Evidence map›Paper›PMID 35233984›Full record

Trial reportJournal of cachexia, sarcopenia and muscle2022

Pharmacological hypogonadism impairs molecular transducers of exercise-induced muscle growth in humans.

Nima Gharahdaghi, Supreeth Rudrappa, Matthew S Brook, Wesam Farrash, Iskandar Idris, Muhammad Hariz Abdul Aziz, Fawzi Kadi, Konstantinos Papaioannou, Bethan E Phillips, Tanvir Sian and 5 more

Open access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Journal of cachexia, sarcopenia and muscle, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.8field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 16 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 2 institutions in 3 countries.

Nima GharahdaghiMRC-Verus Arthritis Centre for Musculoskeletal Ageing Research and Nottingham NIHR BRC, School of Medicine, University of Nottingham, Derby, UK.ORCID 0000-0002-4650-244X
Supreeth RudrappaMRC-Verus Arthritis Centre for Musculoskeletal Ageing Research and Nottingham NIHR BRC, School of Medicine, University of Nottingham, Derby, UK.
Matthew S BrookMRC-Verus Arthritis Centre for Musculoskeletal Ageing Research and Nottingham NIHR BRC, School of Medicine, University of Nottingham, Derby, UK.
Wesam FarrashMRC-Verus Arthritis Centre for Musculoskeletal Ageing Research and Nottingham NIHR BRC, School of Medicine, University of Nottingham, Derby, UK.
Iskandar IdrisMRC-Verus Arthritis Centre for Musculoskeletal Ageing Research and Nottingham NIHR BRC, School of Medicine, University of Nottingham, Derby, UK.
Muhammad Hariz Abdul AzizMRC-Verus Arthritis Centre for Musculoskeletal Ageing Research and Nottingham NIHR BRC, School of Medicine, University of Nottingham, Derby, UK.
Fawzi KadiDivision of Sports Sciences, School of Health and Medical Sciences, Örebro University, Örebro, Sweden.
Konstantinos PapaioannouDivision of Sports Sciences, School of Health and Medical Sciences, Örebro University, Örebro, Sweden.
Bethan E PhillipsMRC-Verus Arthritis Centre for Musculoskeletal Ageing Research and Nottingham NIHR BRC, School of Medicine, University of Nottingham, Derby, UK.
Tanvir SianMRC-Verus Arthritis Centre for Musculoskeletal Ageing Research and Nottingham NIHR BRC, School of Medicine, University of Nottingham, Derby, UK.
Philip J HerrodMRC-Verus Arthritis Centre for Musculoskeletal Ageing Research and Nottingham NIHR BRC, School of Medicine, University of Nottingham, Derby, UK.
Daniel J WilkinsonMRC-Verus Arthritis Centre for Musculoskeletal Ageing Research and Nottingham NIHR BRC, School of Medicine, University of Nottingham, Derby, UK.
Nathaniel J SzewczykMRC-Verus Arthritis Centre for Musculoskeletal Ageing Research and Nottingham NIHR BRC, School of Medicine, University of Nottingham, Derby, UK.
Kenneth SmithMRC-Verus Arthritis Centre for Musculoskeletal Ageing Research and Nottingham NIHR BRC, School of Medicine, University of Nottingham, Derby, UK.
Philip J AthertonMRC-Verus Arthritis Centre for Musculoskeletal Ageing Research and Nottingham NIHR BRC, School of Medicine, University of Nottingham, Derby, UK.ORCID 0000-0002-7286-046X
University of Nottingham · GBÖrebro University · SE

Funding

Medical Research Council MR/P021220/1Medical Research Council MR/R502364/1
6 · The paper itself

Abstract

backgroundThe relative role of skeletal muscle mechano-transduction in comparison with systemic hormones, such as testosterone (T), in regulating hypertrophic responses to exercise is contentious. We investigated the mechanistic effects of chemical endogenous T depletion adjuvant to 6 weeks of resistance exercise training (RET) on muscle mass, function, myogenic regulatory factors, and muscle anabolic signalling in younger men.

methodsNon-hypogonadal men (n = 16; 18-30 years) were randomized in a double-blinded fashion to receive placebo (P, saline n = 8) or the GnRH analogue, Goserelin [Zoladex (Z), 3.6 mg, n = 8], injections, before 6 weeks of supervised whole-body RET. Participants underwent dual-energy X-ray absorptiometry (DXA), ultrasound of m. vastus lateralis (VL), and VL biopsies for assessment of cumulative muscle protein synthesis (MPS), myogenic gene expression, and anabolic signalling pathway responses.

resultsZoladex suppressed endogenous T to within the hypogonadal range and was well tolerated; suppression was associated with blunted fat free mass [Z: 55.4 ± 2.8 to 55.8 ± 3.1 kg, P = 0.61 vs. P: 55.9 ± 1.7 to 57.4 ± 1.7 kg, P = 0.006, effect size (ES) = 0.31], composite strength (Z: 40 ± 2.3% vs. P: 49.8 ± 3.3%, P = 0.03, ES = 1.4), and muscle thickness (Z: 2.7 ± 0.4 to 2.69 ± 0.36 cm, P > 0.99 vs. P: 2.74 ± 0.32 to 2.91 ± 0.32 cm, P < 0.0001, ES = 0.48) gains. Hypogonadism attenuated molecular transducers of muscle growth related to T metabolism (e.g. androgen receptor: Z: 1.2 fold, P > 0.99 vs. P: 1.9 fold, P < 0.0001, ES = 0.85), anabolism/myogenesis (e.g. IGF-1Ea: Z: 1.9 fold, P = 0.5 vs. P: 3.3 fold, P = 0.0005, ES = 0.72; IGF-1Ec: Z: 2 fold, P > 0.99 vs. P: 4.7 fold, P = 0.0005, ES = 0.68; myogenin: Z: 1.3 fold, P > 0.99 vs. P: 2.7 fold, P = 0.002, ES = 0.72), RNA/DNA (Z: 0.47 ± 0.03 to 0.53 ± 0.03, P = 0.31 vs. P: 0.50 ± 0.01 to 0.64 ± 0.04, P = 0.003, ES = 0.72), and RNA/ASP (Z: 5.8 ± 0.4 to 6.8 ± 0.5, P > 0.99 vs. P: 6.5 ± 0.2 to 8.9 ± 1.1, P = 0.008, ES = 0.63) ratios, as well as acute RET-induced phosphorylation of growth signalling proteins (e.g. AKT

conclusionsWe conclude that endogenous T sufficiency has a central role in the up-regulation of molecular transducers of RET-induced muscle hypertrophy in humans that cannot be overcome by muscle mechano-transduction alone.

Indexed as

HypogonadismResistance TrainingExerciseHumansMaleMuscle, SkeletalTransducersExercise trainingHypertrophyMuscle protein synthesisTestosterone

Identifiers

PMID35233984
PMCPMC8977972
OpenAlexW4214851749

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.