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Abstract We examined how resistance exercise (RE), cycling exercise and disuse atrophy affect myosin heavy chain (MyHC) protein fragmentation. The 1boutRE study involved younger men (n = 8; 5 ± 2 years of RE experience) performing a lower body RE bout with vastus lateralis (VL) biopsies being obtained prior to and acutely following exercise. With the 10weekRT study, VL biopsies were obtained in 36 younger adults before and 24 h after their first/naïve RE bout. Participants also engaged in 10 weeks of resistance training and donated VL biopsies before and 24 h after their last RE bout. VL biopsies were also examined in an acute cycling study (n = 7) and a study involving 2 weeks of leg immobilization (n = 20). In the 1boutRE study, fragmentation of all MyHC isoforms (MyHCTotal) increased 3 h post‐RE (∼200%, P = 0.018) and returned to pre‐exercise levels by 6 h post‐RE. Interestingly, a greater magnitude increase in MyHC type IIa versus I isoform fragmentation occurred 3 h post‐RE (8.6 ± 6.3‐fold vs. 2.1 ± 0.7‐fold, P = 0.018). In 10weekRT participants, the first/naïve and last RE bouts increased MyHCTotal fragmentation 24 h post‐RE (+65% and +36%, P

Abstract Migration is one of the most energy-demanding behaviors observed in birds. Mitochondria are the primary source of energy used to support these long-distance movements, yet how mitochondria meet the energetic demands of migration is scarcely studied. We quantified changes in mitochondrial respiratory performance in the White-crowned Sparrow (Zonotrichia leucophrys), which has a migratory and non-migratory subspecies. We hypothesized that the long-distance migratory Gambel’s subspecies (Z. l. gambelii) would show higher mitochondrial respiratory performance compared to the non-migratory Nuttall’s subspecies (Z. l. nuttalli). We sampled Gambel’s individuals during spring pre-migration, active fall migration, and a period with no migration or breeding (winter). We sampled Nuttall’s individuals during periods coinciding with fall migration and the winter period of Gambel’s annual cycle. Overall, Gambel’s individuals had higher citrate synthase, a proxy for mitochondrial volume, than Nuttall’s individuals. This was most pronounced prior to and during migration. We found that both OXPHOS capacity (state 3) and basal respiration (state 4) of mitochondria exhibit high seasonal flexibility within Gambel’s individuals, with values highest during active migration. These values in Nuttall’s individuals were most similar to Gambel’s individuals in winter. Our observations indicate that seasonal changes in mitochondrial respiration play a vital role in migration energetics.

Abstract We recently reported that vastus lateralis (VL) cross‐sectional area (CSA) increases after 7 weeks of resistance training (RT, 2 days/week), with declines occurring following 7 weeks of subsequent treadmill high‐intensity interval training (HIIT) (3 days/week). Herein, we examined the effects of this training paradigm on skeletal muscle proteolytic markers. VL biopsies were obtained from 11 untrained college‐aged males at baseline (PRE), after 7 weeks of RT (MID), and after 7 weeks of HIIT (POST). Tissues were analysed for proteolysis markers, and in vitro experiments were performed to provide additional insights. Atrogene mRNAs (TRIM63, FBXO32, FOXO3A) were upregulated at POST versus both PRE and MID (P 0.05). in vitro experiments recapitulated the training phenotype when stimulated with a hypertrophic stimulus (insulin‐like growth factor 1; IGF1) followed by a subsequent AMP‐activated protein kinase activator (5‐aminoimidazole‐4‐carboxamide ribonucleotide; AICAR), as demonstrated by larger myotube diameter in IGF1‐treated cells versus IGF1 followed by AICAR treatments (I+A; P = 0.017). Muscle protein synthesis (MPS) levels were also greater in IGF1‐treated versus I+A myotubes (P

Aim: To define the role of prophylactic parathyroidectomy in the surgical treatment of medullary thyroid carcinoma (MTC) in multiple endocrine neoplasia type IIa (MEN2A) syndrome through a literature review. Materials and methods: The database of PubMed was searched using the terms “parathyroidectomy” and “medullary” in the fields “Title” and “Abstract”, as well as the Google Scholar database. Articles without references to parathyroid management strategies were mainly excluded. Results: Fourteen articles were reviewed as relevant to this study regarding recommendations for the management of parathyroids during prophylactic thyroidectomy in patients with MTC in MEN2A syndrome. Three of them had the same or similar purpose to our work, and the most recent literature review did not clearly support either one of the two management strategies. References to parathyroid management were found in the rest of the articles, but their purpose was not to determine the appropriate management strategy. The majority of the authors support the preservation of macroscopically normal parathyroid glands, while one study favored routine total parathyroidectomy and autografting. Conclusions: Although there does not seem to be a gold standard, the strategy of preserving macroscopically normal parathyroid glands with routine lab testing and surgical exploration for hyperparathyroidism during thyroidectomy seems to be a safe and effective strategy.

An increase in mechanical loading, such as that which occurs during resistance exercise, induces radial growth of muscle fibers (i.e. an increase in cross-sectional area). Muscle fibers are largely composed of myofibrils, but whether radial growth is mediated by an increase in the size of the myofibrils (i.e. myofibril hypertrophy) and/or the number of myofibrils (i.e. myofibrillogenesis) is not known. Electron microscopy (EM) can provide images with the level of resolution that is needed to address this question, but the acquisition and subsequent analysis of EM images is a time- and cost-intensive process. To overcome this, we developed a novel method for visualizing myofibrils with a standard fluorescence microscope (fluorescence imaging of myofibrils with image deconvolution [FIM-ID]). Images from FIM-ID have a high degree of resolution and contrast, and these properties enabled us to develop pipelines for automated measurements of myofibril size and number. After extensively validating the automated measurements, we used both mouse and human models of increased mechanical loading to discover that the radial growth of muscle fibers is largely mediated by myofibrillogenesis. Collectively, the outcomes of this study offer insight into a fundamentally important topic in the field of muscle growth and provide future investigators with a time- and cost-effective means to study it.

Abstract Background Dietary supplements containing L-arginine are marketed to improve exercise performance, but the efficacy of such supplements is not clear. Therefore, this study examined the efficacy of acute ingestion of L-arginine alpha-ketoglutarate (AAKG) muscular strength and endurance in resistance trained and untrained men. Methods Eight resistance trained and eight untrained healthy males ingested either 3000mg of AAKG or a placebo 45 minutes prior to a resistance exercise protocol in a randomized, double-blind crossover design. One-repetition maximum (1RM) on the standard barbell bench press and leg press were obtained. Upon determination of 1RM, subjects completed repetitions to failure at 60% 1RM on both the standard barbell bench press and leg press. Heart rate was measured pre and post exercise. One week later, subjects ingested the other supplement and performed the identical resistance exercise protocol. Results Our data showed statistical significant differences (p0.05) between supplementation conditions for either resistance trained or untrained men in the bench press or leg press exercises. Heart rate was similar at the end of the upper and lower body bouts of resistance exercise with AAKG vs. placebo. Conclusion The results from our study indicate that acute AAKG supplementation provides no ergogenic benefit on 1RM or TLV as measured by the standard barbell bench press and leg press, regardless of the subjects training status.

Many parameters used to investigate stress in vertebrates are temporally sensitive. The act of capture and sampling can influence them, hindering their functionality for evaluating the effects of stressors. Consequently, the investigation and subsequent incorporation of less time-sensitive parameters are necessary to better evaluate stressors affecting vertebrates. In this study, we investigated how capture stress and handling associated with sampling influence antioxidant status in American Alligators (Alligator mississippiensis (Daudin, 1802); hereinafter Alligator), long-lived, top-trophic carnivores found in the southeastern United States, by measuring levels of two antioxidant enzymes in destructive (brain and pancreas) and nondestructive (tail scutes) tissues: superoxide dismutase 1 (SOD1) and glutathione peroxidase 1 (GPX1). Capture stress had no effect on pancreatic SOD1 and no effect on brain and pancreatic GPX1 (all p > 0.05). However, brain SOD1, scute SOD1, and scute GPX1 were all impacted by capture stress. These disparate results illustrate that the influence of capture stress on antioxidant enzymes in Alligators is tissue and marker dependent, necessitating further investigation. Our results provide a firm foundation to further investigate oxidative status in crocodilians. Key words: Crocodilian, time, oxidative status, health, condition, American Alligator, Alligator mississippiensis De nombreux paramétres employes dans l'étude du stress chez les vertebres varient selon le moment. La capture et l'échantillonnage peuvent les influencer, réduisant du coup leur utilité pour évaluer les effets de facteurs de stress. Par consequent, l'étude, et l'intégration subséquente, de paramétres moins sensibles au moment sont nécessaires pour améliorer l'évaluation des facteurs de stress chez les vertébrés. Nous étudions l'influence du stress associé á la capture et de la manipulation associée á l'échantillonnage sur le statut oxydatif chez les alligators d'Amérique (Alligator mississippiensis (Daudin, 1802)), des carnivores longévifs de niveau trophique supérieur présents dans le sud-est des ?‰tats-Unis, en mesurant les concentrations d'enzymes antioxydantes dans des tissus nécessitant (cerveau et pancréas) ou non (scutelles de la queue) la destruction du spécimen, soit la superoxyde dismutase 1 (SOD1) et la glutathion peroxydase 1 (GPX1). Le stress de capture n'a pas d'effet sur la SOD1 pancréatique ni sur la GPX1 cérébrale et pancréatique (p > 0,05 dans tous les cas). Il a toutefois une incidence sur la SOD1 cérébrale, la SOD1 scutellaire et la GPX1 scutellaire. Ces résultats disparates illustrent le fait que l'influence du stress de capture sur les enzymes antioxydantes chez les alligators dépend du tissu et du marqueur et nécessite donc des études plus poussées. Nos résultats constituent une base solide pour d'autres études du statut oxydatif chez les crocodiliens. [Traduit par la Rédaction] Mots-clés : crocodilien, moment, statut oxydatif, santé, embonpoint, alligator d'Amérique, Alligator mississippiensis, Introduction Physiological biomarkers are often used as important tools to investigate health status and to determine the effects of stressors of wild animals. A large assortment of biomarkers have previously [...]

Developmental environmental stressors can have instructive effects on an organism's phenotype. This developmental plasticity can prepare organisms for potentially stressful future environments, circumventing detrimental effects on fitness. However, the physiological mechanisms underlying such adaptive plasticity are understudied, especially in vertebrates. We hypothesized that captive male zebra finches (Taeniopygia castanotis) exposed to a mild heat conditioning during development would acquire a persisting thermotolerance, and exhibit increased heat‐shock protein (HSP) levels associated with a decrease in oxidative damage when exposed to a high‐intensity stressor in adulthood. To test this, we exposed male finches to a prolonged mild heat conditioning (38°C) or control (22°C) treatment as juveniles. Then in a 2 × 2 factorial manner, these finches were exposed to a high heat stressor (42°C) or control (22°C) treatment as adults. Following the adult treatment, we collected testes and liver tissue and measured HSP70, HSP90, and HSP60 protein levels. In the testes, finches exhibited lower levels of HSP90 and HSP60 when exposed to the high heat stressor in adulthood if they were exposed to the mild heat conditioning as juveniles. In the liver, finches exposed to the high heat stressor in adulthood had reduced HSP90 and HSP60 levels, regardless of whether they were conditioned as juveniles. In some cases, elevated testes HSP60 levels were associated with increased liver oxidative damage and diminishment of a condition‐dependent trait, indicating potential stress‐induced tradeoffs. Our results indicate that a mild conditioning during development can have persisting effects on HSP expression and acquired thermotolerance. Research Highlights: Our results indicate that a mild heat conditioning during development can induce an increase in thermotolerance that persists into adulthood, and results in variation in testes and liver heat‐shock protein expression in response to heat stress. [ABSTRACT FROM AUTHOR]

We examined how resistance exercise (RE), cycling exercise and disuse atrophy affect myosin heavy chain (MyHC) protein fragmentation. The 1boutRE study involved younger men (n = 8; 5 ± 2 years of RE experience) performing a lower body RE bout with vastus lateralis (VL) biopsies being obtained prior to and acutely following exercise. With the 10weekRT study, VL biopsies were obtained in 36 younger adults before and 24 h after their first/naïve RE bout. Participants also engaged in 10 weeks of resistance training and donated VL biopsies before and 24 h after their last RE bout. VL biopsies were also examined in an acute cycling study (n = 7) and a study involving 2 weeks of leg immobilization (n = 20). In the 1boutRE study, fragmentation of all MyHC isoforms (MyHCTotal) increased 3 h post‐RE (∼200%, P = 0.018) and returned to pre‐exercise levels by 6 h post‐RE. Interestingly, a greater magnitude increase in MyHC type IIa versus I isoform fragmentation occurred 3 h post‐RE (8.6 ± 6.3‐fold vs. 2.1 ± 0.7‐fold, P = 0.018). In 10weekRT participants, the first/naïve and last RE bouts increased MyHCTotal fragmentation 24 h post‐RE (+65% and +36%, P < 0.001); however, the last RE bout response was attenuated compared to the first bout (P = 0.045). Although cycling exercise did not alter MyHCTotal fragmentation, ∼8% VL atrophy with 2 weeks of leg immobilization increased MyHCTotal fragmentation (∼108%, P < 0.001). Mechanistic C2C12 myotube experiments indicated that MyHCTotal fragmentation is likely due to calpain proteases. In summary, RE and disuse atrophy increase MyHC protein fragmentation. Research into how ageing and disease‐associated muscle atrophy affect these outcomes is needed. Highlights: What is the central question of this study?How different exercise stressors and disuse affect skeletal muscle myosin heavy chain fragmentation.What is the main finding and its importance?This investigation is the first to demonstrate that resistance exercise and disuse atrophy lead to skeletal muscle myosin heavy chain protein fragmentation in humans. Mechanistic in vitro experiments provide additional evidence that MyHC fragmentation occurs through calpain proteases. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate whether baseline values and acute and chronic changes in androgen receptors (AR) markers, including total AR, cytoplasmic (cAR), and nuclear (nAR) fractions, as well as DNA-binding activity (AR-DNA), are involved in muscle hypertrophy responsiveness by comparing young nonresponder and responder individuals. After 10 wk of resistance training (RT), participants were identified as nonresponders using two typical errors (TE) obtained through two muscle cross-sectional area (mCSA) ultrasound measurements (2 × TE; 4.94%), and the highest responders within our sample were numerically matched. Muscle biopsies were performed at baseline, 24 h after the first RT session (acute responses), and 96 h after the last session (chronic responses). AR, cAR, and nAR were analyzed using Western blotting, and AR-DNA was analyzed using an ELISA-oligonucleotide assay. Twelve participants were identified as nonresponders (ΔmCSA: −1.32%) and 12 as responders (ΔmCSA: 21.35%). There were no baseline differences between groups in mCSA, AR, cAR, nAR, or AR-DNA (P > 0.05). For acute responses, there was a significant difference between nonresponders (+19.5%) and responders (−14.4%) in AR-DNA [effect size (ES) = −1.39; 95% confidence interval (CI): −2.53 to −0.16; P = 0.015]. There were no acute between-group differences in any other AR markers (P > 0.05). No significant differences between groups were observed in chronic responses across any AR markers (P > 0.05). Nonresponders and responders presented similar baseline, acute, and chronic results for the majority of the AR markers. Thus, our findings do not support the influence of AR markers on muscle hypertrophy responsiveness to RT in untrained individuals. NEW & NOTEWORTHY: We explored, for the first time, the influence of androgen receptor (AR) through the separation of cytoplasmic and nuclear cell fractions [i.e., cytoplasmic androgen receptor (cAR), nuclear androgen receptor (nAR), and androgen receptor DNA-binding activity (AR-DNA)] on muscle hypertrophy responsiveness to resistance training. The absence of muscle hypertrophy in naïve individuals does not seem to be explained by baseline values, and acute or chronic changes in AR markers. [ABSTRACT FROM AUTHOR]

Abstract We investigated the effects of aging and long‐term physical activity on markers of mitochondrial function and dynamics in the cortex and cerebellum of female rats. Additionally, we interrogated markers of oxidative damage and antioxidants. Thirty‐four female Lewis rats were separated into three groups. A young group (YNG, n = 10) was euthanized at 6 months of age. Two other groups were aged to 15 months and included a physical activity group (MA‐PA, n = 12) and a sedentary group (MA‐SED, n = 12). There were no age effects for any of the variables investigated, except for SOD2 protein levels in the cortex (+6.5%, p = 0.012). Long‐term physical activity increased mitochondrial complex IV activity in the cortex compared to YNG (+85%, p = 0.016) and MA‐SED (+82%, p = 0.023) and decreased carbonyl levels in the cortex compared to YNG (−12.49%, p = 0.034). Our results suggest that the mitochondrial network and redox state of the brain of females may be more resilient to the aging process than initially thought. Further, voluntary wheel running had minimal beneficial effects on brain markers of oxidative damage and mitochondrial physiology.

Heat shock proteins (HSPs) are important mediators of the normal cellular function and the cellular stress response. As such, HSPs are often utilized to measure the effects of stressors on organisms in vivo. However, multiple variables can influence their expression, including time or season, confounding results. To investigate the utility of HSPs in measuring effects of stressors in a top-trophic carnivore, we captured 20 American Alligators (Alligator mississippiensis (Daudin, 1802)), placed them in burlap sacks for 2 h and collected blood samples over four time points (baseline, 1 and 2 h after placement into burlap sacks, and 24 h after initial capture) to measure plasma corticosterone (the main crocodilian glucocorticoid) and levels of HSP60, HSP70, and HSP90. Time point significantly affected plasma corticosterone levels in Alligators (p < 0.0001), with levels significantly elevated at 1, 2, and 24 h, relative to baseline (all p < 0.05). However, capture stress did not affect HSP60, HSP70, or HSP90 in red blood cells (all p > 0.05). Our results suggest HSPs may be important biomarkers for investigating the impacts of stressors on captive and wild crocodilians, as they are not acutely elevated by capture or handling stress. Key words: body condition index, crocodilian, corticosterone, stress protein, temporal, American Alligator, Alligator mississippiensis. Les protéines de choc thermique (<< heat shock proteins >> ou HSP) sont d'importants médiateurs de la fonction cellulaire normale et de la réaction cellulaire au stress. Elles sont donc souvent utilisées pour mesurer les effets d'agents stressants sur des organismes in vivo. De multiples variables peuvent toutefois influencer leur expression, dont le moment et la saison, ce qui peut compliquer l'interprétation des résultats. Pour étudier l'utilité des HSP pour mesurer les effets d'agents stressants chez un carnivore de troisième ordre, nous avons capturé 20 alligators d'Amérique (Alligator mississippiensis (Daudin, 1802)), les avons placés dans des sacs de jute pendant 2 h et avons prélevé des échantillons sanguins à trois moments (référence, 1 et 2 h après les avoir mis dans les sacs de jute et 24 h après la capture initiale), afin de mesurer les concentrations de corticostérone plasmatique (le principal glucocorticoïde chez l'alligator) et de HSP60, HSP70 et HSP90. Le moment a un effet significatif sur les concentrations de corticostérone plasmatique des alligators (p < 0,0001), ces dernières étant significativement plus grandes après 1, 2 et 24 h que la valeur de référence (tous les p < 0,05). Cependant, le stress associé à la capture n'a pas eu d'incidence sur les concentrations de HSP60, HSP70 et HSP90 dans les globules rouges (tous les p > 0,05). Nos résultats indiqueraient que les HSP pourraient être d'importants biomarqueurs pour l'étude des impacts d'agents stressants sur les crocodiliens vivant en captivité et à l'état sauvage, puisque le stress de capture ou de manipulation ne les rehausse pas de manière aiguë. [Traduit par la Rédaction] Mots-clés: indice d'embonpoint, crocodilien, corticostérone, protéine du stress, temporel, alligator d'Amérique, Alligator mississippiensis., Introduction A multitude of studies have investigated the stress response in avian and non-avian reptiles (e.g., Miles et al. 2007; Lutterschmidt et al. 2009; Wada et al. 2009). However, most [...]

We sought to determine the skeletal muscle genome-wide DNA methylation and mRNA responses to one bout of lower load (LL) versus higher load (HL) resistance exercise. Trained college-aged males (n = 11, 23 ± 4 years old, 4 ± 3 years self-reported training) performed LL or HL bouts to failure separated by one week. The HL bout (i.e., 80 Fail) consisted of four sets of back squats and four sets of leg extensions to failure using 80% of participants estimated one-repetition maximum (i.e., est. 1-RM). The LL bout (i.e., 30 Fail) implemented the same paradigm with 30% of est. 1-RM. Vastus lateralis muscle biopsies were collected before, 3 h, and 6 h after each bout. Muscle DNA and RNA were batch-isolated and analyzed using the 850k Illumina MethylationEPIC array and Clariom S mRNA microarray, respectively. Performed repetitions were significantly greater during the 30 Fail versus 80 Fail (p < 0.001), although total training volume (sets × reps × load) was not significantly different between bouts (p = 0.571). Regardless of bout, more CpG site methylation changes were observed at 3 h versus 6 h post exercise (239,951 versus 12,419, respectively; p < 0.01), and nuclear global ten-eleven translocation (TET) activity, but not global DNA methyltransferase activity, increased 3 h and 6 h following exercise regardless of bout. The percentage of genes significantly altered at the mRNA level that demonstrated opposite DNA methylation patterns was greater 3 h versus 6 h following exercise (~75% versus ~15%, respectively). Moreover, high percentages of genes that were up- or downregulated 6 h following exercise also demonstrated significantly inversed DNA methylation patterns across one or more CpG sites 3 h following exercise (65% and 82%, respectively). While 30 Fail decreased DNA methylation across various promoter regions versus 80 Fail, transcriptome-wide mRNA and bioinformatics indicated that gene expression signatures were largely similar between bouts. Bioinformatics overlay of DNA methylation and mRNA expression data indicated that genes related to “Focal adhesion,” “MAPK signaling,” and “PI3K-Akt signaling” were significantly affected at the 3 h and 6 h time points, and again this was regardless of bout. In conclusion, extensive molecular profiling suggests that post-exercise alterations in the skeletal muscle DNA methylome and mRNA transcriptome elicited by LL and HL training bouts to failure are largely similar, and this could be related to equal volumes performed between bouts.

We sought to determine if manipulating resistance training (RT) variables differentially altered the expression of select sarcoplasmic and myofibril proteins as well as myofibrillar spacing in myofibers. Resistance-trained men (n = 20; 26 ± 3 years old) trained for 8 weeks where a randomized leg performed either a standard (CON) or variable RT protocol (VAR: manipulation of load, volume, muscle action, and rest intervals at each RT session). A pre-training (PRE) vastus lateralis biopsy was obtained from a randomized single leg, and biopsies were obtained from both legs 96 h following the last training bout. The sarcoplasmic protein pool was assayed for proteins involved in energy metabolism, and the myofibril protein pool was assayed for relative myosin heavy chain (MHC) and actin protein abundances. Sections were also histologically analyzed to obtain myofibril spacing characteristics. VAR resulted in ~12% greater volume load (VL) compared to CON (p

Resistance training increases muscle fiber hypertrophy, but the morphological adaptations that occur within muscle fibers remain largely unresolved. Fifteen males with minimal training experience (24±4years, 23.9±3.1kg/m2 body mass index) performed 10weeks of conventional, full-body resistance training (2× weekly). Body composition, the radiological density of the vastus lateralis muscle using peripheral quantitative computed tomography (pQCT), and vastus lateralis muscle biopsies were obtained 1week prior to and 72h following the last training bout. Quantification of myofibril and mitochondrial areas in type I (positive for MyHC I) and II (positive for MyHC IIa/IIx) fibers was performed using immunohistochemistry (IHC) techniques. Relative myosin heavy chain and actin protein abundances per wet muscle weight as well as citrate synthase (CS) activity assays were also obtained on tissue lysates. Training increased whole-body lean mass, mid-thigh muscle cross-sectional area, mean and type II fiber cross-sectional areas (fCSA), and maximal strength values for leg press, bench press, and deadlift (p

Skeletal muscle adaptations to resistance and endurance training include increased ribosome and mitochondrial biogenesis, respectively. Such adaptations are believed to contribute to the notable increases in hypertrophy and aerobic capacity observed with each exercise mode. Data from multiple studies suggest the existence of a competition between ribosome and mitochondrial biogenesis, in which the first adaptation is prioritized with resistance training while the latter is prioritized with endurance training. In addition, reports have shown an interference effect when both exercise modes are performed concurrently. This prioritization/interference may be due to the interplay between the 5’ AMP-activated protein kinase (AMPK) and mechanistic target of rapamycin complex 1 (mTORC1) signaling cascades and/or the high skeletal muscle energy requirements for the synthesis and maintenance of cellular organelles. Negative associations between ribosomal DNA and mitochondrial DNA copy number in human blood cells also provide evidence of potential competition in skeletal muscle. However, several lines of evidence suggest that ribosome and mitochondrial biogenesis can occur simultaneously in response to different types of exercise and that the AMPK-mTORC1 interaction is more complex than initially thought. The purpose of this review is to provide in-depth discussions of these topics. We discuss whether a curious competition between mitochondrial and ribosome biogenesis exists and show the available evidence both in favor and against it. Finally, we provide future research avenues in this area of exercise physiology.

We evaluated mitochondrial dynamics and autophagy by investigating the acute and long-term changes in the liver and skeletal muscle of rats in multiple reproductive stages. A total of 48 rats were used. Rats were randomly assigned to three groups (n = 16 per group): nonreproductive females; females that became pregnant, gave birth, but had their pups removed at birth, and thus, did not lactate; and females that experienced pregnancy, gave birth, and were allowed to lactate. Each group was further divided into two-time subgroups (n = 8 per subgroup) and data were collected at a time-point corresponding to 1) peak lactation (day 14 of lactation) in the lactating animals (4 months of age) and 2) 15 weeks after parturition (12 weeks post-weaning in lactating animals; 7 months of age). Levels of several proteins involved in mitochondrial dynamics and the autophagy system were measured in the liver and skeletal muscle. Beclin1 protein levels in the liver were higher in non-lactating rats two weeks after parturition, while Beclin1 protein levels were highest in 7-month-old animals that had previously experienced a standard reproductive event that included pregnancy and a full 3 week of lactation. These animals also exhibited higher protein levels of the mitochondrial fusion marker Mfn2 in the liver. In skeletal muscle, we also observed increased protein levels of the mitochondrial fission marker DRP1 in non-lactating animals compared to animals that lactated. In summary, our data provide insightful information on the mechanisms that influence liver and skeletal muscle remodeling in response to the metabolic challenges of reproduction, and lactation in particular. Autophagy remodeling and mitochondrial fusion seem to coincide with liver mass size during the lactation stage of reproduction. Our findings highlight the complex changes that occur in the liver and skeletal muscle during reproduction, and highlights the remarkable plasticity required during this demanding metabolic feat.

Dietary carotenoids have been proposed to have physiological benefits in addition to contributing to coloration. Here, Koch et al. compare immune and antioxidant functions in yellow, carotenoid-rich vs. white, carotenoid-deficient canaries and find no difference, suggesting a limited physiological role of carotenoids.