Cited by 351Sports Performance and TrainingMuscle metabolism and nutritionCardiovascular and exercise physiology

Concurrent exercise training: do opposites distract?

Open access
Coffey, Vernon G., Hawley, John A.·2017·The Journal of Physiology

Abstract

Specificity is a core principle of exercise training to promote the desired adaptations for maximising athletic performance. The principle of specificity of adaptation is underpinned by the volume, intensity, frequency and mode of contractile activity and is most evident when contrasting the divergent phenotypes that result after undertaking either prolonged endurance or resistance training. The molecular profiles that generate the adaptive response to different exercise modes have undergone intense scientific scrutiny. Given divergent exercise induces similar signalling and gene expression profiles in skeletal muscle of untrained or recreationally active individuals, what is currently unclear is how the specificity of the molecular response is modified by prior training history. The time course of adaptation and when ‘phenotype specificity’ occurs has important implications for exercise prescription. This context is essential when attempting to concomitantly develop resistance to fatigue (through endurance‐based exercise) and increased muscle mass (through resistance‐based exercise), typically termed ‘concurrent training’. Chronic training studies provide robust evidence that endurance exercise can attenuate muscle hypertrophy and strength but the mechanistic underpinning of this ‘interference’ effect with concurrent training is unknown. Moreover, despite the potential for several key regulators of muscle metabolism to explain an incompatibility in adaptation between endurance and resistance exercise, it now seems likely that multiple integrated, rather than isolated, effectors or processes generate the interference effect. Here we review studies of the molecular responses in skeletal muscle and evidence for the interference effect with concurrent training within the context of the specificity of training adaptation. image

Integrity signals

Registry

Crossref · 10.1113/jp272270

Cites

91 of 91 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

14 of 69 cited sources checked · 7 supported · 0 flagged · accuracy not yet measured

  • Premisecitation

    Compared to trained athletes, untrained individuals have a greater capacity to activate the molecular machinery in muscle in response to contractile activity because any overload stimulus induces large perturbations to cellular homeostasis regardless of the mode of exercise.

    “Compared to trained athletes, untrained individuals have a greater capacity to activate the molecular machinery in muscle in response to contractile activity because any overload stimulus induces large perturbations to cellular homeostasis regardless of the mode of exercise (Benziane et al., 2008b;Perry et al., 2010;Nader et al., 2014).”
    Quote in the paperSubstantial claim1 of 3 sources checked
    • cites Benziane et al., 2008b

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites Perry et al., 2010 source

      Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.

      Experimental — accuracy not yet measured
    • cites Nader et al., 2014 source
  • Premisecitation

    Low responders to each exercise stimulus may be as high as 25% in studies of individuals undertaking resistance and endurance training in isolation.

    “The characterisation of individual responses is not a new phenomenon, but the results of studies of individuals undertaking resistance and endurance training in isolation suggest that 'low responders' to each exercise stimulus may be as high as 25% (Timmons et al., 2005;Phillips et al., 2013;Gurd et al., 2016).”
    Quote in the paperSubstantial claim2 of 3 sources checked
    • cites Timmons et al., 2005 source

      The Methods (Human and physiological measurements; page not supplied) describe a low-responder group selected after supervised endurance training, supporting the existence of low responders to that stimulus. The group was selected from a larger cohort, so its size does not establish that 25% of trainees were low responders. This paper did not study responses to resistance training. (LLM, conf=0.87)

      Experimental — accuracy not yet measured
    • cites Phillips et al., 2013 source
    • cites Gurd et al., 2016 source
  • Premisecitation

    Different exercise modes appear to generate a fibre type specific satellite cell response.

    “The different exercise modes also appear to generate a fibre type specific satellite cell response which may also increase the complexity in delineating its role in the specificity of adaptation and any incompatibility with concurrent training (Babcock et al., 2012;Joanisse et al., 2013;Bellamy et al., 2014).”
    Quote in the paperSubstantial claim1 of 3 sources checked
    • cites Babcock et al., 2012 source
    • cites Joanisse et al., 2013 source
    • cites Bellamy et al., 2014 source

      The Results section reports a fibre-type-specific satellite cell response to resistance exercise: type II-associated cells increased after an acute bout, while cells associated with both fibre types increased after 16 weeks of training. The paper does not compare different exercise modes, so it does not establish that different modes generate different fibre-type-specific responses. (LLM, conf=0.85)

      Experimental — accuracy not yet measured
  • Premisecitation

    Even during a short-term intervention, mRNA responses to exercise are attenuated as the muscle adapts to the exercise challenge, even in the face of an increasing training intensity.

    “Of note was that even during such a short-term intervention, the mRNA responses to exercise were attenuated as the muscle adapted to the exercise challenge, even in the face of an increasing training intensity.”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites Perry et al., 2010 source
  • Premisecitation

    Repeated, transient increases in mRNA induced after each exercise session are necessary to elicit the sustained increases observed in the content of transcription and metabolic proteins.

    “They demonstrated that the repeated, transient increases in mRNA induced after each exercise session were necessary to elicit the sustained increases observed in the content of transcription and metabolic proteins.”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites Perry et al., 2010 source

      The Discussion reports repeated transient mRNA increases followed by sustained increases in transcription and metabolic proteins. It says the findings support a hypothesis that mRNA bursts are required for adaptation, but does not demonstrate that they are necessary; the citing sentence overstates that conclusion. (LLM, conf=0.86)

      Experimental — accuracy not yet measured
  • May combine two claims. 19
  • Classified as probably not a substantial claim. 17
  • The quote only partly states this claim. 1
  • May combine two claims.

    Premisecitation

    After training consisting of either endurance exercise, resistance exercise, or a combination of both endurance and resistance exercise, increases in PGC-1α4 are confined to resistance-only and combined exercise training programmes, with no changes in this transcript after endurance-only training.

    “In this regard, Ruas and co-workers (Ruas et al., 2012) have shown that after training consisting of either endurance exercise, resistance exercise, or a combination of both endurance and resistance exercise, increases in PGC-1α4 are confined to resistance-only and combined exercise training programmes, with no changes in this transcript after endurance-only training (Ruas et al., 2012).”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites Ruas et al., 2012 source
  • May combine two claims.

    Premisecitation

    Others have failed to show a specificity of adaptation response in PGC-1α isoforms with acute bouts of endurance compared to resistance exercise or differences in expression with resistance versus concurrent exercise bouts in untrained individuals.

    “However, in contrast to the early results from Ruas et al. (Ruas et al., 2012), others have failed to show a specificity of adaptation response in PGC-1α isoforms with acute bouts of endurance compared to resistance exercise or indeed differences in expression with resistance versus concurrent exercise bouts albeit in untrained individuals (Ydfors et al., 2013;Lundberg et al., 2014a).”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites Ydfors et al., 2013 source

      Split into 2 atoms — 1 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 1 unverifiable. Expand the claim to see per-atom verdicts.

      Experimental — accuracy not yet measured
    • cites Lundberg et al., 2014a

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • May combine two claims.

    Premisecitation

    PGC-1α4 is abundantly expressed in skeletal muscle and appears to play a role in the adaptive response to exercise, particularly in the setting of resistance training.

    “PGC-1α4, a transcript from the PGC-1 α gene, is abundantly expressed in skeletal muscle and appears to play a role in the adaptive response to exercise, particularly in the setting of resistance training (Ruas et al., 2012;White et al., 2014).”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites Ruas et al., 2012 source
    • cites White et al., 2014 source
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Satellite cells are niche stem cells located in skeletal muscle with the capacity to promote adaptation through the contribution of new myonuclei within existing muscle fibres and/or myocytes that can fuse and form new myofibres.

    “Satellite cells are niche stem cells located in skeletal muscle with the capacity to promote adaptation through the contribution of new myonuclei within existing muscle fibres and/or myocytes that can fuse and form new myofibres (Dumont et al., 2015).”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites Dumont et al., 2015 source
  • May combine two claims.

    Premisecitation

    Resistance and aerobic exercise independently have the potential to induce satellite cell responses for skeletal muscle remodelling.

    “It should be noted that resistance and aerobic exercise independently have the potential to induce satellite cell responses for skeletal muscle remodelling”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites Joanisse et al., 2013 source
    • cites Bellamy et al., 2014 source

      The Abstract reports a satellite-cell response after a bout of resistance exercise, supporting that part of the claim. The paper studies resistance training, and the cited passages do not establish an independent satellite-cell response to aerobic exercise. Page numbers are unavailable in our copy. (LLM, conf=0.88)

      Experimental — accuracy not yet measured
  • Probably not a substantial claim: may not pass S4 (based).

    Premisenone given

    Divergent exercise induces similar signalling and gene expression profiles in skeletal muscle of untrained or recreationally active individuals.

    “Given divergent exercise induces similar signalling and gene expression profiles in skeletal muscle of untrained or recreationally active individuals, what is currently unclear is how the specificity of the molecular response is modified by prior training history.”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Premisecitation

    Resistance training elicits little or no change to the oxidative profile of trained muscles, nor major shifts in fuel utilisation patterns.

    “Such training, even when performed over several months or years, elicits little or no change to the oxidative profile of the trained muscles, nor major shifts in the patterns of fuel utilisation (MacDougall et al., 1982).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites MacDougall et al., 1982 source
  • May combine two claims.

    Premisecitation

    Resistance training stimulates synthesis of myofibrillar proteins and muscle hypertrophy.

    “In contrast, training to increase strength and/or power requires short duration (<60 s) maximal contractile activity and heavy resistance loading to stimulate the synthesis of myofibrillar proteins and muscle hypertrophy (Damas et al., 2015).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Damas et al., 2015 source
  • Probably not a substantial claim: may not pass S4 (based).

    Interpretationnone given

    Primary factors determining the molecular profiles generated by concurrent exercise are the training status of subjects and inter-individual responses.

    “However, perhaps the primary factors determining the molecular profiles generated by concurrent exercise are the training status of subjects and inter-individual responses.”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Premisecitation

    Adding strength training to endurance training benefits short-term (4-8 min) running and cycling performance and long-term (~80 min) endurance cycling capacity in trained runners and cyclists, despite no changes in VO2max.

    “Despite no changes in VO2max there was a clear benefit of adding strength training to endurance training for both short-term (4-8 min) running and cycling performance and longterm (~80 min) endurance cycling capacity.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Hickson et al., 1988 source
  • May combine two claims.

    Interpretationnone given

    Where the interference effect has been unclear, it can typically be attributed to low volume and frequency of training, a limited intervention period, and/or the training status of individuals under investigation.

    “Even where the interference effect has been unclear (McCarthy et al., 1995;McCarthy et al., 2002;Balabinis et al., 2003;Häkkinen et al., 2003;Hendrickson et al., 2010;Lundberg et al., 2013), this can typically be attributed to the low volume and frequency of training undertaken, a limited intervention period and/or the training status of individuals under investigation.”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Premisecitation

    In sedentary middle-aged men, concurrent exercise comprising 50% of total work of separate resistance and aerobic bouts produces no meaningful change in S6K and AMPK phosphorylation between modes, comparable increases in myofibrillar protein synthesis with concurrent vs resistance exercise, and similar rates of mitochondrial protein synthesis between concurrent and aerobic exercise.

    “They reported no meaningful change in S6K and AMPK phosphorylation between the different exercise modes, comparable increases in skeletal muscle myofibrillar protein synthesis with concurrent compared with resistance exercise, and similar rates of mitochondrial protein synthesis between concurrent and aerobic exercise.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Donges et al., 2013 source
  • May combine two claims.

    Premisecitation

    PGC-1α4 does not appear to regulate the same set of oxidative genes induced by PGC-1α but activates the expression of IGF-1 while concomitantly suppressing myostatin pathways.

    “This protein does not appear to regulate the same set of oxidative genes induced by PGC-1α but, rather, activates the expression of IGF-1 while concomitantly suppressing myostatin (an inhibitor of muscle cell differentiation and growth) pathways.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    ACTN3 gene deficiency may be unfavourable for the development of muscular power.

    “ACTN3 gene deficiency, which prevents its subsequent protein expression in type II muscle fibres, may be unfavourable for the development of muscular power”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites Eynon et al., 2013

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites Eynon et al., 2014

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • May combine two claims.

    Premisecitation

    Studies in cell culture and animal models provide compelling evidence for cross-talk between AMPK and mTOR signaling pathways, and support the notion that activation of AMPK-related pathways suppresses translation through decreased S6K and 4E-BP phosphorylation.

    “Studies in cell culture and animal models provide compelling evidence for the cross-talk between AMPK and mTOR signaling pathways, and support the notion that activation of AMPK-related pathways suppresses translation through decreased S6K and 4E-BP phosphorylation (Bolster et al., 2002;Thomson et al., 2008;Lantier et al., 2010;Egawa et al., 2014).”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites Bolster et al., 2002 source
    • cites Thomson et al., 2008 source
    • cites Lantier et al., 2010 source
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    The ACTN3 genotype (577RR) associated with muscular power was underrepresented in team sport compared with power athletes.

    “They showed the ACTN3 genotype (577RR) associated with muscular power was underrepresented in team sport compared with power athletes”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Eynon et al., 2014

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    PGC-1α is an exercise-responsive transcriptional co-activator described as a master regulator of oxidative metabolism and mitochondrial biogenesis, promoting many of the adaptations to endurance training in skeletal muscle.

    “PGC-1α is an exercise-responsive transcriptional co-activator that has been described as a master regulator of oxidative metabolism and mitochondrial biogenesis, promoting many of the adaptations to endurance training in skeletal muscle (Hood, 2009).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Hood, 2009 source
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    ACTN3 gene deficiency could promote an endurance-like phenotype.

    “could promote an endurance-like phenotype (Eynon et al., 2013;Eynon et al., 2014)”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites Eynon et al., 2013

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites Eynon et al., 2014

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).

    Premisenone given

    Similar characterisation of the chronic time-course of adaptation to resistance training is currently lacking.

    “Similar characterisation of the chronic time-course of adaptation to resistance training is currently lacking.”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Premisecitation

    A conventional resistance exercise bout transiently increases muscle fibre satellite cell density (~38%) after 4 days recovery, but the addition of a 90 min cycling bout (~60% Wmax) undertaken immediately after resistance exercise completely suppressed this response.

    “They found that a conventional resistance exercise bout transiently increases muscle fibre satellite cell density (~38%) after 4 days recovery, but the addition of a 90 min cycling bout (~60% Wmax) undertaken immediately after resistance exercise completely suppressed this response.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Babcock et al., 2012 source
  • May combine two claims.

    Premisecitation

    PGC-1α4 expression was not induced in the muscle of untrained subjects in response to an acute bout of resistance exercise undertaken at the beginning of a 12 week training programme, but was selectively up-regulated by the same exercise session at the end of the intervention period.

    “Of note, Nader et al. (Nader et al., 2014) showed PGC-1α4 expression was not induced in the muscle of untrained subjects in response to an acute bout of resistance exercise undertaken at the beginning of a 12 week training programme, but was selectively up-regulated by the same exercise session at the end of the intervention period.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Nader et al., 2014 source
  • May combine two claims.

    Premisecitation

    Increases in mitochondrial proteins occurred within five days and following three sessions of high-intensity interval training, while at the end of 2 weeks, VO2max had also increased by 12%.

    “Increases in mitochondrial proteins occurred within five days and following three sessions of high-intensity interval training, while at the end of the 2 weeks, VO2max had also increased by 12% (Perry et al., 2010).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Perry et al., 2010 source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Muscle-specific overexpression of PGC-1α results in a large increase in functional mitochondria.

    “A single bout of endurance exercise induces a rapid and sustained increase in PGC-1α gene and protein in skeletal muscle (Mathai et al., 2008), whereas muscle-specific overexpression of PGC-1α results in a large increase in functional mitochondria (Lin et al., 2002).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Lin et al., 2002 source
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    The ACTN3 gene has emerged as a candidate that may influence exercise performance capacity.

    “The α-actinin-3 (ACTN3) gene has emerged as a candidate that may influence exercise performance capacity.”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites Eynon et al., 2013

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

    • cites Eynon et al., 2014

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisenone given

    A direct comparison between the transcriptome profiles of resistance- and endurance training-induced gene expression has not been undertaken.

    “a direct comparison between the transcriptome profiles of resistance-and endurance training-induced gene expression has not be undertaken.”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Interpretationreasoning

    When previously sedentary or recreationally active individuals commence any concurrent training programme, the response to the two exercise modes is additive and promotes a generic adaptation in the absence of a true specificity of training effect.

    “It seems reasonable to suggest that when previously sedentary or recreationally active individuals commence any concurrent training programme, the response to the two exercise modes is additive and promotes a generic adaptation in the absence of a true specificity of training effect.”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Premisecitation

    Aerobic interval training (6 weeks, 3 session/week) expands the muscle satellite cell pool and increases satellite cell activity without subsequent hypertrophy, indicating exercise-induced satellite cell activation in skeletal muscle is not limited to resistance exercise.

    “Joanisse and colleagues (2013) have shown that aerobic interval training (6 weeks, 3 session/week) expands the muscle satellite cell pool and increases satellite cell activity without subsequent hypertrophy, indicating exerciseinduced satellite cell activation in skeletal muscle is not limited to resistance exercise.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Joanisse et al., 2013 source
  • Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based). The quote only partly states this claim.

    Interpretationreasoning

    Impaired responses to concurrent training compared with single mode training result from the change in phenotype coinciding with the need for greater training loads to disrupt homeostasis and promote further adaptation.

    “which results in impaired responses to concurrent training compared with single mode training.”
    Quote in the paperNot a substantial claim
    • Rests on an assumption: As training progresses (i.e., months-years) repeated bouts of divergent exercise begin to generate a specificity of training adaptation that initiates transformation of the skeletal muscle phenotype.
    • Rests on an assumption: The change in phenotype coincides with the need for greater training loads to disrupt homeostasis and promote further adaptation.
  • Probably not a substantial claim: may not pass S4 (based).

    Interpretationnone given

    The exercise stimulus initially generates a 'general adaptation profile'.

    “The exercise stimulus initially generates a 'general adaptation profile'”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    The downstream effectors of mTORC1 are S6K and 4E-BP, which have key roles in promoting translation initiation and ribosome biogenesis.

    “The downstream effectors of mTORC1 are the 70KDa ribosomal S6 protein kinase (S6K) and eukaryotic initiation factor 4E binding protein (4E-BP) that have been shown to have key roles in promoting translation initiation and ribosome biogenesis (Philp et al., 2011).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Philp et al., 2011 source
  • Probably not a substantial claim: may not pass S4 (based).

    Interpretationnone given

    There is incompatibility and adaptation interference with concurrent training whereby endurance training attenuates hypertrophy/strength.

    “and there is incompatibility and adaptation interference with concurrent training whereby endurance training attenuates hypertrophy/strength.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S4 (based).

    Interpretationnone given

    As training continues, 'specificity of adaptation' responses are generated.

    “but as training continues, 'specificity of adaptation' responses are generated”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Interpretationnone given

    Endurance training has the potential to induce modest hypertrophy and resistance training has the potential to promote oxidative capacity in the untrained state.

    “the potential for endurance training (blue, hatched bars) to induce modest hypertrophy and resistance training (red, hatched bars) to promote oxidative capacity in the untrained state.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Linked kinases have each been proposed as mechanosensors that initiate the signal that generates greater subsequent activity of mTORC1.

    “linked kinases have each been proposed as mechanosensors that initiate the signal that generates greater subsequent activity of the mechanistic target of rapamycin complex 1 (mTORC1).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Philp et al., 2011 source
34 of 34
  • The paper relies on this without support.

    Concurrent training is a prerequisite for performance in many team sports.

    “as concurrent training is a prerequisite for performance in many team sports”
  • The paper relies on this without support.

    The molecular profiles generated by endurance and resistance exercise are complex.

    “The molecular profiles generated by endurance and resistance exercise are complex”
  • The paper relies on this without support.

    The complexity of molecular profiles is magnified when individuals undertake concurrent training.

    “an effect that is magnified when individuals undertake concurrent training.”
  • The paper relies on this without support.

    Modulation of cellular calcium concentration with contraction upregulates CaMK and/or Calcineurin proteins, which act as a metabolic signal for adaptation responses.

    “Modulation of cellular calcium concentration with contraction upregulates Calmodulin kinase (CaMK) and/or Calcineurin proteins, which also act as a metabolic signal for adaptation responses.”
  • The paper relies on this without support.

    In the first days/weeks when an individual commences training, the initial skeletal muscle adaptation responses are similar between single mode and concurrent training adaptation as are any functional performance measures.

    “In the first days/weeks when an individual commences training, the initial skeletal muscle adaptation responses are similar between single mode and concurrent training adaptation as are any functional performance measures.”
  • The paper relies on this without support.

    During this early phase the mechanosensors and subsequent mechanotransduction of the adaptive signal fails, at least in part, to differentiate between the endurance-and resistance-like stimuli often undertaken at lowmoderate intensity and volume.

    “During this early phase the mechanosensors and subsequent mechanotransduction of the adaptive signal fails, at least in part, to differentiate between the endurance-and resistance-like stimuli often undertaken at lowmoderate intensity and volume.”
  • The paper relies on this without support.

    As training progresses (i.e., months-years) repeated bouts of divergent exercise begin to generate a specificity of training adaptation that initiates transformation of the skeletal muscle phenotype.

    “As training progresses (i.e., months-years) repeated bouts of divergent exercise begin to generate a specificity of training adaptation that initiates transformation of the skeletal muscle phenotype.”
  • The paper relies on this without support.

    The change in phenotype coincides with the need for greater training loads to disrupt homeostasis and promote further adaptation.

    “The change in phenotype coincides with the need for greater training loads to disrupt homeostasis and promote further adaptation”
  • The paper relies on this without support.

    Repeated bouts of single mode training (i.e., either endurance-or resistance-based) generate a specific molecular profile that results in mitochondrial biogenesis and improved resistance to fatigue, or hypertrophy and enhanced strength/power in skeletal muscle.

    “The classic model whereby repeated bouts of single mode training (i.e., either endurance-or resistance-based) generate a specific molecular profile that results in mitochondrial biogenesis and improved resistance to fatigue, or hypertrophy and enhanced strength/power in skeletal muscle.”
  • The paper relies on this without support.

    AMPK is an energy sensing protein.

    “The adenosine monophosphate kinase (AMPK) is an energy sensing protein”
  • The paper relies on this without support.

    Reactive oxygen species (ROS) are a metabolic byproduct of oxidative metabolism.

    “reactive oxygen species (ROS) are a metabolic by product of oxidative metabolism”
  • The paper relies on this without support.

    AMPK, ROS, and p38 MAPK all respond to the metabolic stress generated within skeletal muscle by exercise.

    “which in concert with the p38 mitogen activated protein kinase (MAPK) all respond to the metabolic stress generated within skeletal muscle by exercise.”
12 of 12

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • The energetic stress of endurance training activates AMPK, which subsequently phosphorylates TSC2 to directly inhibit mTORC1, thereby immediately halting acute muscle protein synthesis.

    “For decades, the molecular rationale for this interference was attributed exclusively to a conflict of translational efficiency: the energetic stress of endurance training activates AMP-activated protein kinase (AMPK), which subsequently phosphorylates TSC2 to directly inhibit mTORC1, thereby immediately halting acute muscle protein synthesis [129,130].”

    From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [130]

    In “Potential molecular candidates to explain the interference effect” (page not provided), the paper describes evidence from cell and animal models that AMPK-related pathways can suppress translation through reduced S6K and 4E-BP phosphorylation. It does not establish the claimed AMPK–TSC2 sequence or an immediate halt to muscle protein synthesis; it says there is little evidence for direct AMPK-induced impairment of myofibrillar protein synthesis in humans. “The specificity of training adaptation in skeletal muscle” (page not provided) also reports that elevated AMPK activity did not suppress mTOR signaling when endurance exercise preceded resistance exercise. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • The molecular bases for skeletal muscle oxidative metabolism and hypertrophy training adaptations are different and can be potentially antagonistic.

    “Notably, although NO3− supplementation has been reported to enhance the adaptations to sprint interval training [62,147], the molecular bases for skeletal muscle oxidative metabolism and hypertrophy training adaptations are different and can be potentially antagonistic [148,149].”

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Authors
Coffey, V. G., & Hawley, J. A.
Affiliations
  • Bond University (AU)
  • Liverpool John Moores University (GB)
Corresponding author
Hawley, John A.
Venue
The Journal of Physiology
Publisher
Wiley
Published
2016-10-09
Volume
595
Issue
9
Pages
2883-2896
ISSN
  • 0022-3751 (ISSN-L)
  • 1469-7793
OpenAlex
W2483560356
Cited by
351
References
87
Citations by year
2026: 28 · 2025: 34 · 2024: 28 · 2023: 43 · 2022: 42 · 2021: 42 · 2020: 42 · 2019: 24 · 2018: 34 · 2017: 33 · 2016: 1
FWCI
4.89
Type
journal article
Language
en
Open access
Locations
  • The Journal of Physiology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Liverpool John Moores University (acceptedVersion)
  • Bond University Research Portal (Bond University) (submittedVersion, other-oa)
  • e-publications@bond (Bond University) (submittedVersion)
  • Research Bank (Australian Catholic University) (submittedVersion)
Funders
Department of Education and Training
Topics
  • Health Sciences › Medicine › Orthopedics and Sports Medicine › Sports Performance and Training
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
  • Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
Keywords
concurrent training, endurance training, resistance training, interference effects, skeletal muscle, muscle hypertrophy, muscle strength, fatigue resistance, gene expression, training history, exercise prescription
MeSH terms
Adaptation, Physiological, Humans, Muscle, Skeletal, Physical Conditioning, Human

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-11.

Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-11.

Cited sources are checked by gpt-6-sol.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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