scholarly journals Divergent serum metabolomic, skeletal muscle signalling, transcriptomic and performance adaptations to fasted versus whey protein-fed sprint interval training

2021 ◽  
Author(s):  
Tom P Aird ◽  
Andrew J Farquharson ◽  
Kate M Bermingham ◽  
Aifric O'Sullivan ◽  
Janice E Drew ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mrna Expression ◽  
Endurance Exercise ◽  
Acute Exercise ◽  
Interval Training ◽  
Sprint Interval Training ◽  
Metabolic Adaptations ◽  
Protein Ingestion ◽  
And Performance ◽  
Exercise Induced

Sprint interval training (SIT) is a time efficient alternative to endurance exercise, conferring beneficial skeletal muscle metabolic adaptations. Current literature has investigated the nutritional regulation of acute and chronic exercise-induced metabolic adaptations in muscle following endurance exercise, principally comparing the impact of training in fasted and carbohydrate-fed (CHO) conditions. Alternative strategies such as exercising in low CHO, protein-fed conditions remain poorly characterised, specifically pertaining to adaptations associated with SIT. Thus, this study aimed to compare the metabolic and performance adaptations to acute and short term SIT in the fasted state with pre-exercise hydrolysed (WPH) or concentrate (WPC) whey protein supplementation. In healthy males, pre-exercise protein ingestion did not alter exercise-induced increases in PGC-1α, PDK4, SIRT1, and PPAR-δ mRNA expression following acute SIT. However, supplementation of WPC and WPH beneficially altered acute exercise-induced SIRT4 and CD36 mRNA expression, respectively. Pre-exercise protein ingestion attenuated acute exercise-induced increases in muscle pan-acetylation, and PARP1 protein content compared with fasted SIT. Acute serum metabolomic differences confirmed greater pre-exercise amino acid delivery in protein-fed compared with fasted conditions. Following 3 weeks of SIT, training-induced increases in mitochondrial enzymatic activity and exercise performance were similar across nutritional groups. Interestingly, resting muscle acetylation status was favourably regulated in WPH conditions following training. Such findings suggest pre-exercise WPC and WPH ingestion positively influences metabolic adaptations to SIT compared to fasted training, resulting in either similar or enhanced performance adaptations. Future studies investigating nutritional modulation of metabolic adaptations to exercise are warranted to build upon these novel findings.

scholarly journals Endurance training reduces the contraction-induced interleukin-6 mRNA expression in human skeletal muscle

2004 ◽  
Vol 287 (6) ◽  
pp. E1189-E1194 ◽  
Author(s):  
Christian P. Fischer ◽  
Peter Plomgaard ◽  
Anne K. Hansen ◽  
Henriette Pilegaard ◽  
Bengt Saltin ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mrna Expression ◽  
Muscle Glycogen ◽  
Human Skeletal Muscle ◽  
Acute Exercise ◽  
Glycogen Content ◽  
Knee Extensor ◽  
Exercise Induced ◽  
Response To Exercise ◽  
Resting Muscle

Contracting skeletal muscle expresses large amounts of IL-6. Because 1) IL-6 mRNA expression in contracting skeletal muscle is enhanced by low muscle glycogen content, and 2) IL-6 increases lipolysis and oxidation of fatty acids, we hypothesized that regular exercise training, associated with increased levels of resting muscle glycogen and enhanced capacity to oxidize fatty acids, would lead to a less-pronounced increase of skeletal muscle IL-6 mRNA in response to acute exercise. Thus, before and after 10 wk of knee extensor endurance training, skeletal muscle IL-6 mRNA expression was determined in young healthy men ( n = 7) in response to 3 h of dynamic knee extensor exercise, using the same relative workload. Maximal power output, time to exhaustion during submaximal exercise, resting muscle glycogen content, and citrate synthase and 3-hydroxyacyl-CoA dehydrogenase enzyme activity were all significantly enhanced by training. IL-6 mRNA expression in resting skeletal muscle did not change in response to training. However, although absolute workload during acute exercise was 44% higher ( P < 0.05) after the training period, skeletal muscle IL-6 mRNA content increased 76-fold ( P < 0.05) in response to exercise before the training period, but only 8-fold ( P < 0.05, relative to rest and pretraining) in response to exercise after training. Furthermore, the exercise-induced increase of plasma IL-6 ( P < 0.05, pre- and posttraining) was not higher after training despite higher absolute work intensity. In conclusion, the magnitude of the exercise-induced IL-6 mRNA expression in contracting human skeletal muscle was markedly reduced by 10 wk of training.

Skeletal Muscle Metabolic and Performance Adaptations After Short Sprint Interval Training (SIT).

2004 ◽  
Vol 36 (Supplement) ◽  
pp. S20
Author(s):  
Kirsten A. Burgomaster ◽  
George J.F. Heigenhauser ◽  
Martin J. Gibala
Keyword(s):  
Skeletal Muscle ◽  
Interval Training ◽  
Sprint Interval Training ◽  
And Performance

Skeletal Muscle Metabolic and Performance Adaptations After Short Sprint Interval Training (SIT).

2004 ◽  
Vol 36 (Supplement) ◽  
pp. S20 ◽  
Author(s):  
Kirsten A. Burgomaster ◽  
George J.F. Heigenhauser ◽  
Martin J. Gibala
Keyword(s):  
Skeletal Muscle ◽  
Interval Training ◽  
Sprint Interval Training ◽  
And Performance

scholarly journals Innate immune responses to a single session of sprint interval training

2011 ◽  
Vol 36 (3) ◽  
pp. 395-404 ◽  
Author(s):  
Glen Davison
Keyword(s):  
Interval Training ◽  
Sprint Interval Training ◽  
Innate Immune Responses ◽  
Single Session ◽  
Metabolic Adaptations ◽  
Significant Depression ◽  
Oxidative Burst Activity ◽  
Exercise Induced ◽  
Neutrophil Oxidative Burst ◽  
Time Point

Sprint interval training (SIT) is a potent stimulus for physiological and metabolic adaptations comparable with those induced by traditional “aerobic” endurance training. There has been a great deal of recent research on SIT, which may lead to increased use of this type of training. The purpose of the present study was to determine the acute effects of SIT on aspects of innate immunity not previously researched in this context. Nine males completed 1 SIT and 1 resting control trial in a crossover design. Blood and saliva samples were obtained at pre-, post-, and 30 min postexercise to measure blood neutrophil oxidative burst activity (OBA) in addition to saliva secretary IgA (s-IgA) and lysozyme. SIT induced a significant depression of neutrophil fMLP-stimulated OBA (–30% for the 30-min postexercise time point, p < 0.01), PMA-stimulated OBA (–14% for the postexercise time point, –21% for the 30-min postexercise time point, p < 0.01), and bacterial-stimulated degranulation (–23% for the postexercise time point, –32% for the 30-min postexercise time point, p < 0.01) but not fMLP-then-PMA-stimulated OBA, saliva lysozyme, or s-IgA concentrations or secretion rates (p > 0.05). The main novel finding of the present study is that a single session of SIT causes significant exercise-induced immunodepression of some neutrophil functions but mucosal immunity was not depressed.

scholarly journals Nicotinamide Riboside supplementation does not alter whole-body or skeletal muscle metabolic responses to a single bout of endurance exercise

2020 ◽  
Author(s):  
Ben Stocks ◽  
Stephen P. Ashcroft ◽  
Sophie Joanisse ◽  
Yasir S. Elhassan ◽  
Gareth G. Lavery ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mrna Expression ◽  
Endurance Exercise ◽  
Vastus Lateralis ◽  
Whole Body ◽  
Endurance Capacity ◽  
Similar Response ◽  
Transcriptional Responses ◽  
Nicotinamide Riboside ◽  
Exercise Induced

AbstractOral supplementation of the NAD+ precursor Nicotinamide Riboside (NR) has been reported to increase Sirtuin (SIRT) signalling, mitochondrial biogenesis and endurance capacity in rodent skeletal muscle. However, whether NR supplementation can elicit a similar response in human skeletal muscle is unclear. This study aimed to assess the effect of 7-day NR supplementation on exercise-induced transduction and transcriptional responses in skeletal muscle of young, healthy, recreationally active human volunteers. In a double-blinded, randomised, counter-balanced, crossover design, eight male participants (age: 23 ± 4 years, VO2peak: 46.5 ± 4.4 mL·kg-1·min-1) received one week of NR or cellulose placebo (PLA) supplementation (1000 mg·d-1) before performing one hour of cycling at 60% Wmax. Muscle biopsies were collected prior to supplementation and pre-, immediately and three-hours post-exercise from the medial vastus lateralis, whilst venous blood samples were collected throughout the trial. Global acetylation, auto-PARylation of PARP1, acetylation of p53Lys382 and MnSODLys122 were unaffected by NR supplementation or exercise. Exercise led to an increase in AMPKThr172 (1.6-fold), and ACCSer79 (4-fold) phosphorylation, in addition to an increase in PGC-1α (∼5-fold) and PDK4 (∼10-fold) mRNA expression, however NR had no additional effect on this response. There was also no effect of NR supplementation on substrate utilisation at rest or during exercise or on skeletal muscle mitochondrial respiration. Finally, NR supplementation blunted the exercise induced activation of skeletal muscle NNMT mRNA expression, but had no effect on mRNA expression of NMRK1, NAMPT or NMNAT1, which were not significantly affected by NR supplementation or exercise. In summary, one week of NR supplementation does not augment skeletal muscle signal transduction pathways implicated in mitochondrial adaptation to endurance exercise.

scholarly journals Effect of Physical Training on Exercise-Induced Inflammation and Performance in Mice

2021 ◽  
Vol 9 ◽  
Author(s):  
Luiz Alexandre Medrado de Barcellos ◽  
William Antonio Gonçalves ◽  
Marcos Paulo Esteves de Oliveira ◽  
Juliana Bohnen Guimarães ◽  
Celso Martins Queiroz-Junior ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Physical Training ◽  
Acute Exercise ◽  
Inflammatory Cells ◽  
Cell Interaction ◽  
Leukocyte Recruitment ◽  
Aerobic Performance ◽  
Inflammatory Profile ◽  
And Performance ◽  
Exercise Induced

Acute exercise increases the amount of circulating inflammatory cells and cytokines to maintain physiological homeostasis. However, it remains unclear how physical training regulates exercise-induced inflammation and performance. Here, we demonstrate that acute high intensity exercise promotes an inflammatory profile characterized by increased blood IL-6 levels, neutrophil migratory capacity, and leukocyte recruitment to skeletal muscle vessels. Moreover, we found that physical training amplified leukocyte–endothelial cell interaction induced by acute exercise in skeletal muscle vessels and diminished exercise-induced inflammation in skeletal muscle tissue. Furthermore, we verified that disruption of the gp-91 subunit of NADPH-oxidase inhibited exercise-induced leukocyte recruitment on skeletal muscle after training with enhanced exercise time until fatigue. In conclusion, the training was related to physical improvement and immune adaptations. Moreover, reactive oxygen species (ROS) could be related to mechanisms to limit aerobic performance and its absence decreases the inflammatory response elicited by exercise after training.

scholarly journals Role of PGC-1α during acute exercise-induced autophagy and mitophagy in skeletal muscle

2015 ◽  
Vol 308 (9) ◽  
pp. C710-C719 ◽  
Author(s):  
Anna Vainshtein ◽  
Liam D. Tryon ◽  
Marion Pauly ◽  
David A. Hood
Keyword(s):  
Skeletal Muscle ◽  
Acute Exercise ◽  
Transmembrane Protein ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Lipid Trafficking ◽  
Mitochondrial Transcription Factor ◽  
Energy Demands ◽  
Niemann Pick ◽  
Exercise Induced

Regular exercise leads to systemic metabolic benefits, which require remodeling of energy resources in skeletal muscle. During acute exercise, the increase in energy demands initiate mitochondrial biogenesis, orchestrated by the transcriptional coactivator peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α). Much less is known about the degradation of mitochondria following exercise, although new evidence implicates a cellular recycling mechanism, autophagy/mitophagy, in exercise-induced adaptations. How mitophagy is activated and what role PGC-1α plays in this process during exercise have yet to be evaluated. Thus we investigated autophagy/mitophagy in muscle immediately following an acute bout of exercise or 90 min following exercise in wild-type (WT) and PGC-1α knockout (KO) animals. Deletion of PGC-1α resulted in a 40% decrease in mitochondrial content, as well as a 25% decline in running performance, which was accompanied by severe acidosis in KO animals, indicating metabolic distress. Exercise induced significant increases in gene transcripts of various mitochondrial (e.g., cytochrome oxidase subunit IV and mitochondrial transcription factor A) and autophagy-related (e.g., p62 and light chain 3) genes in WT, but not KO, animals. Exercise also resulted in enhanced targeting of mitochondria for mitophagy, as well as increased autophagy and mitophagy flux, in WT animals. This effect was attenuated in the absence of PGC-1α. We also identified Niemann-Pick C1, a transmembrane protein involved in lysosomal lipid trafficking, as a target of PGC-1α that is induced with exercise. These results suggest that mitochondrial turnover is increased following exercise and that this effect is at least in part coordinated by PGC-1α. Anna Vainshtein received the AJP-Cell 2015 Paper of the Year award. Listen to a podcast with Anna Vainshtein and coauthor David A. Hood at http://ajpcell.podbean.com/e/ajp-cell-paper-of-the-year-2015-award-podcast/ .

Skeletal muscle adaptations to exercise are not influenced by metformin treatment in humans: secondary analyses of two randomised, clinical trials.

2021 ◽  
Author(s):  
Nanna Skytt Pilmark ◽  
Laura Oberholzer ◽  
Jens Frey Halling ◽  
Jonas M. Kristensen ◽  
Christina Pedersen Bønding ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Exercise Training ◽  
Human Skeletal Muscle ◽  
Acute Exercise ◽  
Metformin Treatment ◽  
Ampk Activation ◽  
Double Blind ◽  
Parallel Group ◽  
Exercise Induced

Metformin and exercise both improve glycemic control, but in vitro studies have indicated that an interaction between metformin and exercise occurs in skeletal muscle, suggesting a blunting effect of metformin on exercise training adaptations. Two studies (a double-blind, parallel-group, randomized clinical trial conducted in 29 glucose-intolerant individuals and a double-blind, cross-over trial conducted in 15 healthy lean males) were included in this paper. In both studies, the effect of acute exercise +/- metformin treatment on different skeletal muscle variables, previously suggested to be involved in a pharmaco-physiological interaction between metformin and exercise, was assessed. Furthermore, in the parallel-group trial, the effect of 12 weeks of exercise training was assessed. Skeletal muscle biopsies were obtained before and after acute exercise and 12 weeks of exercise training, and mitochondrial respiration, oxidative stress and AMPK activation was determined. Metformin did not significantly affect the effects of acute exercise or exercise training on mitochondrial respiration, oxidative stress or AMPK activation, indicating that the response to acute exercise and exercise training adaptations in skeletal muscle is not affected by metformin treatment. Further studies are needed to investigate whether an interaction between metformin and exercise is present in other tissues, e.g. the gut. Trial registration: ClinicalTrials.gov (NCT03316690 and NCT02951260). Novelty bullets • Metformin does not affect exercise-induced alterations in mitochondrial respiratory capacity in human skeletal muscle • Metformin does not affect exercise-induced alterations in systemic levels of oxidative stress nor emission of reactive oxygen species from human skeletal muscle • Metformin does not affect exercise-induced AMPK activation in human skeletal muscle

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