This study investigated the effect of nine nights of sleep restriction, with repeated resistance exercise sessions, on the skeletal muscle transcriptome of young, trained females. Sleep restriction and resistance exercise interacted to alter the enrichment of skeletal muscle transcriptomic pathways in young, resistance-trained females. Performing exercise when sleep restricted may not provide the same adaptive response for individuals as if they were fully rested.
Academic career development relies on a combination of teaching and research skills. In Australia, it is common for recent Doctor of Philosophy graduates to have a short-term post-doctoral research experience to build publication track-record and increase grant competitiveness, before securing a combined research and teaching or ‘academic’ role at a university. Other scientists work as full-time researchers for several years before transitioning to academic roles with expectations they can teach. The aim of this study was to explore the experiences of health and biomedical science researchers transitioning into academic roles using a mixed methods design. Sixty-six participants working in health and biomedical sciences at over 20 Australian Universities who had been in an academic role for 5 years or less completed an online survey. Of 66 participants, 18 (27%) had never been in a research-only role before, while 48 (63%) had held a research-only role for up to 11 years before starting their current academic role. Findings showed most academics were not trained nor equipped to successfully undertake scholarly teaching. They reported a lack of awareness of teaching expectations, practical resources, and direct support provision at the start of their appointment. For former researchers specifically, these experiences led to low confidence and poor enjoyment in their academic role, with the potential to decrease overall teaching quality, student learning and student satisfaction. We postulate that these issues may be mitigated by the implementation of teaching-specific training programs catering for the research-only background of staff entering health and biomedical academic roles in the higher education workforce.
Testosterone, the major androgen, influences the reproductive and non-reproductive systems in males and females via binding to the androgen receptor (AR). Both circulating endogenous testosterone and muscle AR protein content are positively associated with muscle mass and strength in males, but there is no such evidence in females. Here, we tested whether circulating testosterone levels were associated with muscle mass, function, or the muscle anabolic response to resistance training in pre-menopausal females. Twenty-seven pre-menopausal, untrained females (aged 23.5 ± 4.8 years) underwent a 12-week resistance training programme. Muscle strength, size, power, and plasma and urine androgen hormone levels were measured. Skeletal muscle biopsies were collected before and after the training programme to quantify the effect of resistance training on AR content and nuclear localisation. Primary muscle cell lines were cultured from a subset (n = 6) of the participants' biopsies and treated with testosterone to investigate its effect on myotube diameter, markers of muscle protein synthesis and AR cellular localisation. Physiological levels of total testosterone were not associated with muscle mass or strength at baseline or with the changes in muscle mass and strength that occurred in response to resistance training in our cohort of pre-menopausal females. In contrast, bioavailable testosterone and the proportion of nuclear-localised AR were positively associated with skeletal muscle mass and strength in pre-menopausal females. In vitro, supra-physiological doses of testosterone increased myocyte diameter, but this did not occur via the Akt/mTOR pathway as previously suggested. Instead, we show a marked increase in AR nuclear localisation with testosterone administration in vitro. KEY POINTS: Total circulating testosterone was not related to muscle mass or strength before or after resistance training in pre-menopausal females. Bioavailable testosterone was positively related to exercise-induced muscle hypertrophy in pre-menopausal females. In vivo nuclear localisation of the androgen receptor was positively related to muscle mass in pre-menopausal females at baseline, but not to resistance training-induced hypertrophy. Testosterone treatment induced androgen receptor nuclear translocation but did not induce mTOR signalling in primary skeletal myocytes cultured from pre-menopausal female muscle.
Key points Testosterone, the major androgen hormone, influences the reproductive and non-reproductive systems in males and females via binding to the androgen receptor (AR). Both circulating endogenous testosterone and muscle AR protein content are positively associated with muscle mass and strength in males, but there is no such evidence in females. Here, we tested whether circulating testosterone levels were associated with muscle mass, function, or the muscle anabolic response to resistance training in pre-menopausal females. Twenty-seven pre-menopausal, untrained females (aged 23.5 ± 4.8) underwent a 12-week resistance training program. Muscle strength, size, power and plasma and urine androgen hormone levels were measured. Skeletal muscle biopsies were collected before and after the training program to quantify the effect of resistance training on AR protein and mRNA content, and nuclear localisation. Primary muscle cell lines were cultured from a subset (n=6) of the participants’ biopsies and treated with testosterone to investigate its effect on myotube diameter, markers of muscle protein synthesis and AR cellular localisation. Total testosterone was not associated with muscle mass or strength at baseline or with the changes in muscle mass and strength that occurred in response to resistance training. In vitro, supra-physiological doses of testosterone increased myocyte diameter, but this did not occur via the Akt/mTOR pathway as previously suggested. Instead, we show a marked increase in AR nuclear localisation with testosterone administration. In conclusion, we found that, bioavailable testosterone and the proportion of nuclear-localised AR, but not total testosterone, with skeletal muscle mass and strength in pre-menopausal females. ### Competing Interest Statement The authors have declared no competing interest.
ABSTRACT Introduction Female athletes sleep less and report more sleep problems than their male counterparts. Inadequate sleep reduces maximal strength in male athletes; however, little is known about the impact of sleep restriction (SR) on the quantity and quality of resistance exercise performed by female athletes. This study investigated the effect of nine nights of moderate SR on repeated resistance exercise performance, hormonal responses, and perceived fatigue in females. Methods Ten healthy, resistance-trained, eumenorrheic females age 18–35 yr underwent nine nights of SR (5-h time in bed) and normal sleep (NS; ≥7-h time in bed) in a randomized, crossover fashion with a minimum 6-wk washout. Participants completed four resistance exercise sessions per trial, with blood samples collected before and after exercise. Exercise performance was assessed using volume load, reactive strength index, and mean concentric velocity with rating of perceived exertion recorded after exercise. Participants completed awakening saliva sampling and the Multi-component Training Distress Scale daily. Results Volume load decreased trivially (<1%, P < 0.05) with SR. Mean concentric velocity per set was slower during SR for the lower-body (up to 15%, P < 0.05), but not the upper-body, compound lifts. Intraset velocity loss was up to 7% greater during SR for back squats (P < 0.05). SR increased salivary cortisol area under the curve (by 42%), total training distress (by 84%), and session perceived exertion (by 11%). Conclusions Sustained SR reduces markers of resistance exercise quality (bar velocity) more than quantity (volume load) and increases perceived effort at the same relative intensity in resistance-trained females. Markers of exercise quality and internal load may be more sensitive than volume load, to advise coaches to the decline in lifting performance for female athletes experiencing SR.
Despite females representing 50% of the human population, there is a lack of research in female physiology including exercise physiology. Factors that are unique to females such as the menstrual cycle, contraceptive use or menopause, may be perceived as barriers for the inclusion of female cohorts. Researchers need to understand the interplay between the female biological and physiological systems and the interaction between their chosen outcomes. The strategies below can be employed to ensure researchers account for potentially confounding variables in female exercise physiology research.
Chronic sleep loss is a potent catabolic stressor, increasing the risk of metabolic dysfunction and loss of muscle mass and function. To provide mechanistic insight into these clinical outcomes, we sought to determine if acute sleep deprivation blunts skeletal muscle protein synthesis and promotes a catabolic environment. Healthy young adults (N=13; 7 male, 6 female) were subjected to one night of total sleep deprivation (DEP) and normal sleep (CON) in a randomized cross-over design. Anabolic and catabolic hormonal profiles, skeletal muscle fractional synthesis rate and markers of muscle protein degradation were assessed across the following day. Acute sleep deprivation reduced muscle protein synthesis by 18% (CON: 0.072 ± 0.015 vs. DEP: 0.059 ± 0.014 %•h-1, p=0.040). In addition, it increased plasma cortisol by 21% (p=0.030) and decreased plasma testosterone, but not IGF-1, by 22% (p=0.029). A single night of total sleep deprivation is sufficient to induce anabolic resistance and a pro-catabolic environment. These acute changes may represent mechanistic precursors driving the metabolic dysfunction and body composition changes associated with chronic sleep deprivation.
The Journal of PhysiologyVolume 598, Issue 11 p. 2059-2060 Journal ClubFree Access No time to sleep on it – start exercising! Olivia E. Knowles, Corresponding Author Olivia E. Knowles l.knowles@deakin.edu.au orcid.org/0000-0002-5579-1247 Institute for Physical Activity and Nutrition (IPAN), School of Exercise and Nutrition Sciences, Deakin University, Geelong, Victoria, Australia E-mail: l.knowles@deakin.edu.auSearch for more papers by this author Olivia E. Knowles, Corresponding Author Olivia E. Knowles l.knowles@deakin.edu.au orcid.org/0000-0002-5579-1247 Institute for Physical Activity and Nutrition (IPAN), School of Exercise and Nutrition Sciences, Deakin University, Geelong, Victoria, Australia E-mail: l.knowles@deakin.edu.auSearch for more papers by this author First published: 02 April 2020 https://doi.org/10.1113/JP279790Citations: 3 Edited by: Michael Hogan & Troy Hornberger Linked articles: This Perspectives article highlights an article by Saner et al. To read this paper, visit https://doi.org/10.1113/JP278828. AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat The evolution of technology and 24 h workplaces has seen an increase in population groups reporting inadequate sleep. Inadequate sleep is an emerging risk factor for reduced skeletal muscle mass and sarcopenia, along with several other chronic and metabolic diseases that have discernible links to skeletal muscle health. The maintenance of skeletal muscle mass is dependent upon a fine balance between protein synthesis (anabolism) and protein degradation (catabolism) in the muscle. Rodent studies have previously shown that sleep deprivation decreases muscle fibre cross-sectional area, at the same time as down-regulating markers of protein synthesis and up-regulating markers of protein degradation (de Sa Souza et al. 2016). In this issue of The Journal of Physiology, Saner et al. (2020) are the first to investigate the effect of sleep restriction on skeletal muscle protein synthesis in humans. Twenty-four young, healthy males were randomly grouped and assigned to five consecutive nights of either normal sleep conditions (n = 8), sleep restriction (4 h in bed, n = 8), or sleep restriction and high intensity interval exercise (HIIT) (n = 8). The participants underwent an oral deuterium oxide ingestion protocol. An assessment of myofibrillar protein synthesis (MyoPS), as well as markers of protein synthesis and degradation, was performed on muscle biopsies sampled from the vastus lateralis at baseline, pre- and post-study. The primary finding was that sleep restriction reduced the rate of skeletal muscle MyoPS compared to normal sleep; however, there were no changes in the corresponding markers of protein synthesis and degradation. In addition, it was shown that performing HIIT maintained MyoPS rates similar to that of the normal sleep group, suggesting that HIIT may exert a protective effect on MyoPS. These novel and important findings warrant further discussion regarding mechanisms, clinical outcomes and their applicability to sleep-restricted populations. Sleep restriction alone decreased muscle protein synthesis compared to well-rested participants (Saner et al. 2020), suggesting that inadequate sleep directly impacts muscle protein synthesis rates in males. This finding has significant public health consequences because, in Australia, 40% of the adult population is chronically sleep deprived and one in four workers undertake shiftwork. We previously suggested that sustained changes to wake, work and sleep periods directly and indirectly impair the muscle protein balance via alterations to light exposure, sleep patterns and feeding patterns (Aisbett et al. 2017). A recent pre-print by our group (Lamon et al. 2020) confirms the findings of Saner et al. (2020) and provides further proof-of-concept that one night of total sleep deprivation is sufficient to decrease MyoPS in healthy, young males. Muscle protein synthesis is regulated by a combination of mechanical (muscle contraction), nutritional (dietary protein intake) and hormonal stimuli. Exercise levels and nutritional intake were standardized in the study by Saner et al. (2020), yet hormonal markers were not investigated. Identifying the hormonal changes associated with acute and chronic sleep deprivation may provide essential insights into the mechanisms at play. Experimental evidence exists suggesting that inadequate sleep alters anabolic and catabolic hormone secretion patterns in humans, providing a possible mechanism for impaired muscle protein metabolism (Aisbett et al. 2017). Specifically, the major androgenic hormone testosterone is a potent activator of muscle protein synthesis in males. Sleep restriction alters testosterone secretion patterns, and our recent study suggests that reduced testosterone might constitute a mechanism underlying the sleep restriction-induced decrease in muscle protein synthesis in males (Lamon et al. 2020). If sustained sleep restriction leads to skeletal muscle atrophy over time, it is essential not only to understand the mechanisms by which this occurs, but also how we can blunt this effect. The identification of an intervention that could mitigate the negative consequences of sleep restriction on skeletal muscle health is perhaps the most important clinical outcome of the study by Saner et al. (2020). HIIT performed during the sleep restriction period was able to return MyoPS rates to control levels (Saner et al. 2020). Before such findings guide exercise prescription for sleep-restricted populations, two important factors should be resolved. First, confirming the protective effects of HIIT using a within-participant design in order to fully unpack the sleep-training interaction would be an immediate next step. Second, identifying the best mode of training for protecting skeletal muscle health during periods of sleep restriction would optimize translation into practice. Saner et al. (2020) acknowledge that resistance exercise has been demonstrated as a superior mode of exercise for stimulating skeletal muscle protein synthesis compared to HIIT (Bell et al. 2015). In their study, Bell et al. (2015) provided a direct comparison of the muscle protein synthesis response to resistance exercise, HIIT and continuous aerobic exercise. All protocols were designed at a moderate to high intensity, matched for training volume and completed within a 30 min timeframe, equivalent to the duration used in Saner et al. (2020) and in line with physical activity recommendations. With these protocols, they found resistance exercise to increase muscle protein synthesis rates by ∼25% more compared to HIIT at 24 and 48 h post-exercise (Bell et al. 2015). The metabolic response to exercise is mode specific, with MyoPS being particularly sensitive to mechanical loading. The increased load that is placed on the muscle during resistance exercise triggers an adaptive response, where muscle hypertrophy occurs via accumulated bursts of muscle protein synthesis. By contrast, HIIT or aerobic exercise is typically performed under a lower load and involves different patterns of neurological activation, muscle fibre recruitment and energy expenditure. In their study, Saner et al. (2020) successfully implemented a HIIT protocol of ∼25 min in duration. They rationalized that HIIT constitutes a time-efficient stimulus for inducing skeletal muscle protein synthesis amongst other health benefits, including cardiometabolic advantages that are important for insulin sensitivity and mitochondrial function. In addition to being the exercise mode of choice for stimulating the protein synthesis response, resistance exercise can be implemented in an equally time efficient manner (Bell et al. 2015), with wide ranging health benefits, and may therefore constitute the gold standard strategy for increasing MyoPS in sleep-deprived males. Future research should therefore compare the benefits of HIIT and resistance exercise with respect to attenuating reduced rates of MyoPS caused by sleep restriction. If the clinical relevance of the findings from Saner et al. (2020) are considered important for improvements in the skeletal muscle health of sleep-restricted populations, it is imperative that the applicability of these findings are discussed. Saner et al. (2020) recruited young, untrained males. The ratio of male to female participants is almost two-fold greater in sports and exercise medicine research (Knowles et al. 2019) and possibly greater in sleep research. It is therefore easier to compare results from this specific population group with previous research findings. Untrained participants, however, display a higher muscle protein synthesis response to exercise, which diminishes as the organism adapts to training (Bell et al. 2015). Therefore, if we are to encourage populations experiencing inadequate sleep to perform frequent exercise, it would be valuable to understand the implications for trained individuals. It is therefore important to investigate the implications of sleep restriction not only for both HIIT and resistance exercise MyoPS responses, but also in trained participants. In their discussion, Saner et al. (2020) acknowledge the importance of future research that investigates female populations. Although current research suggests that MyoPS rates are similar between males and females (Knowles et al. 2019), this is an important recommendation from the authors. Females report more sleep problems than males, yet there remains a sparsity of research on female populations in this field. The hormone profile of females may influence the muscle protein response, which is less dependent on testosterone and more dependent on oestrogen and progesterone (Knowles et al. 2019). The menstrual cycle also plays a role in regulating sleep and circadian rhythms. If follows that the combination of these factors likely alters the MyoPS response to exercise under sleep-restricted conditions. The current literature has only investigated MyoPS under normal sleep conditions at two stages of the menstrual cycle, when the ratio of oestrogen to progesterone is small. Oestrogen plays a role in skeletal muscle hypertrophy by stimulating the activation and proliferation of satellite cells and up-regulating the Akt/mTOR pathway, whereas progesterone may have a catabolic effect (Knowles et al. 2019). Growth hormone and Insulin-like growth factor-1 are two other candidate hormones that might take over some of the anabolic effects of testosterone in females. These hormones undergo different patterns of variation across the menstrual cycle, although there is a lack of evidence regarding the impact of sleep restriction on their expression levels, especially in females. Although skeletal muscle hypertrophy is largely determined by the mechanical activation of intracellular signalling pathways, it remains important to understand the impact of the menstrual cycle and other biological sex differences on the interaction between exercise, MyoPS and sleep. Saner et al. (2020) have made a significant step toward understanding the negative health consequences of sleep restriction, with and without preventative exercise intervention. Their findings provide a promising platform for future research that can assist the many populations facing an increased risk of poor health outcomes as a a result of inadequate sleep. References Aisbett B, Condo D, Zacharewicz E & Lamon S (2017). The impact of shiftwork on skeletal muscle health. Nutrients 9, 248. Bell KE, Séguin C, Parise G, Baker SK & Phillips SM (2015). Day-to-day changes in muscle protein synthesis in recovery from resistance, aerobic, and high-intensity interval exercise in older men. J Gerontol A Biol Sci Med Sci 70, 1024– 1029. de Sa Souza H, Antunes HKM, Dattilo M, Lee KS, Monico-Neto M, de Campos Giampa SQ, Phillips SM, Tufik S & de Mello MT (2016). Leucine supplementation is anti-atrophic during paradoxical sleep deprivation in rats. Amino Acids 48, 949– 957. Knowles OE, Aisbett B, Main LC, Drinkwater EJ, Orellana L & Lamon S (2019). Resistance training and skeletal muscle protein metabolism in eumenorrheic females: implications for researchers and practitioners. Sports Med 49, 1637– 1650. Lamon S, Morabito A, Arentson-Lantz E, Knowles O, Vincent GE, Condo D, Alexander SE, Garnham A, Paddon-Jones D & Aisbett B (2020). The effect of acute sleep deprivation on skeletal muscle protein synthesis and the hormonal environment. bioRxiv https://doi.org/10.1101/2020.03.09.984666 Saner NJ, Lee MJC, Pitchford NW, Kuang J, Roach GD, Garnham A, Stokes T, Phillips SM, Bishop DJ & Bartlett JD (2020). The effect of sleep restriction, with or without high-intensity interval exercise, on myofibrillar protein synthesis in healthy young men. J Physiol 598, 1523– 1536. Additional information Competing interests No competing interests declared. Author contributions Sole author. Funding No funding. Acknowledgements I would like to acknowledge Dr Séverine Lamon and Associate Professor Brad Aisbett for their insightful feedback on drafts of the manuscript. Citing Literature Volume598, Issue111 June 2020Pages 2059-2060 ReferencesRelatedInformation
Post-graduate programs attract older students, who often work part-time or full-time and have child-care responsibilities. In the Information Age, online learning environments can help these students to meet their learning objectives more efficiently and provide a unique opportunity to address individual learning preferences. The aim of this study was to assess the learning experiences of postgraduate students in an online learning environment delivering content in a guided, self-directed way focusing on active learning opportunities. Two-hundred and eighty-seven students participated in the study. A pragmatic descriptive design with purposive sampling was used to examine the impact of a newly developed active online learning environment on student commitment, performance and satisfaction when compared to a passive, pre-recorded lecture. In contrast to our hypothesis that all metrics would improve with subject redevelopment, student performance and commitment did not improve in the active online learning environment; however, student satisfaction increased significantly. These findings might be partly attributed to the increased cognitive load associated to online learning. This study demonstrates how, for postgraduate students choosing online learning, active learning experiences can be used to provide students with a greater sense of satisfaction while acknowledging for the heterogeneity of the cohort and its different learning preferences. However, in the worldwide context of remote learning rapidly and urgently expanding, it also outlines that online learning needs to be carefully scaffolded to ensure deep learning and that the impact of the transition to online learning on performance and commitment should be considered, especially when directed at non-experienced students.
Resistance training is essential for health and performance and confers many benefits such as increasing skeletal muscle mass, increasing strength and power output, and improving metabolic health. Resistance training is a major component of the physical activity guidelines, yet research in female populations is limited. Recent increases in the promotion of, and the participation by, females in sport and exercise, highlight the need for an increase in understanding of evidence-based best practice exercise prescription for females. The aim of this review is to provide an overview of the current research regarding resistance training performance and skeletal muscle adaptation in females, with a focus on the hormonal variables that may influence resistance training outcomes. Findings suggest that the menstrual cycle phase may impact strength, but not skeletal muscle protein metabolism. In comparison, oral contraception use in females may reduce skeletal muscle protein synthesis, but not strength outcomes, when compared to non-users. Future research should investigate the role of resistance training in the maintenance of skeletal muscle protein metabolism during pregnancy, menopause and in athletes experiencing relative energy deficiency in sport. The review concludes with recommendations for researchers to assist them in the inclusion of female participants in resistance training research specifically, with commentary on the most appropriate methods of controlling for, or understanding the implications of, hormonal fluctuations. For practitioners, the current evidence suggests possible resistance training practices that could optimise performance outcomes in females, although further research is warranted.
Objectives: Inadequate sleep (e.g., an insufficient duration of sleep per night) can reduce physical performance and has been linked to adverse metabolic health outcomes. Resistance exercise is an effective means to maintain and improve physical capacity and metabolic health, however, the outcomes for populations who may perform resistance exercise during periods of inadequate sleep are unknown. The primary aim of this systematic review was to evaluate the effect of sleep deprivation (i.e. no sleep) and sleep restriction (i.e. a reduced sleep duration) on resistance exercise performance. A secondary aim was to explore the effects on hormonal indicators or markers of muscle protein metabolism. Methods: A systematic search of five electronic databases was conducted with terms related to three combined concepts: inadequate sleep; resistance exercise; performance and physiological outcomes. Study quality and biases were assessed using the Effective Public Health Practice Project quality assessment tool. Results: Seventeen studies met the inclusion criteria and were rated as 'moderate' or 'weak' for global quality. Sleep deprivation had little effect on muscle strength during resistance exercise. In contrast, consecutive nights of sleep restriction could reduce the force output of multi-joint, but not single-joint movements. Results were conflicting regarding hormonal responses to resistance training. Conclusion: Inadequate sleep impairs maximal muscle strength in compound movements when performed without specific interventions designed to increase motivation. Strategies to assist groups facing inadequate sleep to effectively perform resistance training may include supplementing their motivation by training in groups or ingesting caffeine; or training prior to prolonged periods of wakefulness. (C) 2018 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.
Adolescents who aspire to excel in both sport and academics are provided the opportunity to pursue their ambitions in a focused and integrated manner at sport schools. Sport schools have been established internationally, yet previous literature tells us little about the outcomes of these students. This study investigated: (1) differences in the time commitments and self-reported health and wellbeing of ‘matched’ samples of sport school and non-sport school students, and (2) the impact of weekly sport volume on sport school students’ health and wellbeing outcomes and burnout.