Regulation of glucose and fatty acid metabolism in skeletal muscle during contraction

O ciclo glicose-ácido graxo explica a preferência do tecido muscular pelos ácidos graxos durante atividade moderada de longa duração. Em contraste, durante o exercício de alta intensidade, há aumento na disponibilidade e na taxa de oxidação de glicose. A produção de espécies reativas de oxigênio (EROs) durante a atividade muscular sugere que o balanço redox intracelular é importante na regulação do metabolismo de lipídios/carboidratos. As EROs diminuem a atividade do ciclo de Krebs e aumentam a atividade da proteína desacopladora mitocondrial. O efeito oposto é esperado durante a atividade moderada. Assim, as questões levantadas nesta revisão são: Por que o músculo esquelético utiliza preferencialmente os lipídios no estado basal e de atividade moderada? Por que o ciclo glicose-ácido graxo falha em exercer seus efeitos durante o exercício intenso? Como o músculo esquelético regula o metabolismo de lipídios e carboidratos em regime envolvendo o ciclo contração-relaxamento.The glucose-fatty acid cycle explains the preference for fatty acid during moderate and long duration physical exercise. In contrast, there is a high glucose availability and oxidation rate in response to intense physical exercise. The reactive oxygen species (ROS) production during physical exercise suggests that the redox balance is important to regulate of lipids/carbohydrate metabolism. ROS reduces the activity of the Krebs cycle, and increases the activity of mitochondrial uncoupling proteins. The opposite effects happen during moderate physical activity. Thus, some issues is highlighted in the present review: Why does skeletal muscle prefer lipids in the basal and during moderate physical activity? Why does glucose-fatty acid fail to carry out their effects during intense physical exercise? How skeletal muscles regulate the lipids and carbohydrate metabolism during the contraction-relaxation cycle

Regulation of glucose and fatty acid metabolism in skeletal muscle during contraction

O ciclo glicose-ácido graxo explica a preferência do tecido muscular pelos ácidos graxos durante atividade moderada de longa duração. Em contraste, durante o exercício de alta intensidade, há aumento na disponibilidade e na taxa de oxidação de glicose. A produção de espécies reativas de oxigênio (EROs) durante a atividade muscular sugere que o balanço redox intracelular é importante na regulação do metabolismo de lipídios/carboidratos. As EROs diminuem a atividade do ciclo de Krebs e aumentam a atividade da proteína desacopladora mitocondrial. O efeito oposto é esperado durante a atividade moderada. Assim, as questões levantadas nesta revisão são: Por que o músculo esquelético utiliza preferencialmente os lipídios no estado basal e de atividade moderada? Por que o ciclo glicose-ácido graxo falha em exercer seus efeitos durante o exercício intenso? Como o músculo esquelético regula o metabolismo de lipídios e carboidratos em regime envolvendo o ciclo contração-relaxamento555303313CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQCOORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL DE NÍVEL SUPERIOR - CAPESFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPsem informaçãoThe glucose-fatty acid cycle explains the preference for fatty acid during moderate and long duration physical exercise. In contrast, there is a high glucose availability and oxidation rate in response to intense physical exercise. The reactive oxygen species (ROS) production during physical exercise suggests that the redox balance is important to regulate of lipids/carbohydrate metabolism. ROS reduces the activity of the Krebs cycle, and increases the activity of mitochondrial uncoupling proteins. The opposite effects happen during moderate physical activity. Thus, some issues is highlighted in the present review: Why does skeletal muscle prefer lipids in the basal and during moderate physical activity? Why does glucose-fatty acid fail to carry out their effects during intense physical exercise? How skeletal muscles regulate the lipids and carbohydrate metabolism during the contraction-relaxation cycle

The acute effects of plyometric and sled towing stimuli with and without caffeine ingestion on vertical jump performance in professional soccer players

Abstract Background Post-activation potentiation (PAP) is the phenomenon by which muscular performance is enhanced in response to a conditioning stimulus. PAP has typically been evidenced via improved counter movement jump (CMJ) performance. This study examined the effects of PAP, with and without prior caffeine ingestion, on CMJ performance. Methods Twelve male professional soccer players (23 ± 5 years) performed two trials of plyometric exercises and sled towing 60 min after placebo or caffeine ingestion (5 mg.kg− 1) in a randomized, counterbalanced and double-blinded design. CMJ performance was assessed at baseline and 1, 3 and 5 min after the conditioning stimulus (T1, T3 and T5, respectively). Results Two way ANOVA main effects indicated a significant difference in jump height after the PAP protocol (F[3, 11] = 14.99, P  0.05) compared to placebo. Conclusions The results of this study suggest that acute plyometric and sled towing stimuli enhances jump performance and that this potentiation is augmented by caffeine ingestion in male soccer players

Chronic treatment with the AMP-kinase activator AICAR increases glycogen storage and fatty acid oxidation in skeletal muscles but does not reduce hyperglucagonemia and hyperglycemia in insulin deficient rats.

This study tested whether the glycogen-accumulating effect of chronic in vivo pharmacological 5'AMP-activated protein kinase (AMPK) activation could improve glycemic control under conditions of insulin deficiency. Male Wistar rats were rendered diabetic through the administration of streptozotocin (STZ) and then treated for 7 consecutive days with the AMPK activator 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR). Subsequently, glycogen content and synthesis, glucose oxidation, and fatty acid oxidation (FAO) were determined in oxidative and glycolytic skeletal muscles. Glycemia, insulinemia, glucagonemia, and circulating triglycerides (TG) and non-esterified fatty acids (NEFAs) were measured after AICAR treatment. Insulin was almost undetectable in STZ rats and these animals were severely hyperglycemic. Glycogen content was markedly low mainly in glycolytic muscles of STZ rats and AICAR treatment restored it to control values. No differences were found among all muscles studied with regards to the content and phosphorylation of Akt/protein kinase B and glycogen synthase kinase 3. Even though glycogen synthase content was reduced in all muscles from STZ rats, insulin-induced dephosphorylation/activation of this enzyme was preserved and unaffected by AICAR treatment. Glucagon and NEFAS were 2- and 7.4-fold fold higher in STZ rats than controls, respectively. AICAR did not affect hyperglycemia and hyperglucagonemia in STZ rats; however, it normalized circulating NEFAs and significantly increased FAO in glycolytic muscles. In conclusion, even though AICAR-induced AMPK activation enhanced glycogen accumulation in glycolytic muscles and normalized circulating NEFAs and TG levels, the hyperglycemic effects of glucagon likely offset the potentially glucose-lowering effects of AICAR, resulting in no improvement of glycemic control in insulin-deficient rats

Fat depot-specific anti-catabolic effect of AICAR in rats with streptozotocin (STZ)-induced insulin deficiency.

<p>Subcutaneous (Sc) inguinal (Ing) fat (A) and retroperitoneal (Retro) fat (B) masses of control (Con, saline-injected), AICAR-injected (A), STZ, and STZ plus AICAR (STZ+A) rats were extracted and quantified at the end of the study. *P<0.05 vs. Con, A, and STZ+A. ^#P<0.05 vs. Con, A, and STZ. ^‡P<0.05 vs. Con, STZ, and STZ+A (One-way ANOVA, N = 8).</p

Polyphagia and polydipsia of Streptozotocin (STZ)-induced diabetes is not affected by AICAR treatment.

<p>Time-course of food intake (A) average food intake (B), time-course body weight (BW) (C), average BW (D), feed efficiency (E), and water (F) intake of control (Con, saline-injected), AICAR-injected (A), STZ, and STZ plus AICAR (STZ+A) rats. Time-course graphs show data from animals monitored on a daily basis one week prior to (days 1–7) and during AICAR administration (days 8–14). *P<0.05 vs. Con, STZ, and STZ+A. ^#P<0.05 vs. Con and A (Two-way ANOVA, N = 8).</p

Treatment with AICAR attenuates the catabolic effects of streptozotocin (STZ)-induced diabetes on body composition.

<p>Lean body mass (LBM) (A), soleus (Sol) (B), extensor digitorum longus (EDL) (C), and epitrochlearis (Epit) (D) muscles, and viscera (E) masses were measured in control (Con, saline-injected), AICAR-injected (A), STZ, and STZ plus AICAR (STZ+A) rats at the end of the study. *P<0.05 vs. Con, A, and STZ+A. ^#P<0.05 vs. Con, A, and STZ. ^‡P<0.05 vs. Con and A. (One-way ANOVA, N = 8).</p

Profile of oxygen consumption (VO₂) (A and B), respiratory exchange ratio (RER) (C and D), energy expenditure (heat) (E and F), and ambulatory activity (G and H) in control (Con, saline-injected), AICAR-injected (A), streptozotocin (STZ) diabetic, and streptozotocin plus AICAR (STZ+A) rats.

<p>At the end of the AICAR administration-period all animals were placed in the CLAMS for 24 h. *P<0.05 vs. Con and A light. ^#P<0.05 vs. Con and A dark. ^‡P<0.05 vs. Con light. ^¥P<0.05 vs. Con dark. ^†P<0.05 vs. Con and A light. ^§P<0.05 vs. Con, A, and STZ light and dark. ^&P<0.05 vs. Con, A, and STZ+A dark. ^$P<0.05 vs. Con, A, and STZ+A dark. ^£P<0.05 vs. Con, A, and STZ dark (Two-way ANOVA, N = 8).</p