Publications by authors named "George Heigenhauser"

A lag in the increase in oxygen consumption (MO ) occurs at the start of sustainable exercise in trout. Waterborne dichloroacetate (0.58 and 3.

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Omega-3 polyunsaturated fatty acids (PUFAs) have unique properties purported to influence several aspects of metabolism, including energy expenditure and protein function. Supplementing with n-3 PUFAs may increase whole-body resting metabolic rate (RMR), by enhancing Na /K ATPase (NKA) activity and reducing the efficiency of sarcoplasmic reticulum (SR) Ca ATPase (SERCA) activity by inducing a Ca leak-pump cycle. The purpose of this study was to examine the effects of fish oil (FO) on RMR, substrate oxidation, and skeletal muscle SERCA and NKA pump function in healthy older individuals.

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The application of blood flow restriction (BFR) during resistance exercise is increasingly recognized for its ability to improve rehabilitation and for its effectiveness in increasing muscle hypertrophy and strength among healthy populations. However, direct comparison of the skeletal muscle adaptations to low-load resistance exercise (LL-RE) and low-load BFR resistance exercise (LL-BFR) performed to task failure is lacking. Using a within-subject design, we examined whole muscle group and skeletal muscle adaptations to 6 wk of LL-RE and LL-BFR training to repetition failure.

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Introduction: In skeletal muscle, the Na/K ATPase (NKA) plays essential roles in processes linked to muscle contraction, fatigue, and energy metabolism; however, very little information exists regarding the regulation of NKA activity. The scarcity of information regarding NKA function in skeletal muscle likely stems from methodological constraints, as NKA contributes minimally to total cellular ATP utilization, and therefore contamination from other ATPases prevents the assessment of NKA activity in muscle homogenates. Here we introduce a method that improves accuracy and feasibility for the determination of NKA activity in small rodent muscle samples (5-10 mg) and in human skeletal muscle.

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Fish oil (FO) supplementation in humans results in the incorporation of omega-3 fatty acids (FAs) eicosapentaenoic acid (EPA; C20:5) and docosahexaenoic acid (DHA; C20:6) into skeletal muscle membranes. However, despite the importance of membrane composition in structure-function relationships, a paucity of information exists regarding how different muscle membranes/organelles respond to FO supplementation. Therefore, the purpose of the present study was to determine the effects 12 weeks of FO supplementation (3g EPA/2g DHA daily) on the phospholipid composition of sarcolemmal and mitochondrial fractions, as well as whole muscle responses, in healthy young males.

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General anesthesia (GA) can cause abnormal lung fluid redistribution. Pulmonary circulation transvascular fluid fluxes ( ) are attributed to changes in hydrostatic forces and erythrocyte volume (EV) regulation. Despite the very low hydraulic conductance of pulmonary microvasculature it is possible that GA may affect hydrostatic forces through changes in pulmonary vascular resistance (PVR), and EV through alteration of erythrocyte transmembrane ion fluxes ( ).

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We examined whether slower pulmonary O uptake (V˙O) kinetics in hypoxia is a consequence of: a) hypoxia alone (lowered arterial O pressure), b) hyperventilation-induced hypocapnia (lowered arterial CO pressure), or c) a combination of both. Eleven participants performed 3-5 repetitions of step-changes in cycle ergometer power output from 20W to 80% lactate threshold in the following conditions: i) normoxia (CON; room air); ii) hypoxia (HX, inspired O = 12%; lowered end-tidal O pressure [PO] and end-tidal CO pressure [PCO]); iii) hyperventilation (HV; increased PO and lowered PCO); and iv) normocapnic hypoxia (NC-HX; lowered PO and PCO matched to CON). Ventilation was increased (relative to CON) and matched between HX, HV, and NC-HX conditions.

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This study determined whether ingesting a carbohydrate-electrolyte solution (CES) vs. progressive dehydration affected skeletal muscle glycogen use and performance in ice hockey players during simulated ice hockey exercise comprised of 3 active "periods". Seven males (21.

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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.

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Unlabelled: Dietary inorganic nitrate (NO3) supplementation improves skeletal muscle (SkM) contractile efficiency, and although rodent literature has suggested improvements in calcium handling or redox modifications as likely explanations, the direct mechanism of action in humans remains unknown.

Purpose: This study aimed to examine the effects of 7 d of beetroot juice (BRJ) supplementation on SkM contractile characteristics and function.

Methods: Recreationally active males (n = 8) underwent transcutaneous electrical muscle stimulation of the vastus lateralis for the evaluation of contractile characteristics before and after 7 d of BRJ supplementation (280 mL·d, ~26 mmol NO3).

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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.

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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.

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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.

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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.

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  During intense exercise in horses the transvascular fluid flux in the pulmonary circulation (Jv-a) represents 4% of cardiac output (Q). This fluid flux has been attributed to an increase in pulmonary transmural hydrostatic forces, increases in perfused microvascular surface area, and reversible alterations in capillary permeability under conditions of high flow and pressure. Erythrocyte fluid efflux, however, accounts for a significant fraction of Jv-a.

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Article Synopsis
  • The paper explores how ventilation and acid-base balance interact under different conditions like rest, exercise, and pregnancy, as well as various health issues.
  • It introduces a physicochemical method for assessing acid-base status and shows how this approach helps to identify sources of acid-base disorders through examples from existing research.
  • The study highlights the complex relationship between ventilation and acid-base balance, emphasizing the need for more comprehensive research to better understand these interactions, particularly during exercise and in various medical conditions.
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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.

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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.

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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).

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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.

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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.

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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.

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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.

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