Human Skeletal Muscle mRNA Response to a Single Hypoxic Exercise Bout

Slivka, Dustin; Heesch, Matthew; Dumke, Charles L.; Cuddy, John S.; Hailes, Walter; Ruby, Brent C.

doi:10.1016/j.wem.2014.06.011

Cited by 22 publications

(19 citation statements)

References 12 publications

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“…In a previous human study, 1 hour of moderate-intensity cycling (60% of cycling peak power output) at simulated altitude (3000 m) had no effect on PGC-1a mRNA in the skeletal muscle of recreationally active men. 72 In agreement, PGC-1a total and isoform mRNA levels were unaffected by systemic hypoxia (3250 m) in the present study, despite deoxygenated HHb was matched between the BFR and HYP condition ( Figure 4A). Thus, the severity of exercise-induced muscle hypoxia was not decisive for the effects of BFR on PGC-1a levels in the present study.…”

Section: Augmented Pgc-1a-isoform Mrna Content After Blood Flow-ressupporting

confidence: 88%

Increased FXYD1 and PGC‐1α mRNA after blood flow‐restricted running is related to fibre type‐specific AMPK signalling and oxidative stress in human muscle

et al. 2018

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AimThis study explored the effects of blood flow restriction (BFR) on mRNA responses of PGC‐1α (total, 1α1, and 1α4) and Na+,K+‐ATPase isoforms (NKA; α1‐3, β1‐3, and FXYD1) to an interval running session and determined whether these effects were related to increased oxidative stress, hypoxia, and fibre type‐specific AMPK and CaMKII signalling, in human skeletal muscle.MethodsIn a randomized, crossover fashion, 8 healthy men (26 ± 5 year and 57.4 ± 6.3 mL kg−1 min−1) completed 3 exercise sessions: without (CON) or with blood flow restriction (BFR), or in systemic hypoxia (HYP, ~3250 m). A muscle sample was collected before (Pre) and after exercise (+0 hour, +3 hours) to quantify mRNA, indicators of oxidative stress (HSP27 protein in type I and II fibres, and catalase and HSP70 mRNA), metabolites, and α‐AMPK Thr172/α‐AMPK, ACC Ser221/ACC, CaMKII Thr287/CaMKII, and PLBSer16/PLB ratios in type I and II fibres.ResultsMuscle hypoxia (assessed by near‐infrared spectroscopy) was matched between BFR and HYP, which was higher than CON (~90% vs ~70%; P < .05). The mRNA levels of FXYD1 and PGC‐1α isoforms (1α1 and 1α4) increased in BFR only (P < .05) and were associated with increases in indicators of oxidative stress and type I fibre ACC Ser221/ACC ratio, but dissociated from muscle hypoxia, lactate, and CaMKII signalling.ConclusionBlood flow restriction augmented exercise‐induced increases in muscle FXYD1 and PGC‐1α mRNA in men. This effect was related to increased oxidative stress and fibre type‐dependent AMPK signalling, but unrelated to the severity of muscle hypoxia, lactate accumulation, and modulation of fibre type‐specific CaMKII signalling.

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Section: Augmented Pgc-1a-isoform Mrna Content After Blood Flow-ressupporting

confidence: 88%

Increased FXYD1 and PGC‐1α mRNA after blood flow‐restricted running is related to fibre type‐specific AMPK signalling and oxidative stress in human muscle

et al. 2018

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“…This is consistent with a previous human study, in which contraction-stimulated increases in leg muscle PGC-1α mRNA content was unaffected by promoted systemic levels of epinephrine and lactate invoked by simultaneous arm exercise (Brandt et al, 2016). The present observation of unaltered PGC-1α levels after exercise in systemic hypoxia agrees with a previous human study that reported unchanged PGC-1α mRNA content after a single exercise session at simulated altitude (3000 m) in recreationally active men (Slivka et al, 2014). Since deoxygenated HHb was similar during exercise with ischaemia and in systemic hypoxia (Fig.…”

Section: Increases In Human Muscle Pgc-1α-isoform Mrna Content Are Unsupporting

confidence: 93%

Repeated-ischaemic exercise enhances mitochondrial and ion transport gene adaptations in human skeletal muscle – Role of muscle redox state and AMPK

Christiansen

Bangsbo

et al. 2017

Preprint

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in key points (150 words): We investigated if ischaemia would augment the exercise-induced mRNA response of PGC-1α and Na + ,K + -ATPase (NKA) isoforms (α1-3, β1-3, and FXYD1), and examined whether this effect could be related to oxidative stress and fibre type-dependent AMPK and CaMKII signalling in the skeletal muscle of trained men. Repeated-ischaemic exercise increased the mRNA content of PGC-1α total, -1α1, and -1α4, and of the NKA regulatory subunit FXYD1, whereas exercise in systemic hypoxia or alone was without effect on these genes. These responses to ischaemia were complemented by increased oxidative stress (as assessed by catalase and HSP70 mRNA) and ACC phosphorylation (an indicator of AMPK activation) in type I fibres. However, they were unrelated to CaMKII signalling, muscle hypoxia, and lactate accumulation. Thus, repeated ischaemic exercise augments the muscle gene response associated with mitochondrial biogenesis and ion homeostasis in trained men. This effect seems partly attributable to promoted oxidative stress and AMPK activation. AbstractThis study assessed the effect of repeated-ischaemic exercise on the mRNA content of PGC-1α (total, 1α1, and 1α4) and Na + ,K + -ATPase (NKA; α1-3, β1-3, and FXYD1) isoforms in human skeletal muscle, and studied some of the potential molecular mechanisms involved. Eight trained men (26 ± 5 y and 57.4 ± 6.3 mL•kg -1 •min -1 ) completed three interval running sessions with (ISC) or without ischaemia (CON), or in hypoxia (HYP, ~3250 m), in a randomised, crossover fashion separated by 1 week. A muscle sample was collected from the dominant leg before (Pre) and after exercise (+0h, +3h) in all sessions to measure the mRNA content of PGC-1α and NKA isoforms, oxidative stress markers (i.e. catalase and HSP70 mRNA), muscle lactate, and phosphorylation of AMPK, ACC, CaMKII, and PLB protein in type I and II fibres. Muscle hypoxia (i.e. deoxygenated haemoglobin) was matched between ISC and HYP, which was higher than in CON (~90% vs. ~70%; p<0.05). The levels of PGC-1α total, -1α1, -1α4, and FXYD1 mRNA increased in ISC only (p<0.05). These changes were associated with increases in oxidative stress markers and higher p-ACCSer 221 /ACC in type I fibres, but were unrelated to muscle hypoxia, lactate, and CaMKII and PLB phosphorylation. These findings highlight that repeated-ischaemic exercise augments the skeletal muscle gene response related to mitochondrial biogenesis and ion transport in trained men. This effect seems attributable, in part, to increased oxidative stress and AMPK activation, whereas it appears unrelated to altered CaMKII signalling, and the muscle hypoxia and lactate accumulation induced by ischaemia. AbbreviationsACC, Acetyl-CoA carboxylase; AMPK, 5' AMP-activated protein kinase subunit; β2M, β2 microglobulin; CaMKII, Ca2+-calmodulin-dependent protein kinase isoform II

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“…Finally, these investigations should be conducted in well-defined populations in order to minimize confounding outcomes from heterogeneous participant groups that often result from convenience sampling. These recommendations are essential for understanding highly variable tissue level responses that are sensitive to fitness level and exercise habituation (Mounier et al 2009;Slivka et al 2014;Peters et al 2015).…”

Section: Altitude Considerations For Living and Trainingmentioning

confidence: 99%

“…Recent examination of mitochondrial biogenesis gene transcripts in human vastus lateralis obtained following an acute bout of hypoxic exercise reinforces the notion that adaptive responses to high altitude exercise are redox sensitive (Slivka et al . ). Nonetheless, human performance studies of hypoxic exercise on sea level performance are equivocal (Ventura et al .…”

Section: Introductionmentioning

confidence: 97%

Impact of extreme exercise at high altitude on oxidative stress in humans

Quindry

Dumke

Slivka

et al. 2015

The Journal of Physiology

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Exercise and oxidative stress research continues to grow as a physiological subdiscipline. The influence of high altitude on exercise and oxidative stress is among the recent topics of intense study in this area. Early findings indicate that exercise at high altitude has an independent influence on free radical generation and the resultant oxidative stress. This review provides a detailed summary of oxidative stress biochemistry as gleaned mainly from studies of humans exercising at high altitude. Understanding of the human response to exercise at altitude is largely derived from field-based research at altitudes above 3000 m in addition to laboratory studies which employ normobaric hypoxia. The implications of oxidative stress incurred during high altitude exercise appear to be a transient increase in oxidative damage followed by redox-sensitive adaptations in multiple tissues. These outcomes are consistent for lowland natives, high altitude acclimated sojourners and highland natives, although the latter group exhibits a more robust adaptive response. To date there is no evidence that altitude-induced oxidative stress is deleterious to normal training or recovery scenarios. Limited evidence suggests that deleterious outcomes related to oxidative stress are limited to instances where individuals are exposed to extreme elevations for extended durations. However, confirmation of this tentative conclusion requires further investigation. More applicably, altitude-induced hypoxia may have an independent influence on redox-sensitive adaptive responses to exercise and exercise recovery. If correct, these findings may hold important implications for athletes, mountaineers, and soldiers working at high altitude. These points are raised within the confines of published research on the topic of oxidative stress during exercise at altitude.

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Human Skeletal Muscle mRNA Response to a Single Hypoxic Exercise Bout

Abstract: The improvements in mitochondrial function reported with intermittent hypoxic training may not be explained by a single acute hypoxic exposure, and thus it appears that a longer period of preacclimatization than a single exposure may be required.

Cited by 22 publications

References 12 publications

Increased FXYD1 and PGC‐1α mRNA after blood flow‐restricted running is related to fibre type‐specific AMPK signalling and oxidative stress in human muscle

Increased FXYD1 and PGC‐1α mRNA after blood flow‐restricted running is related to fibre type‐specific AMPK signalling and oxidative stress in human muscle

Repeated-ischaemic exercise enhances mitochondrial and ion transport gene adaptations in human skeletal muscle – Role of muscle redox state and AMPK

Impact of extreme exercise at high altitude on oxidative stress in humans

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