A Brief Review on Concurrent Training: From Laboratory to the Field

Abstract

The majority of sports rely on concurrent training (CT; e.g., the simultaneous training of strength and endurance). However, a phenomenon called "Concurrent training effect" (CTE), which is a compromise in adaptation resulting from concurrent training, appears to be mostly affected by the interference of the molecular pathways of the underlying adaptations from each type of training segments. Until now, it seems that the volume, intensity, type, frequency of endurance training, as well as the training history and background strongly affect the CTE. High volume, moderate, continuous and frequent endurance training, are thought to negatively affect the resistance training-induced adaptations, probably by inhibition of the Protein kinase B-mammalian target of rapamycin pathway activation, of the adenosine monophosphate-activated protein kinase (AMPK). In contrast, it seems that short bouts of high-intensity interval training (HIIT) or sprint interval training (SIT) minimize the negative effects of concurrent training. This is particularly the case when HIIT and SIT incorporated in cycling have even lower or even no negative effects, while they provide at least the same metabolic adaptations, probably through the peroxisome proliferator-activated receptor-γ coactivator (PGC-1a) pathway. However, significant questions about the molecular events underlying the CTE remain unanswered.

Keywords: adenosine monophosphate-activated protein kinase; concurrent exercise; mammalian target of rapamycin; peroxisome proliferator-activated receptor-γ coactivator.

Figure 1

Molecular events after a concurrent training incorporating resistance exercise and high-volume, low-moderate intensity endurance exercise leads to a high increase of AMPK phosphorylation, leading to inhibited myofibrillar protein synthesis, via the de-activation of the mTOR cascade through the AMPK-mediated phosphorylation of TSC 1/2, but also to increased mitochondrial protein synthesis, via the AMPK, ROS, CaMKII, Calcineurin, Sirt1 and p38 MAPK activation of PGC-1a. In addition, the increased phosphorylation of AMPK mediates the increase of protein degradation, by activating FOXO, MaFbx, MuRF 1, ULK-1, MyoD and Atrogin-1 molecules. 4EBP1: Eukaryotic initiation factor 4E-binding protein 1; AKT: Protein kinase B; AMP:ATP: Adenosine monophosphate: Adenosine triphosphate ratio; AMPK: Adenosine monophosphate-activated protein kinase; Ca²⁺: Calcium ions; CaMK II: Ca²⁺/calmodulin-dependent kinases II; eEF2: Eukaryotic elongation factor 2; eEF2K: Eukaryotic elongation factor-2 kinase; eIF4B: Eukaryotic translation initiation factor 4B; eIF4E: Eukaryotic translation initiation factor 4E; ERK 1/2: extracellular signal–regulated kinases ½; ERRs: Estrogen receptor related receptor (ERR) family; FAK: Focal adhesion kinase; FOXO: Forkhead box O (FoxO) transcription factors; IGF-1: Insulin-like growth factor 1; IRS-1: Insulin receptor substrate 1; JNK: Jun amino-terminal kinase; MaFbx: Muscle-atrophy f-box; MEF 2: myocyte enhancer factor-2; mTOR: mammalian target of rapamycin (in this text we are referring to Raptor mTOR); MuRF 1: Muscle ring-finger 1; MyoD: Myoblast determination protein; NRF 1: Nuclear respiratory factor 1; NRF 2: Nuclear factor (erythroid-derived 2)-like 2 (also known as NFE2L2); p38 MAPK: p38 mitogen-activated protein kinase; p70S6k: Ribosomal protein S6 kinase beta-1 (also known as S6K1); PDK1: 3-phosphoinositide-dependent protein kinase-1; PGC-1a: peroxisome proliferator-activated receptor-γ coactivator 1a; PI3K: phosphatidylinositol 3-kinase/Phosphatidylinositol-4,5-bisphosphate 3-kinase; PIP3: Phosphatidylinositol (3,4,5)-trisphosphate; PPARs: Seroxisome proliferator–activated receptor family; ROS: Reactive Oxygen Species; S6: Ribosomal s6 kinase (also known as rsk and p70^rsk); SIRT: Sirtuin; TFAM: Mitochondrial transcription factor A; TSC 1/2: Tuberous sclerosis complex ½; ULK 1: Unc-51-like kinase.

Figure 2

Molecular events after a concurrent training including low-volume high-intensity interval training (HIIT) or sprint interval training (SIT). A concurrent training incorporating resistance exercise, low-volume, high-intensity endurance exercise leads to a significant lower activation of AMPK, and thus to a very low activation of TSC 1/2, FOXO, MaFbx, MuRF 1, ULK-1, MyoD and Atrogin-1 molecules, allowing the increased myofibrillar and mitochondrial protein synthesis, and keeping low the rates of proteins degradation. 4EBP1: Eukaryotic initiation factor 4E-binding protein 1; AKT: Protein kinase B; AMP:ATP: Adenosine monophosphate: Adenosine triphosphate ratio; AMPK: Adenosine monophosphate-activated protein kinase; Ca²⁺: Calcium ions; CaMK II: Ca²⁺/calmodulin-dependent kinases II; eEF2: Eukaryotic elongation factor 2; eEF2K: Eukaryotic elongation factor-2 kinase; eIF4B: Eukaryotic translation initiation factor 4B; eIF4E: Eukaryotic translation initiation factor 4E; ERK 1/2: extracellular signal–regulated kinases ½; ERRs: Estrogen receptor related receptor (ERR) family; FAK: Focal adhesion kinase; FOXO: Forkhead box O (FoxO) transcription factors; IGF-1: Insulin-like growth factor 1; IRS-1: Insulin receptor substrate 1; JNK: Jun amino-terminal kinase; MaFbx: Muscle-atrophy f-box; MEF 2: myocyte enhancer factor-2; mTOR: mammalian target of rapamycin (in this text we are referring to Raptor mTOR); MuRF 1: Muscle ring-finger 1; MyoD: Myoblast determination protein; NRF 1: Nuclear respiratory factor 1; NRF 2: Nuclear factor (erythroid-derived 2)-like 2 (also known as NFE2L2); p38 MAPK: p38 mitogen-activated protein kinase; p70S6k: Ribosomal protein S6 kinase beta-1 (also known as S6K1); PDK1: 3-phosphoinositide-dependent protein kinase-1; PGC-1a: peroxisome proliferator-activated receptor-γ coactivator 1a; PI3K: phosphatidylinositol 3-kinase/Phosphatidylinositol-4,5-bisphosphate 3-kinase; PIP3: Phosphatidylinositol (3,4,5)-trisphosphate; PPARs: Seroxisome proliferator–activated receptor family; ROS: Reactive Oxygen Species; S6: Ribosomal s6 kinase (also known as rsk and p70^rsk); SIRT: Sirtuin; TFAM: Mitochondrial transcription factor A; TSC 1/2: Tuberous sclerosis complex ½; ULK 1: Unc-51-like kinase.