Short-term intensified training temporarily impairs mitochondrial respiratory capacity in elite endurance athletes

Cardinale, Daniele A.; Gejl, Kasper Degn; Petersen, Kristine Grøsfjeld; Nielsen, Joachim; Ørtenblad, Niels; Larsen, Filip J.

doi:10.1152/japplphysiol.00829.2020

Cited by 12 publications

(8 citation statements)

References 74 publications

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“…Our data demonstrated that, following three weeks of high-volume HIIT in humans, there was an increase in basal LC3B-II protein level, suggesting an increase in autophagosome content ( Figure 3 ). Our findings are in agreement with a recent study showing that four weeks of HIIT led to significant increases in LC3B-II protein content despite no significant increase in LC3B-I or LC3B-II/I ratio [ 19 ], and are in line with the results of a previous study where three weeks of one-legged knee extensor training led to an increase in LC3B-II protein levels [ 13 ]. However, others have not shown any effect of endurance training on LC3A/B-II protein levels, despite an increase in LC3A/B-I protein levels [ 17 ].…”

Section: Discussionsupporting

confidence: 93%

“…Eight weeks of endurance exercise showed that only LC3A/B-I, but not LC3A/B-II, protein content changed [ 17 ]. Conversely, a recent study showed that intensifying the training of elite endurance athletes, by adding three extra exercise sessions per week for four weeks, increased the protein content of LC3B-II [ 19 ]. Future studies should explore whether exercise training volume is important for training-induced changes in markers of autophagy.…”

Section: Introductionmentioning

confidence: 99%

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Exercise and Training Regulation of Autophagy Markers in Human and Rat Skeletal Muscle

Botella

Jamnick

Granata

et al. 2022

IJMS

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Autophagy is a key intracellular mechanism by which cells degrade old or dysfunctional proteins and organelles. In skeletal muscle, evidence suggests that exercise increases autophagosome content and autophagy flux. However, the exercise-induced response seems to differ between rodents and humans, and little is known about how different exercise prescription parameters may affect these results. The present study utilised skeletal muscle samples obtained from four different experimental studies using rats and humans. Here, we show that, following exercise, in the soleus muscle of Wistar rats, there is an increase in LC3B-I protein levels immediately after exercise (+109%), and a subsequent increase in LC3B-II protein levels 3 h into the recovery (+97%), despite no change in Map1lc3b mRNA levels. Conversely, in human skeletal muscle, there is an immediate exercise-induced decrease in LC3B-II protein levels (−24%), independent of whether exercise is performed below or above the maximal lactate steady state, which returns to baseline 3.5 h following recovery, while no change in LC3B-I protein levels or MAP1LC3B mRNA levels is observed. SQSTM1/p62 protein and mRNA levels did not change in either rats or humans following exercise. By employing an ex vivo autophagy flux assay previously used in rodents we demonstrate that the exercise-induced decrease in LC3B-II protein levels in humans does not reflect a decreased autophagy flux. Instead, effect size analyses suggest a modest-to-large increase in autophagy flux following exercise that lasts up to 24 h. Our findings suggest that exercise-induced changes in autophagosome content markers differ between rodents and humans, and that exercise-induced decreases in LC3B-II protein levels do not reflect autophagy flux level.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Exercise and Training Regulation of Autophagy Markers in Human and Rat Skeletal Muscle

Botella

Jamnick

Granata

et al. 2022

IJMS

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“…However, whether training intensity or volume is the most important to increase mitochondrial oxidative capacity remains highly debated (Bishop et al, 2019 ; MacInnis et al, 2019 ). Recent evidence suggests that too much high-intensity training may also adversely affect mitochondrial adaptations (Granata et al, 2020 ; Cardinale et al, 2021 ; Flockhart et al, 2021 ). Polarized training may therefore have an advantageous mix of low- and high-intensity exercise for maximizing mitochondrial adaptations.…”

Section: Training-induced Adaptations To Maximize Endurance Performancementioning

confidence: 99%

Under the Hood: Skeletal Muscle Determinants of Endurance Performance

Zwaard¹,

Brocherie²,

Jaspers³

2021

Front. Sports Act. Living

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In the past decades, researchers have extensively studied (elite) athletes' physiological responses to understand how to maximize their endurance performance. In endurance sports, whole-body measurements such as the maximal oxygen consumption, lactate threshold, and efficiency/economy play a key role in performance. Although these determinants are known to interact, it has also been demonstrated that athletes rarely excel in all three. The leading question is how athletes reach exceptional values in one or all of these determinants to optimize their endurance performance, and how such performance can be explained by (combinations of) underlying physiological determinants. In this review, we advance on Joyner and Coyle's conceptual framework of endurance performance, by integrating a meta-analysis of the interrelationships, and corresponding effect sizes between endurance performance and its key physiological determinants at the macroscopic (whole-body) and the microscopic level (muscle tissue, i.e., muscle fiber oxidative capacity, oxygen supply, muscle fiber size, and fiber type). Moreover, we discuss how these physiological determinants can be improved by training and what potential physiological challenges endurance athletes may face when trying to maximize their performance. This review highlights that integrative assessment of skeletal muscle determinants points toward efficient type-I fibers with a high mitochondrial oxidative capacity and strongly encourages well-adjusted capillarization and myoglobin concentrations to accommodate the required oxygen flux during endurance performance, especially in large muscle fibers. Optimisation of endurance performance requires careful design of training interventions that fine tune modulation of exercise intensity, frequency and duration, and particularly periodisation with respect to the skeletal muscle determinants.

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“…In addition, we have recently found intrinsic mitochondrial respiration (IMR), aconitase activity and glucose tolerance to be reduced in healthy subjects after excessive high intensity interval training (HIIT) [ 7 ]. A reduced mitochondrial quality has also been found in a cohort of elite triathletes and cyclists after intensified training [ 8 ]. It is under debate whether or not a loss of performance is at all needed or desired during OR in order to achieve a supercompensation [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

A Simple Model for Diagnosis of Maladaptations to Exercise Training

et al. 2022

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Background The concept of overreaching and super compensation is widely in use by athletes and coaches seeking to maximize performance and adaptations to exercise training. The physiological aspects of acute fatigue, overreaching and non-functional overreaching are, however, not well understood, and well-defined negative physiological outcomes are missing. Instead, the concept relies heavily on performance outcomes for differentiating between the states. Recent advancements in the field of integrated exercise physiology have associated maladaptations in muscular oxidative function to high loads of exercise training. Method Eleven female and male subjects that exercised regularly but did not engage in high-intensity interval training (HIIT) were recruited to a 4-week long training intervention where the responses to different training loads were studied. Highly monitored HIIT sessions were performed on a cycle ergometer in a progressive fashion with the intent to accomplish a training overload. Throughout the intervention, physiological and psychological responses to HIIT were assessed, and the results were used to construct a diagnostic model that could indicate maladaptations during excessive training loads. Results We here use mitochondrial function as an early marker of excessive training loads and show the dynamic responses of several physiological and psychological measurements during different training loads. During HIIT, a loss of mitochondrial function was associated with reduced glycolytic, glucoregulatory and heart rate responses and increased ratings of perceived exertion in relation to several physiological measurements. The profile of mood states was highly affected after excessive training loads, whereas performance staled rather than decreased. By implementing five of the most affected and relevant measured parameters in a diagnostic model, we could successfully, and in all the subjects, identify the training loads that lead to maladaptations. Conclusions As mitochondrial parameters cannot be assessed without donating a muscle biopsy, this test can be used by coaches and exercise physiologists to monitor adaptation to exercise training for improving performance and optimizing the health benefits of exercise. Clinical trial registry numberNCT04753021. Retrospectively registered 2021-02-12.

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Short-term intensified training temporarily impairs mitochondrial respiratory capacity in elite endurance athletes

Cited by 12 publications

References 74 publications

Exercise and Training Regulation of Autophagy Markers in Human and Rat Skeletal Muscle

Exercise and Training Regulation of Autophagy Markers in Human and Rat Skeletal Muscle

Under the Hood: Skeletal Muscle Determinants of Endurance Performance

A Simple Model for Diagnosis of Maladaptations to Exercise Training

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