Muscle damage in response to a single bout of high intensity concentric exercise in patients with Pompe disease

Introduction: Aerobic training with an acyclic and intermittent character triggers high metabolic stress, responsible for generating alterations in several blood biomarkers. Thus, investigations that clarify understanding of metabolic behavior in response to exercise seem pertinent, when considering the dynamics of prescription of physical training and recovery. Objective: Demonstrate and discuss the behavior of blood biomarkers in response to High Intensity Interval Training (HIIT) and High Intensity Functional Training (HIFT). Methods: The PubMed/MEDLINE, Scielo, Lilacs, Bireme, Google Scholar, and Scopus databases were searched from the oldest records available until January 16, 2020. The search was carried out by combining descriptors related to the terms: “HIIT”, “HIFT”, and “blood biomarkers”. To be included, studies were required to: 1) have a clinical trial design; 2) evaluate the effects of an HIIT and/or HIFT protocol; and 3) measure blood biomarkers before and after the training protocol. No restrictions were applied to the characteristics of the participants regarding health condition, age, sex, and level of training. Results: In total, seven studies were included (n=221 participants, aged between 18 and 63 years) that analyzed different population profiles such as athletes, sedentary young people, patients with breast cancer, and diabetics. The biomarkers evaluated included analysis of muscle damage (C Reactive protein and CK); oxidative stress (antioxidant capacity); kidney injury (creatinine and urea); hormones (testosterone and cortisol); cytokines (TNF-α, IL-6, IL-1β, IL-10, IL-4, and IF-γ); and hemogram. In general, the results demonstrated specific patterns for the investigated markers. Thus, there were increases in muscle damage markers, while in the inflammatory markers, there was a reduction in pro-inflammatory cytokines and an increase in anti-inflammatory cytokines. Despite the reduced values of the general blood count, markers such as neutrophils and basophils did not demonstrate statistically significant alterations. Serum testosterone levels were higher and cortisol was lower in the post-exercise period when compared to pre-exercise. Conclusion: These data are of practical relevance when demonstrating patterns of physiological responses, which also characterize knowledge and understanding essential to determine adequate periodization.

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Exercise-Induced Lactate Release Mediates Mitochondrial Biogenesis in the Hippocampus of Mice via Monocarboxylate Transporters

Frontiers in Physiology ◽

10.3389/fphys.2021.736905 ◽

2021 ◽

Vol 12 ◽

Author(s):

Jonghyuk Park ◽

Jimmy Kim ◽

Toshio Mikami

Keyword(s):

Blood Lactate ◽

Mitochondrial Biogenesis ◽

High Intensity ◽

Lactate Concentration ◽

High Intensity Exercise ◽

Mtdna Copy Number ◽

Single Bout ◽

Extracellular Lactate ◽

Exercise Induced ◽

The Brain

Regular exercise training induces mitochondrial biogenesis in the brain via activation of peroxisome proliferator-activated receptor gamma-coactivator 1α (PGC-1α). However, it remains unclear whether a single bout of exercise would increase mitochondrial biogenesis in the brain. Therefore, we first investigated whether mitochondrial biogenesis in the hippocampus is affected by a single bout of exercise in mice. A single bout of high-intensity exercise, but not low- or moderate-intensity, increased hippocampal PGC-1α mRNA and mitochondrial DNA (mtDNA) copy number at 12 and 48h. These results depended on exercise intensity, and blood lactate levels observed immediately after exercise. As lactate induces mitochondrial biogenesis in the brain, we examined the effects of acute lactate administration on blood and hippocampal extracellular lactate concentration by in vivo microdialysis. Intraperitoneal (I.P.) lactate injection increased hippocampal extracellular lactate concentration to the same as blood lactate level, promoting PGC-1α mRNA expression in the hippocampus. However, this was suppressed by administering UK5099, a lactate transporter inhibitor, before lactate injection. I.P. UK5099 administration did not affect running performance and blood lactate concentration immediately after exercise but attenuated exercise-induced hippocampal PGC-1α mRNA and mtDNA copy number. In addition, hippocampal monocarboxylate transporters (MCT)1, MCT2, and brain-derived neurotrophic factor (BDNF) mRNA expression, except MCT4, also increased after high-intensity exercise, which was abolished by UK5099 administration. Further, injection of 1,4-dideoxy-1,4-imino-D-arabinitol (glycogen phosphorylase inhibitor) into the hippocampus before high-intensity exercise suppressed glycogen consumption during exercise, but hippocampal lactate, PGC-1α, MCT1, and MCT2 mRNA concentrations were not altered after exercise. These results indicate that the increased blood lactate released from skeletal muscle may induce hippocampal mitochondrial biogenesis and BDNF expression by inducing MCT expression in mice, especially during short-term high-intensity exercise. Thus, a single bout of exercise above the lactate threshold could provide an effective strategy for increasing mitochondrial biogenesis in the hippocampus.

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The Influence of a Single Bout of High-Intensity Interval Exercise on Postprandial Lipemia and Glycemia

Medicine & Science in Sports & Exercise ◽

10.1249/01.mss.0000517604.78250.1d ◽

2017 ◽

Vol 49 (5S) ◽

pp. 273

Author(s):

James Rowe ◽

Stephen Decker

Keyword(s):

High Intensity ◽

Postprandial Lipemia ◽

Interval Exercise ◽

Single Bout ◽

High Intensity Interval

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INCREASED C-FOS EXPRESSION FOLLOWING A SINGLE BOUT OF ECCENTRIC VERSUS CONCENTRIC EXERCISE

Medicine & Science in Sports & Exercise ◽

10.1097/00005768-200205001-01041 ◽

2002 ◽

Vol 34 (5) ◽

pp. S186

Author(s):

M J. Hubal ◽

Y W. Chen ◽

P D. Thompson ◽

E P. Hoffman ◽

P M. Clarkson

Keyword(s):

Concentric Exercise ◽

Single Bout ◽

Fos Expression

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Different responses of apoptotic, inflammatory and heat shock protein gene expression to a single bout of high intensity interval exercise between physically active and inactive men

Applied Physiology Nutrition and Metabolism ◽

10.1139/apnm-2020-0783 ◽

2021 ◽

Author(s):

Selma Arzu Vardar ◽

Zeynep Banu Doğanlar ◽

Oktay Kaya ◽

Pınar Tayfur ◽

Necdet Sut ◽

...

Keyword(s):

Heat Shock ◽

High Intensity ◽

Pcr Analysis ◽

Mrna Levels ◽

Physically Active ◽

Hsp70 Mrna ◽

Interval Exercise ◽

Single Bout ◽

Group 5 ◽

High Intensity Interval

High mechanical load of muscles may induce muscular apoptosis on the one hand and adaptation to exercise on the other. This study aimed to explore whether changes of circulatory levels of inflammation, apoptosis and heat shock proteins (HSPs) mRNA following single bout of high intensity interval exercise (HIIE) differs between physically active (PA) and inactive (PI) men. Nine PA and nine PI (peak VO2 2.6±0.4 vs. 2.0 ± 0.2 L.min-1) healthy men (age: 28.7+/-6.3 vs. 30.2+/-4.5 years and BMI: 2.6±2.1 vs. 23.3±2.8 kg.m-2) performed HIIE comprising 4 repeats of a Wingate test (load:0.050 kg.kg-1 body weight). Blood samples were collected before exercise, 5 min and 24 h after HIIE for measuring mRNA of inflammation markers IL6 and TNFα, apoptosis markers including Bcl-2, Bax, and HSP27, HSP60, HSP70, HSP90 using quantitative real-time PCR analysis. Post-HIIE IL6, TNFα and HSP60 were higher in the PI than the PA group 5 min after exercise (p=0.003, ES=1.59; p=0.007, ES=1.59 and p=0.027, ES=1.10 respectively). HSP70 acutely increased only in the PA group (p=0.024, ES=1.20). The increase in Bcl-2 (p=0.047, ES=1.08) and Bax (p=0.024, ES=1.20) levels were higher in the PI group 5 min after HIIE. The present study indicated that the response of inflammatory, apoptosis and HSP gene expressions to HIIE in blood of healthy male volunteers strongly depends on their level of regular physical activity. Novelty • Blood IL-6 and HSP60 mRNA levels following high intensity exercise may indicate metabolic stress. • Increased blood HSP70 mRNA in physically active men may show an alternative apoptosis suppression pathway.

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Activation of JNK in rat heart by exercise: effect of training

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00596.2003 ◽

2003 ◽

Vol 285 (6) ◽

pp. H2639-H2647 ◽

Cited By ~ 11

Author(s):

M. O. Boluyt ◽

A. M. Loyd ◽

M. H. Roth ◽

M. J. Randall ◽

E. Y. M. Song

Keyword(s):

High Intensity ◽

Rat Heart ◽

Dependent Manner ◽

High Intensity Training ◽

Long Duration ◽

Single Bout ◽

Exercise Effect ◽

No Activation ◽

Intensity Training ◽

Training Protocol

The purpose of the study was to determine whether exercise would activate JNK in the heart and whether chronic exercise training would alter the response. Untrained rats were familiarized with the treadmill and assigned to one of four groups: low intensity (LI), 10 min, 0%, 15 m/min; medium intensity (MI), 10 min, 0%, 33 m/min; high intensity (HI), 10 min, 25%, 33 m/min; long duration (LD), 30 min, 0%, 15 m/min. Another cohort of rats was subjected to a progressive 6 wk high-intensity training protocol that produced a 12% increase in heart mass. In untrained rats, JNK activity was LI: 1.5 (fold nonrun control), MI: 2.0, HI: 2.5, LD: 1.25 immediately after a single bout of exercise. In trained rats, no activation of JNK above baseline was detected after either a 10-min or 1-h bout of exercise. We concluded that treadmill exercise activates JNK in the rat heart in an intensity-dependent manner and that chronic training abrogates the myocardial JNK response to a bout of exercise.

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