Resistance exercise initiates mechanistic target of rapamycin (mTOR) translocation and protein complex co-localisation in human skeletal muscle.

The mechanistic target of rapamycin (mTOR) is a central mediator of protein synthesis in skeletal muscle. We utilized immunofluorescence approaches to study mTOR cellular distribution and protein-protein co-localisation in human skeletal muscle in the basal state as well as immediately, 1 and 3 h after an acute bout of resistance exercise in a fed (FED; 20 g Protein/40 g carbohydrate/1 g fat) or energy-free control (CON) state. mTOR and the lysosomal protein LAMP2 were highly co-localised in basal samples.

Mild Dehydration Does Not Influence Performance Or Skeletal Muscle Metabolism During Simulated Ice Hockey Exercise In Men.

This study determined whether mild dehydration influenced skeletal muscle glycogen use, core temperature or performance during high-intensity, intermittent cycle-based exercise in ice hockey players vs. staying hydrated with water. Eight males (21.

The effect of dehydration on muscle metabolism and time trial performance during prolonged cycling in males.

This study combined overnight fluid restriction with lack of fluid intake during prolonged cycling to determine the effects of dehydration on substrate oxidation, skeletal muscle metabolism, heat shock protein 72 (Hsp72) response, and time trial (TT) performance. Nine males cycled at ~65% VO2peak for 90 min followed by a TT (6 kJ/kg BM) either with fluid (HYD) or without fluid (DEH). Blood samples were taken every 20 min and muscle biopsies were taken at 0, 45, and 90 min of exercise and after the TT.

Rapid Repression of ADP Transport by Palmitoyl-CoA Is Attenuated by Exercise Training in Humans: A Potential Mechanism to Decrease Oxidative Stress and Improve Skeletal Muscle Insulin Signaling.

Mitochondrial ADP transport may represent a convergence point unifying two prominent working models for the development of insulin resistance, as reactive lipids (specifically palmitoyl-CoA [P-CoA]) can inhibit ADP transport and subsequently increase mitochondrial reactive oxygen species emissions. In the current study, we aimed to determine if exercise training in humans diminished P-CoA attenuation of mitochondrial ADP respiratory sensitivity. Six weeks of exercise training increased whole-body glucose homeostasis and skeletal muscle Akt signaling and reduced markers of oxidative stress without reducing maximal mitochondrial H2O2 emissions.

Effect of voluntary hyperventilation with supplemental CO2 on pulmonary O2 uptake and leg blood flow kinetics during moderate-intensity exercise.

Pulmonary O2 uptake (V(O₂p)) and leg blood flow (LBF) kinetics were examined at the onset of moderate-intensity exercise, during hyperventilation with and without associated hypocapnic alkalosis. Seven male subjects (25 ± 6 years old; mean ± SD) performed alternate-leg knee-extension exercise from baseline to moderate-intensity exercise (80% of estimated lactate threshold) and completed four to six repetitions for each of the following three conditions: (i) control [CON; end-tidal partial pressure of CO2 (P(ET, CO₂)) ~40 mmHg], i.e.

Pulmonary gas exchange and acid-base balance during exercise.

As the first step in the oxygen-transport chain, the lung has a critical task: optimizing the exchange of respiratory gases to maintain delivery of oxygen and the elimination of carbon dioxide. In healthy subjects, gas exchange, as evaluated by the alveolar-to-arterial PO2 difference (A-aDO2), worsens with incremental exercise, and typically reaches an A-aDO2 of approximately 25 mmHg at peak exercise. While there is great individual variability, A-aDO2 is generally largest at peak exercise in subjects with the highest peak oxygen consumption.

AMP-activated protein kinase is required for exercise-induced peroxisome proliferator-activated receptor co-activator 1 translocation to subsarcolemmal mitochondria in skeletal muscle.

In skeletal muscle, mitochondria exist as two subcellular populations known as subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria. SS mitochondria preferentially respond to exercise training, suggesting divergent transcriptional control of the mitochondrial genomes. The transcriptional co-activator peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) and mitochondrial transcription factor A (Tfam) have been implicated in the direct regulation of the mitochondrial genome in mice, although SS and IMF differences may exist, and the potential signalling events regulating the mitochondrial content of these proteins have not been elucidated.

Increase in skeletal-muscle glycogenolysis and perceived exertion with progressive dehydration during cycling in hydrated men.

This study investigated the effects of progressive mild dehydration during cycling on whole-body substrate oxidation and skeletal-muscle metabolism in recreationally active men. Subjects (N = 9) cycled for 120 min at ~65% peak oxygen uptake (VO2peak 22.7 °C, 32% relative humidity) with water to replace sweat losses (HYD) or without fluid (DEH).

Mitochondrial creatine kinase activity and phosphate shuttling are acutely regulated by exercise in human skeletal muscle.

Energy transfer between mitochondrial and cytosolic compartments is predominantly achieved by creatine-dependent phosphate shuttling (PCr/Cr) involving mitochondrial creatine kinase (miCK). However, ADP/ATP diffusion through adenine nucleotide translocase (ANT) and voltage-dependent anion carriers (VDACs) is also involved in this process. To determine if exercise alters the regulation of this system, ADP-stimulated mitochondrial respiratory kinetics were assessed in permeabilized muscle fibre bundles (PmFBs) taken from biopsies before and after 2 h of cycling exercise (60% ) in nine lean males.

Effects of dehydration during cycling on skeletal muscle metabolism in females.

Introduction: This study investigated the effects of progressive dehydration on the time course of changes to whole body substrate oxidation and skeletal muscle metabolism during 120 min of cycling in hydrated females.

Methods: Subjects (n = 9) cycled for 120 min at approximately 65% VO(2peak) on two occasions: with no fluid (DEH) and with fluid (HYD) replacement to match sweat losses. Venous blood samples were taken at rest and every 20 min and muscle biopsies taken at 0, 60, and 120 min of exercise.

Acute endurance exercise increases plasma membrane fatty acid transport proteins in rat and human skeletal muscle.

Fatty acid transport proteins are present on the plasma membrane and are involved in the uptake of long-chain fatty acids into skeletal muscle. The present study determined whether acute endurance exercise increased the plasma membrane content of fatty acid transport proteins in rat and human skeletal muscle and whether the increase was accompanied by an increase in long-chain fatty acid transport in rat skeletal muscle. Sixteen subjects cycled for 120 min at ∼60 ± 2% Vo(2) peak.

The relationship between human skeletal muscle pyruvate dehydrogenase phosphatase activity and muscle aerobic capacity.

Pyruvate dehydrogenase (PDH) is a mitochondrial enzyme responsible for regulating the conversion of pyruvate to acetyl-CoA for use in the tricarboxylic acid cycle. PDH is regulated through phosphorylation and inactivation by PDH kinase (PDK) and dephosphorylation and activation by PDH phosphatase (PDP). The effect of endurance training on PDK in humans has been investigated; however, to date no study has examined the effect of endurance training on PDP in humans.

Nuclear SIRT1 activity, but not protein content, regulates mitochondrial biogenesis in rat and human skeletal muscle.

Silent mating type information regulator 2 homolog 1 (SIRT1)-mediated peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) deacetylation is potentially key for activating mitochondrial biogenesis. Yet, at the whole muscle level, SIRT1 is not associated with mitochondrial biogenesis (Gurd, BJ, Yoshida Y, Lally J, Holloway GP, Bonen A. J Physiol 587: 1817-1828, 2009).

Repeated transient mRNA bursts precede increases in transcriptional and mitochondrial proteins during training in human skeletal muscle.

Exercise training induces mitochondrial biogenesis, but the time course of molecular sequelae that accompany repetitive training stimuli remains to be determined in human skeletal muscle. Therefore, throughout a seven-session, high-intensity interval training period that increased (12%), we examined the time course of responses of (a) mitochondrial biogenesis and fusion and fission proteins, and (b) selected transcriptional and mitochondrial mRNAs and proteins in human muscle. Muscle biopsies were obtained 4 and 24 h after the 1st, 3rd, 5th and 7th training session.

High-intensity interval training increases SIRT1 activity in human skeletal muscle.

The effects of training on silent mating-type information regulator 2 homolog 1 (SIRT1) activity and protein in relationship to peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha) and mitochondrial content were determined in human skeletal muscle. Six weeks of high-intensity interval training ( approximately 1 h of 10 x 4 min intervals at 90% peak oxygen consumption separated by 2 min rest, 3 days per week) increased maximal activities of mitochondrial enzymes in skeletal muscle by 28% to 36% (citrate synthase, beta-hydroxyacyl-coenzyme A dehydrogenase, and cytochrome c oxidase subunit IV) and PGC-1alpha protein (16%) when measured 4 days after training. Interestingly, total muscle SIRT1 activity (31%) and activity per SIRT1 protein (58%) increased despite decreased SIRT1 protein (20%).

Exercise training increases sarcolemmal and mitochondrial fatty acid transport proteins in human skeletal muscle.

Fatty acid oxidation is highly regulated in skeletal muscle and involves several sites of regulation, including the transport of fatty acids across both the plasma and mitochondrial membranes. Transport across these membranes is recognized to be primarily protein mediated, limited by the abundance of fatty acid transport proteins on the respective membranes. In recent years, evidence has shown that fatty acid transport proteins move in response to acute and chronic perturbations; however, in human skeletal muscle the localization of fatty acid transport proteins in response to training has not been examined.

Pulmonary O2 uptake and leg blood flow kinetics during moderate exercise are slowed by hyperventilation-induced hypocapnic alkalosis.

The effect of hyperventilation-induced hypocapnic alkalosis (Hypo) on the adjustment of pulmonary O2 uptake (VO2p) and leg femoral conduit artery ("bulk") blood flow (LBF) during moderate-intensity exercise (Mod) was examined in eight young male adults. Subjects completed four to six repetitions of alternate-leg knee-extension exercise during normal breathing [Con; end-tidal partial pressure of CO2 (PetCO2) approximately 40 mmHg] and sustained hyperventilation (Hypo; PetCO2 approximately 20 mmHg). Increases in work rate were made instantaneously from baseline (3 W) to Mod (80% estimated lactate threshold).

Prolonged moderate-intensity aerobic exercise does not alter apoptotic signaling and DNA fragmentation in human skeletal muscle.

Apoptosis in skeletal muscle plays an important role in age- and disease-related tissue dysfunction. Physical activity can influence apoptotic signaling; however, this process has not been well studied in human skeletal muscle. The purpose of this study was to perform a comprehensive analysis of apoptosis-related proteins/enzymes, DNA fragmentation, and oxidative stress in skeletal muscle of humans during an acute bout of prolonged moderate-intensity exercise.

Effect of hyperventilation and prior heavy exercise on O2 uptake and muscle deoxygenation kinetics during transitions to moderate exercise.

The effect of hyperventilation-induced hypocapnic alkalosis (HYPO) and prior heavy-intensity exercise (HVY) on pulmonary O(2) uptake (VO(2p)) kinetics were examined in young adults (n = 7) during moderate-intensity exercise (MOD). Subjects completed leg cycling exercise during (1) normal breathing (CON, P(ET)CO(2) approximately 40 mmHg) and (2) controlled hyperventilation (HYPO, P(ET)CO(2) approximately 20 mmHg) throughout the protocol, with each condition repeated on four occasions. The protocol consisted of two MOD transitions (MOD1, MOD2) to 80% estimated lactate threshold with MOD2 preceded by HVY (Delta50%); each transition lasted 6 min and was preceded by 20 W cycling.

Skeletal muscle lipogenic protein expression is not different between lean and obese individuals: a potential factor in ceramide accumulation.

Context: Skeletal muscle lipid content is increased in obesity. Recent evidence suggests that fatty acid (FA) storage as triacylglycerol (TAG) represents a metabolically safe pool compared to the more bioactive diacylglycerol (DAG) and ceramide.

Objective/design: The purpose of this study was to compare the expression of lipogenic proteins and ceramide and DAG content in skeletal muscle of lean and obese humans.

Carbohydrate refeeding after a high-fat diet rapidly reverses the adaptive increase in human skeletal muscle PDH kinase activity.

Pyruvate dehydrogenase (PDH) regulates oxidative carbohydrate disposal in skeletal muscle and is downregulated by reversible phosphorylation catalyzed by PDH kinase (PDK). Previous work has demonstrated increased PDK activity and PDK4 expression in human skeletal muscle following a high-fat low-carbohydrate (HF) diet, which leads to decreased PDH in the active form (PDHa activity) and carbohydrate oxidation. The purpose of this study was to examine the time course of changes in PDK and PDHa activities with refeeding of carbohydrates after an HF diet in human skeletal muscle.

Prior heavy exercise elevates pyruvate dehydrogenase activity and muscle oxygenation and speeds O2 uptake kinetics during moderate exercise in older adults.

The adaptation of pulmonary oxygen uptake (VO(2)(p)) kinetics during the transition to moderate-intensity exercise is slowed in older compared with younger adults; however, this response is faster following a prior bout of heavy-intensity exercise. We have examined VO(2)(p) kinetics, pyruvate dehydrogenase (PDH) activation, muscle metabolite contents, and muscle deoxygenation in older adults [n = 6; 70 +/- 5 (67-74) yr] during moderate-intensity exercise (Mod(1)) and during moderate-intensity exercise preceded by heavy-intensity warm-up exercise (Mod(2)). The phase 2 VO(2)(p) time constant (tauVO(2)(p)) was reduced (P < 0.

Oral acetate supplementation after prolonged moderate intensity exercise enhances early muscle glycogen resynthesis in horses.

Oral acetate supplementation enhances glycogen synthesis in some mammals. However, while acetate is a significant energy source for skeletal muscle at rest in horses, its effects on glycogen resynthesis are unknown. We hypothesized that administration of an oral sodium acetate-acetic acid solution with a typical grain and hay meal after glycogen-depleting exercise would result in a rapid appearance of acetate in blood with rapid uptake by skeletal muscle.