Acute low-intensity cycling with blood-flow restriction has no effect on metabolic signaling in human skeletal muscle compared to traditional exercise

Smiles, William J.; Conceição, Miguel Soares; Telles, Guilherme Defante; Chacon-Mikahil, Mara Patrícia Traina; Cavaglieri, Cláudia Regina; Vechin, Felipe Cassaro; Libardi, Cleiton Augusto; Hawley, John A.; Camera, Donny M.

doi:10.1007/s00421-016-3530-8

Cited by 12 publications

(8 citation statements)

References 60 publications

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“…In the current study, signaling responses for metabolic adaptations were similar between BFRRE and HLRE. In a previous study, it has been shown that acute low-intensity cycling with blood flow restriction has little effect on metabolic signaling compared to traditional resistance training and endurance training (Smiles et al, 2017). Furthermore, it has been shown that application of external restriction of blood flow after sprint-interval training does not further accentuate phosphorylation of p-38 MAPK (Taylor et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Skeletal Muscle Mitochondrial Protein Synthesis and Respiration Increase With Low-Load Blood Flow Restricted as Well as High-Load Resistance Training

et al. 2018

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Purpose: It is well established that high-load resistance exercise (HLRE) can stimulate myofibrillar accretion. Additionally, recent studies suggest that HLRE can also stimulate mitochondrial biogenesis and respiratory function. However, in several clinical situations, the use of resistance exercise with high loading may not constitute a viable approach. Low-load blood flow restricted resistance exercise (BFRRE) has emerged as a time-effective low-load alternative to stimulate myofibrillar accretion. It is unknown if BFRRE can also stimulate mitochondrial biogenesis and respiratory function. If so, BFRRE could provide a feasible strategy to stimulate muscle metabolic health.Methods: To study this, 34 healthy previously untrained individuals (24 ± 3 years) participated in BFRRE, HLRE, or non-exercise control intervention (CON) 3 times per week for 6 weeks. Skeletal muscle biopsies were collected; (1) before and after the 6-week intervention period to assess mitochondrial biogenesis and respiratory function and; (2) during recovery from single-bout exercise to assess myocellular signaling events involved in transcriptional regulation of mitochondrial biogenesis. During the 6-week intervention period, deuterium oxide (D2O) was continuously administered to the participants to label newly synthesized skeletal muscle mitochondrial proteins. Mitochondrial respiratory function was assessed in permeabilized muscle fibers with high-resolution respirometry. Mitochondrial content was assessed with a citrate synthase activity assay. Myocellular signaling was assessed with immunoblotting.Results: Mitochondrial protein synthesis rate was higher with BFRRE (1.19%/day) and HLRE (1.15%/day) compared to CON (0.92%/day) (P < 0.05) but similar between exercise groups. Mitochondrial respiratory function increased to similar degree with both exercise regimens and did not change with CON. For instance, coupled respiration supported by convergent electron flow from complex I and II increased 38% with BFRRE and 24% with HLRE (P < 0.01). Training did not alter citrate synthase activity compared to CON. BFRRE and HLRE elicited similar myocellular signaling responses.Conclusion: These results support recent findings that resistance exercise can stimulate mitochondrial biogenesis and respiratory function to support healthy skeletal muscle and whole-body metabolism. Intriquingly, BFRRE produces similar mitochondrial adaptations at a markedly lower load, which entail great clinical perspective for populations in whom exercise with high loading is untenable.

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Section: Discussionmentioning

confidence: 99%

Skeletal Muscle Mitochondrial Protein Synthesis and Respiration Increase With Low-Load Blood Flow Restricted as Well as High-Load Resistance Training

et al. 2018

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“…Muscle biopsies obtained after a 150 km running competition (18 hours) revealed a fivefold increase in LC3‐II, indicating increased autophagosome content . In contrast, a reduction of LC3‐II has been observed after less strenuous endurance exercise protocols, whereas LC3‐II did not change after 30 minutes cycling at 70% of VO 2 max or 15 cycling at 40% of VO 2 max with blood flow restriction . Moller et al .…”

Section: Endurance Exercise and Autophagy In Skeletal Musclementioning

confidence: 99%

“…Exercise‐elicited AMPKα Thr 172 phosphorylation depends on the training status and the characteristics of the exercise . Animal studies indicate that AMPK activation is necessary for exercise to induce autophagy while myristoylation of AMPKß is needed to induce mitophagy . AMPK promotes autophagy by directly phosphorylating and activating ULK.…”

Section: Molecular Markers Of Autophagic Flux In Skeletal Musclementioning

confidence: 99%

Exercise‐mediated modulation of autophagy in skeletal muscle

Martin‐Rincon

Morales-Álamo

Calbet

2017

Scandinavian Med Sci Sports

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Although exercise exerts multiple beneficial health effects, it may also damage cellular structures. Damaged elements are continuously degraded and its constituents recycled to produce renovated structures through a process called autophagy, which is essential for the adaptation to training. Autophagy is particularly active in skeletal muscle, where it can be evaluated using specific molecular markers of activation (unc-51-like kinase 1 [ULK1] phosphorylation) and specific proteins indicating increased autophagosome content (increased total LC3, LC3-II, LC3-II/LC3-I ratio). Studies in humans are technically limited but have provided evidence suggesting the activation of autophagy in skeletal muscle through AMP-activated protein kinase (AMPK) and its downstream target ULK1. Autophagy activation is more likely when the intensity is elevated and the exercise performed in the fasted state. The autophagy-gene program and autophagosome content are upregulated after ultraendurance running competitions. However, autophagosome content is reduced after endurance exercise at moderate intensities (50% and 70% of VO max) for 60-120 minutes. Autophagosome content is decreased within the first few hours after resistance training. The effects of regular endurance and strength training on basal autophagy remain to be established in humans. One study has reported that acute severe hypoxia increases autophagosome content in human skeletal muscle, which is reverted by 20 minutes of low-intensity exercise. Experiments with transgenic mice have shown that autophagy is necessary for skeletal muscle adaptation to training. Little is known on how genetic factors, environment, nutrition, drugs and diseases may interact with exercise to modulate autophagy at rest and during exercise in humans.

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“…AMPK has been reported to regulate autophagy and mitophagy by activating unc-51-like autophagy activating kinase 1 (ULK1) [106]. Endurance exercise at the intensity of 70% of VO 2 max for 30 min significantly increased the phosphorylation of ULK1 Ser757 in the vastus lateralis muscle of young subjects [107]. In studies on mice, the increase in mitophagy markers of BNIP3 and Parkin suggest that mitophagy was increased after 90 min running with 10 m/min speed in animals who run at fasted conditions compared to fed control groups [108].…”

Section: Mitophagymentioning

confidence: 99%

Exercise effects on physiological function during aging

Radák

Torma

Berkes

et al. 2019

Free Radical Biology and Medicine

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A B S T R A C TThe decrease in cognitive/motor functions and physical abilities severely affects the aging population in carrying out daily activities. These disabilities become a burden on individuals, families and society in general. It is known that aging conditions are ameliorated with regular exercise, which attenuates the age-associated decline in maximal oxygen uptake (VO2max), production of reactive oxygen species (ROS), decreases in oxidative damage to molecules, and functional impairment in various organs. While benefits of physical exercise are welldocumented, the molecular mechanisms responsible for functional improvement and increases in health span are not well understood. Recent findings imply that exercise training attenuates the age-related deterioration in the cellular housekeeping system, which includes the proteasome, Lon protease, autophagy, mitophagy, and DNA repair systems, which beneficially impacts multiple organ functions. Accumulating evidence suggests that exercise lessens the deleterious effects of aging. However, it seems unlikely that systemic effects are mediated through a specific biomarker. Rather, complex multifactorial mechanisms are involved to maintain homeostatic functions that tend to decline with age. Increased levels of VO 2 max not only decrease the incidence of

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Acute low-intensity cycling with blood-flow restriction has no effect on metabolic signaling in human skeletal muscle compared to traditional exercise

Cited by 12 publications

References 60 publications

Skeletal Muscle Mitochondrial Protein Synthesis and Respiration Increase With Low-Load Blood Flow Restricted as Well as High-Load Resistance Training

Skeletal Muscle Mitochondrial Protein Synthesis and Respiration Increase With Low-Load Blood Flow Restricted as Well as High-Load Resistance Training

Exercise‐mediated modulation of autophagy in skeletal muscle

Exercise effects on physiological function during aging

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