducida por el ejercicio. Por lo tanto, dado la menor activación de la señalización de NF-kB en los miembros que perdieron menor masa muscular, los resultados sugieren que los efectos protectores del ejercicio físico sobre el tejido contráctil podrían ser mediados a una menor activación de la señalización de NF-kB.

    El ejercicio físico desempeña una función preservadora sobre la masa muscular durante la restricción calórica severa. La preservación de masa muscular es dosis-dependiente (a mayor volumen, mayor preservación) y está mediada, al menos parcialmente, por una menor activación de la señalización por NF-kB.

    1.Hill, J. O., H. R. Wyatt, et al. (2012). Circulation 126(1): 126-132.2.Di Angelantonio, E., N. Bhupathiraju Sh, et al. (2016). Lancet 388(10046): 776-786. 3.Chaston, T. B., J. B. Dixon, et al. (2007). Int J Obes (Lond) 31(5): 743-750. 4.Calbet, J. A., J. G. Ponce-Gonzalez, et al. (2017). Front Physiol (Accepted, In press).5.Cai, D., J. D. Frantz, et al. (2004). Cell 119(2): 285-298.6.Tantiwong, P., K. Shanmugasundaram, et al. (2010). Am J Physiol Endocrinol Metab 299(5): E794-801.7.NCD-RisC (2016). Lancet 387(10026): 1377-1396.

  • 3. Beaven, Christopher
    Dose effect of caffeine on testosterone and cortisol responses to resistance exercise2008In: International Journal of Sport Nutrition & Exercise Metabolism, ISSN 1526-484X, E-ISSN 1543-2742, Vol. 18, no 2, p. 131-141Article in journal (Refereed)
    Abstract [en]

    Introduction: Interest in the use of caffeine as an ergogenic aid has increased since the International Olympic Committee lifted the partial ban on its use. Caffeine has beneficial effects on various aspects of athletic performance, but its effects on training have been neglected.

    Purpose: To investigate the acute effect of caffeine on the exercise-associated increases in testosterone and cortisol in a double-blind crossover study.

    Methods: 24 professional rugby-league players ingested caffeine doses of 0, 200, 400 and 800 mg in random order 1 h before a resistance-exercise session. Saliva was sampled at the time of caffeine ingestion, at 15-min intervals throughout each session, and at 15 and 30 min after the session. Data were log transformed to estimate percent effects with mixed modeling, and effects were standardized to assess magnitudes.

    Results: Testosterone concentration showed a small increase of 15% (90% confidence limits, ±19%) during exercise. Caffeine raised this concentration in a dose-dependent manner by a further small 21% (±24%) at the highest dose. The 800-mg dose also produced a moderate 52% (±44%) increase in cortisol. The effect of caffeine on the testosterone/cortisol ratio was a small decline (14; ±21%).

    Conclusion: Caffeine has some potential to benefit training outcomes via the anabolic effects of the increase in testosterone concentration, but this benefit may be counteracted by the opposing catabolic effects of the increase in cortisol and resultant decline in the testosterone/cortisol ratio.

  • 4.
    Cook, C
    et al.
    United Kingdom Sports Council, London, England .
    Beaven, C. Martyn
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences.
    Kilduff, L P
    Swansea Univ, Coll Engn, Swansea, W Glam, Wales.
    Drawer, S
    United Kingdom Sports Council, London, England .
    Acute caffeine ingestion increases voluntarily chosen resistance training load following limited sleep2012In: International Journal of Sport Nutrition & Exercise Metabolism, ISSN 1526-484X, E-ISSN 1543-2742, Vol. 22, no 3, p. 157-164Article in journal (Refereed)
    Abstract [en]

    INTRODUCTION:This study aimed to determine whether caffeine ingestion would increase the workload voluntarily chosen by athletes in a limited sleep state.

    METHODS:In a double-blind, crossover study, sixteen professional rugby players ingested either a placebo or 4 mg·kg-1 caffeine 1 h before exercise. Athletes classified themselves into non-deprived (8 h+) or sleep-deprived states (6 h or less). Exercise comprised four sets of bench press, squats, and bent rows at 85% 1-RM. Athletes were asked to perform as many repetitions on each set as possible without failure. Saliva was collected prior to administration of placebo or caffeine, and again prior to and immediately after exercise and assayed for testosterone and cortisol.

    RESULTS:Sleep deprivation produced a very large decrease in total load (p = 1.98 x 10-7).Caffeine ingestion in the non-deprived state resulted in a moderate increase in total load with a larger effect in the sleep deprived state resulting in total load similar to those observed in the non-deprived placebo condition.Eight of the sixteen athletes were identified as caffeine responders.Baseline testosterone was higher (p < 0.05) and cortisol trended lower in non-sleep deprived states.Changes in hormones from pre-dose to pre-exercise correlated to individual workload responses to caffeine.Testosterone response to exercise increased with caffeine compared to placebo, as did cortisol response.

    CONCLUSIONS:Caffeine increased voluntary workload in professional athletes, emphasised further under conditions of self-reported limited sleep. Caffeine may prove worthwhile when athletes are perceived as tired, especially in individuals identified as responders.

  • 5.
    PÉREZ-SUÁREZ, I
    et al.
    University of Las Palmas, Gran Canaria, Spain.
    CALLE-HERRERO, J
    University of Las Palmas, Gran Canaria, Spain.
    PONCE-GONZÁLEZ, JG
    University of Las Palmas, Gran Canaria, Spain.
    LOSA-REYNA, J
    University of Las Palmas, Gran Canaria, Spain.
    SANTANA, A
    University of Las Palmas, Gran Canaria, Spain.
    Holmberg, Hans-Christer
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences.
    CALBET, JAL
    University of Las Palmas, Gran Canaria, Spain.
    LEPTIN RECEPTOR MOLECULAR VARIANTS ARE DIFFERENTLY REGULATED BY EXERCISE AND ENERGY DEFICIT IN HUMAN SKELETAL MUSCLE2014Conference paper (Refereed)
    Abstract [en]

    Introduction

    Leptin signals in skeletal muscles through pathways which share some steps with the insulin and IGF1. We have recently shown that LEPR (OBR-170) is increased in the dominant arm of tennis players 1 and is reduced in deltoid and vastus lateralis (VL) of obese compared to control subjects 2. The aim of this study was to determine whether exercise up-regulates the protein abundance and phosphorylation status of the different molecular variations of the LEPR (OBR-170, 128, 98A or 98B) in human skeletal muscle. We hypothesized that exercise will up-regulate leptin signaling in skeletal muscle.

     

    Methods

    Fifteen overweight men underwent three experimental phases: pre-test (PRE); caloric restriction (3.2 Kcal/kg body Wt/d) + exercise (45min unilateral arm cranking/d + 8h walking/d) for 4 days (CRE); and control isoenergetic diet + reduced exercise for 3 days (CD). During CRE, the diet consisted solely of whey protein (PRO, n=8) or sucrose (SU, n=7) (0.8 g/kg body Wt/d). Muscle biopsies (135 biopsies in all) were obtained from the trained and untrained deltoid, and VL, after 12h fast at PRE, and end of CRE and CD. The molecular variants of LEPR (OBR-170, 128, 98A and 98B) were determined by western blot and LEPR mRNA by PCR.

      

    Results

    Serum leptin was reduced by ~60% following CRE and CD (P<0.05). LEPRs were more abundant in arm than leg muscles. LEPR mRNA was increased in exercised muscles after CRE. OBR-170 was reduced after CRE and CD only in the control arm (P<0.05). OBR-128 was increased after CD in exercised extremities (P<0.05). OBR-98A was increased after CRE in trained arm, and after CD in legs (P<0.05). However, OBR-98B was increased after CRE and CD in both arms and exercised extremities (P<0.05), being these effects more pronounced in the PRO group (P<0.05). After CD, LEPR mRNA returned to basal levels while LEPR expression was increased in all muscles (P<0.05). The fraction of LEPR activated (Tyr1141 phosphorylated) was reduced in arms but not in leg muscles. LEPR phosphorylation was correlated with JAK2 (upstream) and STAT3 (downstream) phosphorylation (r=0.67-0.89, P<0.05).

     

    Discussion

    Caloric restriction seems to reduce the abundance of LEPR, but this effect varies depending on specific molecular variants of the receptor. The reduction of LEPR is partly counteracted by exercise, likely contributing to increase muscle leptin sensitivity. Whey protein ingestion facilitates these effects. Resuming normal food ingestion after a period of severe energy deficit is accompanied by increased expression LEPR in skeletal muscle. 

  • 6.
    Ørtenblad, Niels
    et al.
    University of Southern Denmark, Odense, Denmark.
    Nielsen, Joachim
    University of Southern Denmark, Odense, Denmark.
    Saltin, Bengt
    Copenhagen Muscle Research Centre, Copenhagen, Denmark.
    Holmberg, Hans-Christer
    Mid Sweden University, Faculty of Human Sciences, Department of Health Sciences.
    Role of glycogen availability in sarcoplasmic reticulum Ca(2+) kinetics in human skeletal muscle2011In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 589, no 3, p. 711-725Article in journal (Refereed)
    Abstract [en]

    Little is known about the precise mechanism that relates skeletal muscle glycogen to muscle fatigue. The aim of the present study was to examine the effect of glycogen on sarcoplasmic reticulum (SR) function in the arm and leg muscles of elite cross-country skiers (n = 10, (V) over dot(O2 max) 72 +/- 2 ml kg(-1) min(-1)) before, immediately after, and 4 h and 22 h after a fatiguing 1 h ski race. During the first 4 h recovery, skiers received either water or carbohydrate (CHO) and thereafter all received CHO-enriched food. Immediately after the race, arm glycogen was reduced to 31 +/- 4% and SR Ca2+ release rate decreased to 85 +/- 2% of initial levels. Glycogen noticeably recovered after 4 h recovery with CHO (59 +/- 5% initial) and the SR Ca2+ release rate returned to pre-exercise levels. However, in the absence of CHO during the first 4 h recovery, glycogen and the SR Ca2+ release rate remained unchanged (29 +/- 2% and 77 +/- 8%, respectively), with both parameters becoming normal after the remaining 18 h recovery with CHO. Leg muscle glycogen decreased to a lesser extent (71 +/- 10% initial), with no effects on the SR Ca2+ release rate. Interestingly, transmission electron microscopy (TEM) analysis revealed that the specific pool of intramyofibrillar glycogen, representing 10-15% of total glycogen, was highly significantly correlated with the SR Ca2+ release rate. These observations strongly indicate that low glycogen and especially intramyofibrillar glycogen, as suggested by TEM, modulate the SR Ca2+ release rate in highly trained subjects. Thus, low glycogen during exercise may contribute to fatigue by causing a decreased SR Ca2+ release rate.

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