Acute and chronic sleep loss are linked with a range of negative physiological and psychological outcomes. Sleep deprivation and restriction have the potential to profoundly affect muscle health by altering gene regulation and substrate metabolism. Even relatively short periods of sleep restriction (less than a week) can compromise glucose metabolism, reduce insulin sensitivity, and impair muscle function.
Skeletal muscle is made up of 80% proteins and maintaining optimal muscle protein metabolism is equally critical for muscle health. In situations where skeletal muscle protein synthesis chronically lags protein degradation, a loss of muscle mass is inevitable. Growing body of evidence suggests that a lack of sleep may directly affect muscle protein metabolism, which in turn elevates the risk of various chronic health conditions.
Previous study reported a catabolic gene signature in skeletal muscle following one night of total sleep deprivation in healthy young males. Five consecutive nights of sleep restriction (4 h per night) reduced myofibrillar protein synthesis when compared to normal sleep patterns. The possible mechanisms underlying these effects might involve the hormonal environment.
This study aimed to determine if one night of complete sleep deprivation promotes a catabolic hormonal environment and compromises postprandial muscle protein synthesis and markers of muscle protein degradation.
Thirteen young (18–35 years old), healthy males (7) and females (6) participated in the study. Participants were required to have habitual bed (22:00–00:00) and wake (06:00–08:00) times that were broadly consistent with the experimental protocol and to self-report obtaining a minimum of 7 h of sleep per night.
Participants completed a control (CON) and experimental (DEP; sleep deprivation) trial in a randomized, crossover design. Trials were separated by at least 4 weeks to allow for a full recovery.
On the night before CON or DEP trial, a standardized meal was provided to participants at 19:00. At 07:30 participants consumed a standardized breakfast.
On the night of the sleep deprivation trial (DEP), participants reported to the laboratory at 21:00 where they were limited to sedentary activities (i.e., reading a book, watching a movie). Participants were constantly observed by research personnel and monitored by actigraphy to ensure they did not fall asleep.
For the control trial (CON), participants were permitted to sleep from 22:00 to 07:00 at home. At 07:00, the participants were woken up, and venous blood samples were immediately collected prior to any physical activity or light exposure.
At 08:00, an 18-gauge cannula was inserted into the antecubital vein of each arm for blood sampling and the primed, constant infusion of L-[ring-13C6]-phenylalanine from 10:00 to 15:00.
Venous blood samples were collected every hour from 07:00 to 17:00. Plasma cortisol, testosterone, and insulin growth factor-1 (IGF-1) concentrations were measured.
Blood amino acids were extracted by cation exchange chromatography. Phenylalanine enrichments were determined by gas chromatography-mass spectrometry (GC-MS).
Skeletal muscle samples were obtained at 13:00 and 15:00 under local anesthesia at separate locations from the belly of the vastus lateralis muscle using a percutaneous needle biopsy technique. Muscle samples were used for the measurement of isotopic enrichment and gene expression analysis.
Muscle proteins were extracted from biopsy samples. Isotopic enrichments of L-[ring-13C6]-phenylalanine in tissue fluid were determined by GC-MS and used as a precursor pool for the calculation of the fractionalsynthesis rate.
Muscle biopsies collected at 13:00 were used for gene expression analysis. mRNA levels for ARNTL (BMAL1), CRY1, PER1, IGF-1Ea, IGF-1Eb, FBX032 (atrogin-1), TRIM63 (MuRF-1), FOXO1, and FOXO3 were measured
Sleep deprivation reduced postprandial muscle protein fractional synthesis rate (FSR) by 18% (CON: 0.072 ± 0.015% vs. DEP: 0.059 ± 0.014%・h-1, p = 0.040).
Sleep deprivation decreased plasma testosterone by 24% (CON: 6.40 ± 5.28 AU vs. DEP: 4.86 ± 3.64 AU, p =0.029).
Plasma cortisol levels were significantly higher (p = 0.014) in the CON condition than in the DEP condition at 07:00 (wake time for CON). At 10:00, plasma cortisol was similar in both sleep conditions (p = 0.940), but by 16:00, cortisol was significantly higher in the DEP condition (p = 0.048). Plasma cortisol area under the curve (10:00–16:00) was 21% higher during DEP than CON (CON: 186 ± 41.7 AU vs. DEP: 226 ± 44.6 AU, p = 0.011).
Sleep deprivation did not influence the plasma IGF-1 concentrations and muscle expression levels of IGF1mRNA isoforms IGF1-Ea and IGF1-Eb when measured in the postprandial state. Plasma insulin concentrations varied across the day, but there was no effect of sleep deprivation.
The muscle expression levels of core clock genes ARNTL, CRY1, and PER1 or muscle protein degradation markers FBOX-32, MURF1, FOXO1, and FOXO3 did not change in response to sleep deprivation.
The study demonstrated that total sleep deprivation induces anabolic resistance by reducing postprandial muscle protein synthesis in young males and females. Sleep deprivation also promoted a catabolic environment, providing insights into the possible mechanisms underlying this process.
Lamon S et al. (2021) The effect of acute sleep deprivation on skeletal muscle protein synthesis and the hormonal environment. Physiological Reports 9, e14660.
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