scholarly journals Exercise mitigates sleep-loss-induced changes in glucose tolerance, mitochondrial function, sarcoplasmic protein synthesis, and circadian rhythms

2020 ◽  
Author(s):  
Nicholas J Saner ◽  
Matthew J-C Lee ◽  
Jujiao Kuang ◽  
Nathan W Pitchford ◽  
Gregory D Roach ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Circadian Rhythms ◽  
Glucose Tolerance ◽  
Mitochondrial Function ◽  
Sleep Loss ◽  
Physiological Processes ◽  
Sarcoplasmic Protein ◽  
Concomitant Reduction ◽  
High Intensity Interval ◽  
Inadequate Sleep

AbstractSleep loss has emerged as a risk factor for the development of impaired glucose tolerance. The mechanisms underpinning this observation are unknown; however, both mitochondrial dysfunction and circadian misalignment have been proposed. Given that exercise improves glucose tolerance, mitochondrial function, and alters circadian rhythms, we investigated whether exercise may counteract the effects induced by inadequate sleep. We report that sleeping 4 hours per night, for five nights, reduced glucose tolerance, with novel observations of associated reductions in mitochondrial function, sarcoplasmic protein synthesis, and measures of circadian rhythmicity; however, incorporating three sessions of high-intensity interval exercise (HIIE) during this period mitigates these effects. These data demonstrate, for the first time, a sleep loss-induced concomitant reduction in a range of physiological processes linked to metabolic function. These same effects are not observed when exercise is performed during a period of inadequate sleep, supporting the use of HIIE as an intervention to mitigate the detrimental physiological effects of sleep loss.

scholarly journals Hypoenergetic diet-induced reductions in myofibrillar protein synthesis are restored with resistance training and balanced daily protein ingestion in older men

2015 ◽  
Vol 308 (9) ◽  
pp. E734-E743 ◽  
Author(s):  
Caoileann H. Murphy ◽  
Tyler A. Churchward-Venne ◽  
Cameron J. Mitchell ◽  
Nathan M. Kolar ◽  
Amira Kassis ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Resistance Training ◽  
Older Men ◽  
Myofibrillar Protein ◽  
Energy Restriction ◽  
Protein Distribution ◽  
Protein Meal ◽  
Fed State ◽  
Sarcoplasmic Protein ◽  
Myofibrillar Protein Synthesis

Strategies to enhance weight loss with a high fat-to-lean ratio in overweight/obese older adults are important since lean loss could exacerbate sarcopenia. We examined how dietary protein distribution affected muscle protein synthesis during energy balance (EB), energy restriction (ER), and energy restriction plus resistance training (ER + RT). A 4-wk ER diet was provided to overweight/obese older men (66 ± 4 yr, 31 ± 5 kg/m2) who were randomized to either a balanced (BAL: 25% daily protein/meal × 4) or skewed (SKEW: 7:17:72:4% daily protein/meal; n = 10/group) pattern. Myofibrillar and sarcoplasmic protein fractional synthetic rates (FSR) were measured during a 13-h primed continuous infusion of l-[ ring-13C6]phenylalanine with BAL and SKEW pattern of protein intake in EB, after 2 wk ER, and after 2 wk ER + RT. Fed-state myofibrillar FSR was lower in ER than EB in both groups ( P < 0.001), but was greater in BAL than SKEW ( P = 0.014). In ER + RT, fed-state myofibrillar FSR increased above ER in both groups and in BAL was not different from EB ( P = 0.903). In SKEW myofibrillar FSR remained lower than EB ( P = 0.002) and lower than BAL ( P = 0.006). Fed-state sarcoplasmic protein FSR was reduced similarly in ER and ER + RT compared with EB ( P < 0.01) in both groups. During ER in overweight/obese older men a BAL consumption of protein stimulated the synthesis of muscle contractile proteins more effectively than traditional, SKEW distribution. Combining RT with a BAL protein distribution “rescued” the lower rates of myofibrillar protein synthesis during moderate ER.

scholarly journals The amnestic agent anisomycin disrupts intrinsic membrane properties of hippocampal neurons via a loss of cellular energetics

2019 ◽  
Vol 122 (3) ◽  
pp. 1123-1135 ◽  
Author(s):  
C. J. Scavuzzo ◽  
M. J. LeBlancq ◽  
F. Nargang ◽  
H. Lemieux ◽  
T. J. Hamilton ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Mitochondrial Function ◽  
Neural Activity ◽  
Memory Consolidation ◽  
Hippocampal Neurons ◽  
Membrane Properties ◽  
Long Term Memory ◽  
Term Memory ◽  
Cellular Energetics

The nearly axiomatic idea that de novo protein synthesis is necessary for long-term memory consolidation is based heavily on behavioral studies using translational inhibitors such as anisomycin. Although inhibiting protein synthesis has been shown to disrupt the expression of memory, translational inhibitors also have been found to profoundly disrupt basic neurobiological functions, including the suppression of ongoing neural activity in vivo. In the present study, using transverse hippocampal brain slices, we monitored the passive and active membrane properties of hippocampal CA1 pyramidal neurons using intracellular whole cell recordings during a brief ~30-min exposure to fast-bath-perfused anisomycin. Anisomycin suppressed protein synthesis to 46% of control levels as measured using incorporation of radiolabeled amino acids and autoradiography. During its application, anisomycin caused a significant depolarization of the membrane potential, without any changes in apparent input resistance or membrane time constant. Anisomycin-treated neurons also showed significant decreases in firing frequencies and spike amplitudes, and showed increases in spike width across spike trains, without changes in spike threshold. Because these changes indicated a loss of cellular energetics contributing to maintenance of ionic gradients across the membrane, we confirmed that anisomycin impaired mitochondrial function by reduced staining with 2,3,5-triphenyltetrazolium chloride and also impaired cytochrome c oxidase (complex IV) activity as indicated through high-resolution respirometry. These findings emphasize that anisomycin-induced alterations in neural activity and metabolism are a likely consequence of cell-wide translational inhibition. Critical reevaluation of studies using translational inhibitors to promote the protein synthesis dependent idea of long-term memory is absolutely necessary. NEW & NOTEWORTHY Memory consolidation is thought to be dependent on the synthesis of new proteins because translational inhibitors produce amnesia when administered just after learning. However, these agents also disrupt basic neurobiological functions. We show that blocking protein synthesis disrupts basic membrane properties of hippocampal neurons that correspond to induced disruptions of mitochondrial function. It is likely that translational inhibitors cause amnesia through their disruption of neural activity as a result of dysfunction of intracellular energetics.

The Acquisition and Maintenance of Thermotolerance in Australian Wheats

1990 ◽  
Vol 17 (1) ◽  
pp. 37 ◽  
Author(s):  
C Blumenthal ◽  
F Bekes ◽  
CW Wrigley ◽  
EWR Barlow
Keyword(s):  
Heat Treatment ◽  
Triticum Aestivum ◽  
Protein Synthesis ◽  
High Temperature ◽  
Heat Shock ◽  
High Temperature Stress ◽  
Time Interval ◽  
Degree Of Protection ◽  
Concomitant Reduction ◽  
Shock Proteins

The exposure of wheat (Triticum aestivum) coleoptiles to a transient high temperature stress results in the synthesis of a group of proteins known as the heat shock proteins (hsps). The appearance of these proteins is associated with a concomitant reduction in normal protein synthesis and has been correlated with the acquisition of thermotolerance (assessed as growth of coleoptiles). Pretreatment with a sublethal heat shock confers protection to a subsequent heat shock that would otherwise have been lethal. In addition, we find that increasing the time interval between the sublethal heat treatment and the subsequent heat shock from 0 to 72 h reduces the protective effect of the sublethal heat treatment considerably. The five cultivars examined (Sunelg, Sunco, Hartog, Vulcan, Halberd) showed differences in the degree of protection acquired, and in the length of time for which protection was maintained. Hartog was found to be the most thermotolerant, and acquired the greatest degree of protection from exposure to a sublethal heat treatment, but the duration of this acquired protection was shorter than in the remaining cultivars. Sunelg was most susceptible to a heat shock but the duration of acquired protection was the greatest.

scholarly journals Physiological responses to food intake throughout the day

2014 ◽  
Vol 27 (1) ◽  
pp. 107-118 ◽  
Author(s):  
Jonathan D. Johnston
Keyword(s):  
Circadian Rhythms ◽  
Unmet Need ◽  
Time Of Day ◽  
Research Field ◽  
Biological Data ◽  
Model Systems ◽  
Physiological Processes ◽  
Circadian Timing System ◽  
Glucose Profiles ◽  
Molecular Components

Circadian rhythms act to optimise many aspects of our biology and thereby ensure that physiological processes are occurring at the most appropriate time. The importance of this temporal control is demonstrated by the strong associations between circadian disruption, morbidity and disease pathology. There is now a wealth of evidence linking the circadian timing system to metabolic physiology and nutrition. Relationships between these processes are often reciprocal, such that the circadian system drives temporal changes in metabolic pathways and changes in metabolic/nutritional status alter core molecular components of circadian rhythms. Examples of metabolic rhythms include daily changes in glucose homeostasis, insulin sensitivity and postprandial response. Time of day alters lipid and glucose profiles following individual meals whereas, over a longer time scale, meal timing regulates adiposity and body weight; these changes may occur via the ability of timed feeding to synchronise local circadian rhythms in metabolically active tissues. Much of the work in this research field has utilised animal and cellular model systems. Although these studies are highly informative and persuasive, there is a largely unmet need to translate basic biological data to humans. The results of such translational studies may open up possibilities for using timed dietary manipulations to help restore circadian synchrony and downstream physiology. Given the large number of individuals with disrupted rhythms due to, for example, shift work, jet-lag, sleep disorders and blindness, such dietary manipulations could provide widespread improvements in health and also economic performance.

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