FitProven
Evidence Breakdown
Based on 3 studies
THE BIGGER QUESTION
Whether this one statement holds is settled above. What to actually do about it is a wider question, weighed across every claim that bears on it.
- What's the right way to train for muscle growth? — this claim is one of 5 weighed there
Evidence map
For & against, at a glance
Crossover Trial
Pro
Lamon S et al. · 2021Physiological Reports**This is not a review.** The paper matching this author list is an original randomised crossover trial (Physiological Reports 2021, doi 10.14814/phy2.14660): 13 healthy young adults (7 male, 6 female) each underwent one night of total sleep deprivation and one night of normal sleep, in randomised order. Postprandial myofibrillar protein fractional synthesis rate was measured from muscle biopsies with stable-isotope tracers between 13:00 and 15:00, and hormones across the following day. One night of total sleep deprivation reduced muscle protein synthesis by 18% (0.072 ± 0.015 vs 0.059 ± 0.014 %·h⁻¹, p = .040), raised plasma cortisol by 21% (p = .030) and lowered plasma testosterone by 24% (p = .029). Markers of muscle protein degradation were unchanged. IGF-1 and systemic inflammation were not among the outcomes. The authors conclude that a single night of total sleep deprivation is enough to induce anabolic resistance and a pro-catabolic environment — an acute mechanistic result, not the chronic sleep restriction the claim is usually about.
0.26
**This is not a review.** The paper matching this author list is an original randomised crossover trial (Physiological Reports 2021, doi 10.14814/phy2.14660): 13 healthy young adults (7 male, 6 female) each underwent one night of total sleep deprivation and one night of normal sleep, in randomised order. Postprandial myofibrillar protein fractional synthesis rate was measured from muscle biopsies with stable-isotope tracers between 13:00 and 15:00, and hormones across the following day. One night of total sleep deprivation reduced muscle protein synthesis by 18% (0.072 ± 0.015 vs 0.059 ± 0.014 %·h⁻¹, p = .040), raised plasma cortisol by 21% (p = .030) and lowered plasma testosterone by 24% (p = .029). Markers of muscle protein degradation were unchanged. IGF-1 and systemic inflammation were not among the outcomes. The authors conclude that a single night of total sleep deprivation is enough to induce anabolic resistance and a pro-catabolic environment — an acute mechanistic result, not the chronic sleep restriction the claim is usually about.
Design Crossover Trial (0.75) × quality 0.35 = impact 0.26
View sourceNon-Randomized Trial
Neutral
Leproult R & Van Cauter E · 2011JAMATen healthy young men spent 3 nights with 10 h in bed (rested condition) and then 8 consecutive nights restricted to 5 h in bed, with blood sampled across the following day. Daytime testosterone (08:00–22:00) fell by 10–15% versus the rested condition, the drop being clearest in the afternoon and evening (15.5 vs 17.9 nmol/L, p = 0.02). Note the design is **sequential within-subject, not randomised or crossover** — the rested condition always came first — so order and adaptation effects cannot be separated from the sleep-restriction effect. The paper measures a hormonal surrogate over one week; it does **not** measure muscle mass, strength or protein synthesis, and the authors draw no conclusion about muscle-building capacity. Any link to hypertrophy is an inference laid on top of this study, not a finding in it.
0.27
Ten healthy young men spent 3 nights with 10 h in bed (rested condition) and then 8 consecutive nights restricted to 5 h in bed, with blood sampled across the following day. Daytime testosterone (08:00–22:00) fell by 10–15% versus the rested condition, the drop being clearest in the afternoon and evening (15.5 vs 17.9 nmol/L, p = 0.02). Note the design is **sequential within-subject, not randomised or crossover** — the rested condition always came first — so order and adaptation effects cannot be separated from the sleep-restriction effect. The paper measures a hormonal surrogate over one week; it does **not** measure muscle mass, strength or protein synthesis, and the authors draw no conclusion about muscle-building capacity. Any link to hypertrophy is an inference laid on top of this study, not a finding in it.
Design Non-Randomized Trial (0.6) × quality 0.45 = impact 0.27
View sourceExpert Opinion
Neutral
Dattilo M et al. · 2011Medical Hypotheses**A three-page hypothesis paper in Medical Hypotheses (pp. 220–222), not a systematic review** — it contains no search strategy, no included studies, no participants and no data. The authors set out a mechanistic proposal: because sleep deprivation raises cortisol and lowers testosterone and IGF-1, they "hypothesize that sleep debt decreases protein synthesis pathways and increases degradation pathways, favoring the loss of muscle mass and thus hindering muscle recovery." That is a conjecture the paper advances, not a finding it demonstrates. Treat it as a mechanistic rationale to be tested, not as evidence that the effect exists.
0.04
**A three-page hypothesis paper in Medical Hypotheses (pp. 220–222), not a systematic review** — it contains no search strategy, no included studies, no participants and no data. The authors set out a mechanistic proposal: because sleep deprivation raises cortisol and lowers testosterone and IGF-1, they "hypothesize that sleep debt decreases protein synthesis pathways and increases degradation pathways, favoring the loss of muscle mass and thus hindering muscle recovery." That is a conjecture the paper advances, not a finding it demonstrates. Treat it as a mechanistic rationale to be tested, not as evidence that the effect exists.
Design Expert Opinion (0.2) × quality 0.20 = impact 0.04
View sourceCrossover Trial
Pro
Lamon S et al. · 2021Physiological Reports**This is not a review.** The paper matching this author list is an original randomised crossover trial (Physiological Reports 2021, doi 10.14814/phy2.14660): 13 healthy young adults (7 male, 6 female) each underwent one night of total sleep deprivation and one night of normal sleep, in randomised order. Postprandial myofibrillar protein fractional synthesis rate was measured from muscle biopsies with stable-isotope tracers between 13:00 and 15:00, and hormones across the following day. One night of total sleep deprivation reduced muscle protein synthesis by 18% (0.072 ± 0.015 vs 0.059 ± 0.014 %·h⁻¹, p = .040), raised plasma cortisol by 21% (p = .030) and lowered plasma testosterone by 24% (p = .029). Markers of muscle protein degradation were unchanged. IGF-1 and systemic inflammation were not among the outcomes. The authors conclude that a single night of total sleep deprivation is enough to induce anabolic resistance and a pro-catabolic environment — an acute mechanistic result, not the chronic sleep restriction the claim is usually about.
0.26
**This is not a review.** The paper matching this author list is an original randomised crossover trial (Physiological Reports 2021, doi 10.14814/phy2.14660): 13 healthy young adults (7 male, 6 female) each underwent one night of total sleep deprivation and one night of normal sleep, in randomised order. Postprandial myofibrillar protein fractional synthesis rate was measured from muscle biopsies with stable-isotope tracers between 13:00 and 15:00, and hormones across the following day. One night of total sleep deprivation reduced muscle protein synthesis by 18% (0.072 ± 0.015 vs 0.059 ± 0.014 %·h⁻¹, p = .040), raised plasma cortisol by 21% (p = .030) and lowered plasma testosterone by 24% (p = .029). Markers of muscle protein degradation were unchanged. IGF-1 and systemic inflammation were not among the outcomes. The authors conclude that a single night of total sleep deprivation is enough to induce anabolic resistance and a pro-catabolic environment — an acute mechanistic result, not the chronic sleep restriction the claim is usually about.
Design Crossover Trial (0.75) × quality 0.35 = impact 0.26
View sourceNon-Randomized Trial
Neutral
Leproult R & Van Cauter E · 2011JAMATen healthy young men spent 3 nights with 10 h in bed (rested condition) and then 8 consecutive nights restricted to 5 h in bed, with blood sampled across the following day. Daytime testosterone (08:00–22:00) fell by 10–15% versus the rested condition, the drop being clearest in the afternoon and evening (15.5 vs 17.9 nmol/L, p = 0.02). Note the design is **sequential within-subject, not randomised or crossover** — the rested condition always came first — so order and adaptation effects cannot be separated from the sleep-restriction effect. The paper measures a hormonal surrogate over one week; it does **not** measure muscle mass, strength or protein synthesis, and the authors draw no conclusion about muscle-building capacity. Any link to hypertrophy is an inference laid on top of this study, not a finding in it.
0.27
Ten healthy young men spent 3 nights with 10 h in bed (rested condition) and then 8 consecutive nights restricted to 5 h in bed, with blood sampled across the following day. Daytime testosterone (08:00–22:00) fell by 10–15% versus the rested condition, the drop being clearest in the afternoon and evening (15.5 vs 17.9 nmol/L, p = 0.02). Note the design is **sequential within-subject, not randomised or crossover** — the rested condition always came first — so order and adaptation effects cannot be separated from the sleep-restriction effect. The paper measures a hormonal surrogate over one week; it does **not** measure muscle mass, strength or protein synthesis, and the authors draw no conclusion about muscle-building capacity. Any link to hypertrophy is an inference laid on top of this study, not a finding in it.
Design Non-Randomized Trial (0.6) × quality 0.45 = impact 0.27
View sourceExpert Opinion
Neutral
Dattilo M et al. · 2011Medical Hypotheses**A three-page hypothesis paper in Medical Hypotheses (pp. 220–222), not a systematic review** — it contains no search strategy, no included studies, no participants and no data. The authors set out a mechanistic proposal: because sleep deprivation raises cortisol and lowers testosterone and IGF-1, they "hypothesize that sleep debt decreases protein synthesis pathways and increases degradation pathways, favoring the loss of muscle mass and thus hindering muscle recovery." That is a conjecture the paper advances, not a finding it demonstrates. Treat it as a mechanistic rationale to be tested, not as evidence that the effect exists.
0.04
**A three-page hypothesis paper in Medical Hypotheses (pp. 220–222), not a systematic review** — it contains no search strategy, no included studies, no participants and no data. The authors set out a mechanistic proposal: because sleep deprivation raises cortisol and lowers testosterone and IGF-1, they "hypothesize that sleep debt decreases protein synthesis pathways and increases degradation pathways, favoring the loss of muscle mass and thus hindering muscle recovery." That is a conjecture the paper advances, not a finding it demonstrates. Treat it as a mechanistic rationale to be tested, not as evidence that the effect exists.
Design Expert Opinion (0.2) × quality 0.20 = impact 0.04
View sourceTap any node to expand its detail.
Evidence
PRO (1)
PRO Crossover Trialn=130.35 Lamon S, Morabito A et al. (2021)
One night of total sleep deprivation cut myofibrillar protein synthesis by 18% (p = 0.040), raised plasma cortisol by 21% (p = 0.030) and lowered plasma testosterone by 24% (p = 0.029); markers of protein degradation were unchanged
This is not a review. The paper matching this author list is an original randomised crossover trial (Physiological Reports 2021, doi 10.14814/phy2.14660): 13 healthy young adults (7 male, 6 female) each underwent one night of total sleep deprivation and one night of normal sleep, in randomised order. Postprandial myofibrillar protein fractional synthesis rate was measured from muscle biopsies with stable-isotope tracers between 13:00 and 15:00, and hormones across the following day. One night of total sleep deprivation reduced muscle protein synthesis by 18% (0.072 ± 0.015 vs 0.059 ± 0.014 %·h⁻¹, p = .040), raised plasma cortisol by 21% (p = .030) and lowered plasma testosterone by 24% (p = .029). Markers of muscle protein degradation were unchanged. IGF-1 and systemic inflammation were not among the outcomes. The authors conclude that a single night of total sleep deprivation is enough to induce anabolic resistance and a pro-catabolic environment — an acute mechanistic result, not the chronic sleep restriction the claim is usually about.
Weighted 0.35 — CITATION METADATA IN THIS RECORD IS WRONG. The DOI 10.1016/j.smrv.2021.101490 resolves to Boardman et al. on sleep loss and error-monitoring -- a different paper, different authors, nothing to do with muscle. The source matching this author list is Lamon et al., Physiological Reports 2021, doi 10.14814/phy2.14660, which is an ORIGINAL randomised crossover (n=13; 7 male, 6 female), NOT a narrative review -- so journal and study_type in this record are also wrong. The metadata recorded here describes the real paper. On its own merits it is a small but rigorous crossover using muscle biopsies and stable-isotope tracers; it tests a single night of TOTAL deprivation rather than the chronic restriction the claim is usually about, and it contains no funding statement. Weight held down pending correction of the citation.
Physiological Reports
NEUTRAL (2)
NEUTRAL Non-Randomized Trialn=100.45 Leproult R, Van Cauter E (2011)
Daytime testosterone fell 10-15% after eight nights restricted to 5 hours in bed, compared with the rested condition
Ten healthy young men spent 3 nights with 10 h in bed (rested condition) and then 8 consecutive nights restricted to 5 h in bed, with blood sampled across the following day. Daytime testosterone (08:00–22:00) fell by 10–15% versus the rested condition, the drop being clearest in the afternoon and evening (15.5 vs 17.9 nmol/L, p = 0.02). Note the design is sequential within-subject, not randomised or crossover — the rested condition always came first — so order and adaptation effects cannot be separated from the sleep-restriction effect. The paper measures a hormonal surrogate over one week; it does not measure muscle mass, strength or protein synthesis, and the authors draw no conclusion about muscle-building capacity. Any link to hypertrophy is an inference laid on top of this study, not a finding in it.
Weighted 0.45 — Only 10 young healthy men, and the design is a sequential within-subject comparison (3 nights of 10 h in bed, then 8 nights of 5 h) rather than a randomised or crossover trial -- order, adaptation and carry-over effects cannot be separated from the sleep-restriction effect, so the 'rct' type label is generous. Publicly funded with no disclosures. It measures a hormonal surrogate over one week, not muscle mass or strength, so it is indirect evidence for any muscle-building claim.
Funding: US National Institutes of Health (NHLBI 5R01HL72694-5; NIDDK P60DK-020595; NIH MO1-RR-00055)
JAMA
NEUTRAL Expert Opinion0.20 Dattilo M, Antunes HK et al. (2011)
No primary data and no pooled estimate — the paper HYPOTHESISES that sleep debt lowers protein synthesis (via reduced GH/IGF-1 and testosterone) and raises degradation (via cortisol), favouring muscle loss
A three-page hypothesis paper in Medical Hypotheses (pp. 220–222), not a systematic review — it contains no search strategy, no included studies, no participants and no data. The authors set out a mechanistic proposal: because sleep deprivation raises cortisol and lowers testosterone and IGF-1, they "hypothesize that sleep debt decreases protein synthesis pathways and increases degradation pathways, favoring the loss of muscle mass and thus hindering muscle recovery." That is a conjecture the paper advances, not a finding it demonstrates. Treat it as a mechanistic rationale to be tested, not as evidence that the effect exists.
Weighted 0.20 — This is a 3-page hypothesis paper in Medical Hypotheses, not a systematic review: no search strategy, no included-studies table, no data synthesis, and no participants — so no sample size applies. Its own abstract says "we hypothesize". It should be read as a mechanistic proposal, not as evidence that the effect exists, and the multiplier is set near the floor to stop the systematic-review base weight from crediting it with rigour it does not have. No funding statement is retrievable (paywalled), and the DOI recorded here does not resolve to this paper.
Medical Hypotheses