Resistance exercise enhances the molecular signaling of mitochondrial biogenesis induced by endurance exercise in human skeletal muscle
Abstract
Combining endurance and strength training (concurrent training) may change the adaptation compared with single mode training. However, the site of interaction and the mechanisms are unclear. We have investigated the hypothesis that molecular signaling of mitochondrial biogenesis after endurance exercise is impaired by resistance exercise. Ten healthy subjects performed either only endurance exercise (E; 1-h cycling at ∼65% of maximal oxygen uptake), or endurance exercise followed by resistance exercise (ER; 1-h cycling + 6 sets of leg press at 70-80% of 1 repetition maximum) in a randomized cross-over design. Muscle biopsies were obtained before and after exercise (1 and 3 h postcycling). The mRNA of genes related to mitochondrial biogenesis [(peroxisome proliferator-activated receptor-γ coactivator-1 (PGC-1)α, PGC-1-related coactivator (PRC)] related coactivator) and substrate regulation (pyruvate dehydrogenase kinase-4) increased after both E and ER, but the mRNA levels were about twofold higher after ER (P < 0.01). Phosphorylation of proteins involved in the signaling cascade of protein synthesis [mammalian target of rapamycin (mTOR), ribosomal S6 kinase 1, and eukaryotic elongation factor 2] was altered after ER but not after E. Moreover, ER induced a larger increase in mRNA of genes associated with positive mTOR signaling (cMyc and Rheb). Phosphorylation of AMP-activated protein kinase, acetyl-CoA carboxylase, and Akt increased similarly at 1 h postcycling (P < 0.01) after both types of exercise. Contrary to our hypothesis, the results demonstrate that ER, performed after E, amplifies the adaptive signaling response of mitochondrial biogenesis compared with single-mode endurance exercise. The mechanism may relate to a cross talk between signaling pathways mediated by mTOR. The results suggest that concurrent training may be beneficial for the adaptation of muscle oxidative capacity.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
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?
Wang et al. (2011) found concomitant activation of AMPK and mTOR and increased expression of PGC-1a and PGC-1-related coactivator (PRC).
“The authors found a concomitant activation of AMPK and mTOR and an increased expression of PGC-1a and PGC-1-related coactivator (PRC).”
From Skeletal Muscle Ribosome and Mitochondrial Biogenesis in Response to Different Exercise Training Modalities (2021) · cites this paper as Wang et al. (2011)
Wang et al. (2011) showed that performing resistance exercise after cycling enhanced markers of mitochondrial adaptations compared to cycling-only.
“This is supported by the work of Wang et al. (2011), which showed that performing resistance exercise after cycling enhanced markers of mitochondrial adaptations compared to cycling-only.”
From Skeletal Muscle Ribosome and Mitochondrial Biogenesis in Response to Different Exercise Training Modalities (2021) · cites this paper as Wang et al. (2011)
Markers of ribosome biogenesis were not examined in Wang et al. (2011), making it difficult to determine if mitochondrial and ribosome biogenesis coincided.
“However, markers of ribosome biogenesis were not examined making it difficult to determine if mitochondrial and ribosome biogenesis coincided.”
From Skeletal Muscle Ribosome and Mitochondrial Biogenesis in Response to Different Exercise Training Modalities (2021) · cites this paper as Wang et al. (2011)
Wang et al. (2011) showed that performing a bout of resistance exercise after endurance exercise enhanced the signaling cascade for mitochondrial biogenesis.
“Wang et al. (2011) showed that performing a bout of resistance exercise after endurance exercise enhanced the signaling cascade for mitochondrial biogenesis.”
From Skeletal Muscle Ribosome and Mitochondrial Biogenesis in Response to Different Exercise Training Modalities (2021) · cites this paper as Wang et al. (2011)
Other studies have shown that AMPK and mTORC1 can be concomitantly activated.
“However, it is important to note that as previously mentioned, other studies have shown that AMPK and mTORC1 can be concomitantly activated (Wang et al., 2011; Fyfe et al., 2016).”
From Skeletal Muscle Ribosome and Mitochondrial Biogenesis in Response to Different Exercise Training Modalities (2021) · cites this paper as Wang et al., 2011
Performing a strength session immediately after a low-intensity endurance session results in a greater stimulus for endurance adaptation than the low-intensity endurance session alone.
“Performing a strength session immediately after a low-intensity endurance session results in a greater stimulus for endurance adaptation than the low-intensity endurance session alone [68]”
From Using Molecular Biology to Maximize Concurrent Training (2014) · cites this paper as [68]
The citation lists haven’t been fetched yet
References 43 · Cited by 181
- Authors
- Wang, L., Mascher, H., Psilander, N., Blomstrand, E., & Sahlin, K.
- Affiliations
- Swedish School of Sport and Health Sciences (SE)
- Karolinska Institutet (SE)
- Corresponding author
- Sahlin, Kent
- Venue
- Journal of Applied Physiology
- Publisher
- American Physiological Society
- Published
- 2011-11
- Volume
- 111
- Issue
- 5
- Pages
- 1335-1344
- ISSN
- 0161-7567 (ISSN-L)
- 8750-7587
- 1522-1601
- OpenAlex
- W1976972166
- Cited by
- 181
- References
- 43
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 18 · 2023: 6 · 2022: 4 · 2021: 9 · 2020: 12 · 2019: 8 · 2018: 11 · 2017: 21 · 2016: 17 · 2015: 18 · 2014: 15 · 2013: 19 · 2012: 12
- FWCI
- 7.05
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Applied Physiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Vetenskapsrådet
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Sports Performance and Training
- Keywords
- concurrent training, endurance exercise, resistance training, mitochondrial biogenesis, skeletal muscle, PGC-1α, PDK4, mTOR signaling, AMPK, c-Myc, Rheb, oxidative capacity, signaling crosstalk
- MeSH terms
- Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Pyruvate Dehydrogenase Acetyl-Transferring Kinase, Adaptation, Physiological, Adult, Organelle Biogenesis, Female, Heat-Shock Proteins, Humans, Male, Mitochondria, Oxidation-Reduction, Phosphorylation, Physical Endurance, RNA, Messenger, Transcription Factors, Signal Transduction, Biomarkers, Exercise, Protein Serine-Threonine Kinases, Muscle, Skeletal, Cross-Over Studies, Resistance Training, TOR Serine-Threonine Kinases
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.
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 ›
Are you an author, or do you see a problem with this page? Request a review
