Cost savings through continuous vital sign monitoring in the medical-surgical unit.

OBJECTIVE: This study aimed to determine the potential cost-savings for implementing continuous vital sign monitoring in a hospital's medical-surgical units. METHODS: A cost-savings analysis was designed to calculate potential cost-savings for an average-sized U.S. community hospital (153 total beds) over a 1-year time horizon. Analysis parameters were extracted from national databases and previous studies that compared outcomes for patients receiving continuous vital sign monitoring (SpO2, HR, and RR) or standard of care (intermittent vital sign measurements) in medical-surgical units based on a targeted literature review. Clinical parameters and associated costs served as analysis inputs. The analysis outputs were costs and potential cost-savings using a 50% and 100% adoption rate of continuous monitoring technologies across the medical-surgical unit. RESULTS: Potential annual cost-savings for in-hospital medical-surgical stays were estimated at $3,414,709 (2022 USD) and $6,829,418 for a 50% and 100% adoption rate, respectively. The cost-savings for an adoption rate of 100% equated to a ∼14% reduction in the overall annual cost of medical-surgical unit stays for an average-sized hospital. The largest contribution to potential cost-savings came from patients that avoided serious adverse events that require transfer to the intensive care unit; this resulted in annual cost-savings from reduced average length of stay between $1,756,613 and $3,513,226 (50% and 100% adoption rate, respectively). Additional cost-savings can be attained from reductions in in-hospital cardiac arrest-associated hospitalizations and decreased rapid response team activation. CONCLUSIONS: Our findings demonstrate that there is the potential for cost-savings of over $6.8 million dollars per year in an average-sized US community hospital by improving patient outcomes through implementation of continuous monitoring technologies in medical-surgical units. Continuous vital sign monitoring technologies that increase patient mobility and facilitate recovery may further contribute to cost-savings and should be considered for economic analyses. Future research is needed to explore these health-related outcomes.

Brain total creatine differs between primary progressive aphasia (PPA) subtypes and correlates with disease severity.

Primary progressive aphasia (PPA) is comprised of three subtypes: logopenic (lvPPA), non-fluent (nfvPPA), and semantic (svPPA). We used magnetic resonance spectroscopy (MRS) to measure tissue-corrected metabolite levels in the left inferior frontal gyrus (IFG) and right sensorimotor cortex (SMC) from 61 PPA patients. We aimed to: (1) characterize subtype differences in metabolites; and (2) test for metabolite associations with symptom severity. tCr differed by subtype across the left IFG and right SMC. tCr levels were lowest in lvPPA and highest in svPPA. tCr levels predicted lvPPA versus svPPA diagnosis. Higher IFG tCr and lower Glx correlated with greater disease severity. As tCr is involved in brain energy metabolism, svPPA pathology might involve changes in specific cellular energy processes. Perturbations to cellular energy homeostasis in language areas may contribute to symptoms. Reduced cortical excitatory capacity (i.e. lower Glx) in language regions may also contribute to symptoms. Thus, tCr may be useful for differentiating between PPA subtypes, and both tCr and Glx might have utility in understanding PPA mechanisms and tracking progression.

Intensive Care Unit Acquired Weakness Is Associated with Rapid Changes to Skeletal Muscle Proteostasis.

Intensive care unit (ICU)-acquired weakness is a frequent consequence of critical illness that impacts both the limb and respiratory muscles. The cause of ICU-acquired weakness is multifactorial, but both prolonged limb muscle inactivity and mechanical ventilation are risk factors for muscle wasting, which predisposes ICU patients to both short-term complications and long-term disabilities resulting from muscle weakness. Unfortunately, the current research does not provide a detailed understanding of the cellular etiology of ICU-acquired weakness, and no standard treatment exists. Therefore, improving knowledge of the mechanisms promoting muscle atrophy in critically ill patients is essential to developing therapeutic strategies to protect against ICU-induced skeletal muscle wasting. To advance our understanding of the mechanism(s) responsible for ICU-acquired weakness, we tested the hypothesis that ICU-induced muscle inactivity promotes a rapid decrease in anabolic signaling/protein synthesis and accelerates proteolysis in both limb and respiratory muscles. To investigate ICU-induced changes in skeletal muscle proteostasis, adult Sprague Dawley rats were anesthetized and mechanically ventilated for 12 h to simulate ICU care. Measurements of anabolic signaling, protein synthesis, and proteolytic activity in the limb muscles (plantaris and soleus) and respiratory muscles (parasternal and intercostal) revealed ICU-induced reductions in both anabolic signaling (i.e., AKT/mTOR pathway) and muscle protein synthesis. Moreover, simulated ICU care resulted in increased biomarkers of accelerated proteolysis in both limb and respiratory muscles. These novel findings reveal that disturbances in limb and respiratory muscle proteostasis occur rapidly during ICU-induced muscle inactivity, irrespective of the muscle function or muscle fiber type.

Activation of Calpain Contributes to Mechanical Ventilation-Induced Depression of Protein Synthesis in Diaphragm Muscle.

Mechanical ventilation (MV) is a clinical tool that provides respiratory support to patients unable to maintain adequate alveolar ventilation on their own. Although MV is often a life-saving intervention in critically ill patients, an undesired side-effect of prolonged MV is the rapid occurrence of diaphragmatic atrophy due to accelerated proteolysis and depressed protein synthesis. Investigations into the mechanism(s) responsible for MV-induced diaphragmatic atrophy reveal that activation of the calcium-activated protease, calpain, plays a key role in accelerating proteolysis in diaphragm muscle fibers. Moreover, active calpain has been reported to block signaling events that promote protein synthesis (i.e., inhibition of mammalian target of rapamycin (mTOR) activation). While this finding suggests that active calpain can depress muscle protein synthesis, this postulate has not been experimentally verified. Therefore, we tested the hypothesis that active calpain plays a key role in the MV-induced depression of both anabolic signaling events and protein synthesis in the diaphragm muscle. MV-induced activation of calpain in diaphragm muscle fibers was prevented by transgene overexpression of calpastatin, an endogenous inhibitor of calpain. Our findings indicate that overexpression of calpastatin averts MV-induced activation of calpain in diaphragm fibers and rescues the MV-induced depression of protein synthesis in the diaphragm muscle. Surprisingly, deterrence of calpain activation did not impede the MV-induced inhibition of key anabolic signaling events including mTOR activation. However, blockade of calpain activation prevented the calpain-induced cleavage of glutaminyl-tRNA synthetase in diaphragm fibers; this finding is potentially important because aminoacyl-tRNA synthetases play a central role in protein synthesis. Regardless of the mechanism(s) responsible for calpain's depression of protein synthesis, these results provide the first evidence that active calpain plays an important role in promoting the MV-induced depression of protein synthesis within diaphragm fibers.

Short and long-term effect of reproduction on mitochondrial dynamics and autophagy in rats.

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.

Mitochondrial Dysfunction Is a Common Denominator Linking Skeletal Muscle Wasting Due to Disease, Aging, and Prolonged Inactivity.

Skeletal muscle is the most abundant tissue in the body and is required for numerous vital functions, including breathing and locomotion. Notably, deterioration of skeletal muscle mass is also highly correlated to mortality in patients suffering from chronic diseases (e.g., cancer). Numerous conditions can promote skeletal muscle wasting, including several chronic diseases, cancer chemotherapy, aging, and prolonged inactivity. Although the mechanisms responsible for this loss of muscle mass is multifactorial, mitochondrial dysfunction is predicted to be a major contributor to muscle wasting in various conditions. This systematic review will highlight the biochemical pathways that have been shown to link mitochondrial dysfunction to skeletal muscle wasting. Importantly, we will discuss the experimental evidence that connects mitochondrial dysfunction to muscle wasting in specific diseases (i.e., cancer and sepsis), aging, cancer chemotherapy, and prolonged muscle inactivity (e.g., limb immobilization). Finally, in hopes of stimulating future research, we conclude with a discussion of important future directions for research in the field of muscle wasting.

Angiotensin 1-7 protects against ventilator-induced diaphragm dysfunction.

Mechanical ventilation (MV) is a life-saving instrument used to provide ventilatory support for critically ill patients and patients undergoing surgery. Unfortunately, an unintended consequence of prolonged MV is the development of inspiratory weakness due to both diaphragmatic atrophy and contractile dysfunction; this syndrome is labeled ventilator-induced diaphragm dysfunction (VIDD). VIDD is clinically important because diaphragmatic weakness is an important contributor to problems in weaning patients from MV. Investigations into the pathogenesis of VIDD reveal that oxidative stress is essential for the rapid development of VIDD as redox disturbances in diaphragm fibers promote accelerated proteolysis. Currently, no standard treatment exists to prevent VIDD and, therefore, developing a strategy to avert VIDD is vital. Guided by evidence indicating that activation of the classical axis of the renin-angiotensin system (RAS) in diaphragm fibers promotes oxidative stress and VIDD, we hypothesized that activation of the nonclassical RAS signaling pathway via angiotensin 1-7 (Ang1-7) will protect against VIDD. Using an established animal model of prolonged MV, our results disclose that infusion of Ang1-7 protects the diaphragm against MV-induced contractile dysfunction and fiber atrophy in both fast and slow muscle fibers. Further, Ang1-7 shielded diaphragm fibers against MV-induced mitochondrial damage, oxidative stress, and protease activation. Collectively, these results reveal that treatment with Ang1-7 protects against VIDD, in part, due to diminishing oxidative stress and protease activation. These important findings provide robust evidence that Ang1-7 has the therapeutic potential to protect against VIDD by preventing MV-induced contractile dysfunction and atrophy of both slow and fast muscle fibers.

Alterations in renin-angiotensin receptors are not responsible for exercise preconditioning of skeletal muscle fibers.

Endurance exercise training promotes a protective phenotype in skeletal muscle known as exercise preconditioning. Exercise preconditioning protects muscle fibers against a variety of threats including inactivity-induced muscle atrophy. The mechanism(s) responsible for exercise preconditioning remain unknown and are explored in these experiments. Specifically, we investigated the impact of endurance exercise training on key components of the renin-angiotensin system (RAS). The RAS was targeted because activation of the classical axis of the RAS pathway via angiotensin II type I receptors (AT1Rs) promotes muscle atrophy whereas activation of the non-classical RAS axis via Mas receptors (MasRs) inhibits the atrophic signaling of the classical RAS pathway. Guided by prior studies, we hypothesized that an exercise-induced decrease in AT1Rs and/or increases in MasRs in skeletal muscle fibers is a potential mechanism responsible for exercise preconditioning. Following endurance exercise training in rats, we examined the abundance of AT1Rs and MasRs in both locomotor and respiratory muscles. Our results indicate that endurance exercise training does not alter the protein abundance of AT1Rs or MasRs in muscle fibers from the diaphragm, plantaris, and soleus muscles compared to sedentary controls (p â€‹> â€‹0.05). Furthermore, fluorescent angiotensin II (AngII) binding analyses confirm our results that exercise preconditioning does not alter the protein abundance of AT1Rs in the diaphragm, plantaris, and soleus (p â€‹> â€‹0.05). This study confirms that exercise-induced changes in RAS receptors are not a key mechanism that contributes to the beneficial effects of exercise preconditioning in skeletal muscle fibers.

Calpains play an essential role in mechanical ventilation-induced diaphragmatic weakness and mitochondrial dysfunction.

Mechanical ventilation (MV) is a life-saving intervention for many critically ill patients. Unfortunately, an unintended consequence of prolonged MV is the rapid development of diaphragmatic atrophy and contractile dysfunction, known as ventilator-induced diaphragm dysfunction (VIDD). Although the mechanism(s) responsible for VIDD are not fully understood, abundant evidence reveals that oxidative stress leading to the activation of the major proteolytic systems (i.e., autophagy, ubiquitin-proteasome, caspase, and calpain) plays a dominant role. Of the proteolytic systems involved in VIDD, calpain has received limited experimental attention due to the longstanding dogma that calpain plays a minor role in inactivity-induced muscle atrophy. Guided by preliminary experiments, we tested the hypothesis that activation of calpains play an essential role in MV-induced oxidative stress and the development of VIDD. This premise was rigorously tested by transgene overexpression of calpastatin, an endogenous inhibitor of calpains. Animals with/without transfection of the calpastatin gene in diaphragm muscle fibers were exposed to 12 h of MV. Results confirmed that overexpression of calpastatin barred MV-induced activation of calpain in diaphragm fibers. Importantly, deterrence of calpain activation protected the diaphragm against MV-induced oxidative stress, fiber atrophy, and contractile dysfunction. Moreover, prevention of calpain activation in the diaphragm forstalled MV-induced mitochondrial dysfunction and prevented MV-induced activation of caspase-3 along with the transcription of muscle specific E3 ligases. Collectively, these results support the hypothesis that calpain activation plays an essential role in the early development of VIDD. Further, these findings provide the first direct evidence that calpain plays an important function in inactivity-induced mitochondrial dysfunction and oxidative stress in skeletal muscle fibers.

Comparative Efficacy of Angiotensin II Type 1 Receptor Blockers Against Ventilator-Induced Diaphragm Dysfunction in Rats.

Mechanical ventilation (MV) is a life-saving intervention for many critically ill patients. Unfortunately, prolonged MV results in the rapid development of inspiratory muscle weakness due to diaphragmatic atrophy and contractile dysfunction (termed ventilator-induced diaphragm dysfunction (VIDD)). Although VIDD is a major risk factor for problems in weaning patients from MV, a standard therapy to prevent VIDD does not exist. However, emerging evidence suggests that pharmacological blockade of angiotensin II type 1 receptors (AT1Rs) protects against VIDD. Nonetheless, the essential characteristics of AT1R blockers (ARBs) required to protect against VIDD remain unclear. To determine the traits of ARBs that are vital for protection against VIDD, we compared the efficacy of two clinically relevant ARBs, irbesartan and olmesartan; these ARBs differ in molecular structure and effects on AT1Rs. Specifically, olmesartan blocks both angiotensin II (AngII) binding and mechanical activation of AT1Rs, whereas irbesartan prevents only AngII binding to AT1Rs. Using a well-established preclinical model of prolonged MV, we tested the hypothesis that compared with irbesartan, olmesartan provides greater protection against VIDD. Our results reveal that irbesartan does not protect against VIDD whereas olmesartan defends against both MV-induced diaphragmatic atrophy and contractile dysfunction. These findings support the hypothesis that olmesartan is superior to irbesartan in protecting against VIDD and are consistent with the concept that blockade of mechanical activation of AT1Rs is a required property of ARBs to shield against VIDD. These important findings provide a foundation for future clinical trials to evaluate ARBs as a therapy to protect against VIDD.

The Role of Calpains in Skeletal Muscle Remodeling with Exercise and Inactivity-induced Atrophy.

Calpains are cysteine proteases expressed in skeletal muscle fibers and other cells. Although calpain was first reported to act as a kinase activating factor in skeletal muscle, the consensus is now that calpains play a canonical role in protein turnover. However, recent evidence reveals new and exciting roles for calpains in skeletal muscle. This review will discuss the functions of calpains in skeletal muscle remodeling in response to both exercise and inactivity-induced muscle atrophy. Calpains participate in protein turnover and muscle remodeling by selectively cleaving target proteins and creating fragmented proteins that can be further degraded by other proteolytic systems. Nonetheless, an often overlooked function of calpains is that calpain-mediated cleavage of proteins can result in fragmented proteins that are biologically active and have the potential to actively influence cell signaling. In this manner, calpains function beyond their roles in protein turnover and influence downstream signaling effects. This review will highlight both the canonical and noncanonical roles that calpains play in skeletal muscle remodeling including sarcomere transformation, membrane repair, triad junction formation, regulation of excitation-contraction coupling, protein turnover, cell signaling, and mitochondrial function. We conclude with a discussion of key unanswered questions regarding the roles that calpains play in skeletal muscle.

Human and Rodent Skeletal Muscles Express Angiotensin II Type 1 Receptors.

Abundant evidence reveals that activation of the renin-angiotensin system promotes skeletal muscle atrophy in several conditions including congestive heart failure, chronic kidney disease, and prolonged mechanical ventilation. However, controversy exists about whether circulating angiotensin II (AngII) promotes skeletal muscle atrophy by direct or indirect effects; the centerpiece of this debate is the issue of whether skeletal muscle fibers express AngII type 1 receptors (AT1Rs). While some investigators assert that skeletal muscle expresses AT1Rs, others argue that skeletal muscle fibers do not contain AT1Rs. These discordant findings in the literature are likely the result of study design flaws and additional research using a rigorous experimental approach is required to resolve this issue. We tested the hypothesis that AT1Rs are expressed in both human and rat skeletal muscle fibers. Our premise was tested using a rigorous, multi-technique experimental design. First, we established both the location and abundance of AT1Rs on human and rat skeletal muscle fibers by means of an AngII ligand-binding assay. Second, using a new and highly selective AT1R antibody, we carried out Western blotting and determined the abundance of AT1R protein within isolated single muscle fibers from humans and rats. Finally, we confirmed the presence of AT1R mRNA in isolated single muscle fibers from rats. Our results support the hypothesis that AT1Rs are present in both human and rat skeletal muscle fibers. Moreover, our experiments provide the first evidence that AT1Rs are more abundant in fast, type II muscle fibers as compared with slow, type I fibers. Together, these discoveries provide the foundation for an improved understanding of the mechanism(s) responsible for AngII-induced skeletal muscle atrophy.

Exercise-induced oxidative stress: Friend or foe?

The first report demonstrating that prolonged endurance exercise promotes oxidative stress in humans was published more than 4 decades ago. Since this discovery, many ensuing investigations have corroborated the fact that muscular exercise increases the production of reactive oxygen species (ROS) and results in oxidative stress in numerous tissues including blood and skeletal muscles. Although several tissues may contribute to exercise-induced ROS production, it is predicted that muscular contractions stimulate ROS production in active muscle fibers and that skeletal muscle is a primary source of ROS production during exercise. This contraction-induced ROS generation is associated with (1) oxidant damage in several tissues (e.g., increased protein oxidation and lipid peroxidation), (2) accelerated muscle fatigue, and (3) activation of biochemical signaling pathways that contribute to exercise-induced adaptation in the contracting muscle fibers. While our understanding of exercise and oxidative stress has advanced rapidly during the last decades, questions remain about whether exercise-induced increases in ROS production are beneficial or harmful to health. This review addresses this issue by discussing the site(s) of oxidant production during exercise and detailing the health consequences of exercise-induced ROS production.

Mechanisms of exercise-induced preconditioning in skeletal muscles.

Endurance exercise training promotes numerous biochemical adaptations within skeletal muscle fibers culminating into a phenotype that is safeguarded against numerous perils including doxorubicin-induced myopathy and inactivity-induced muscle atrophy. This exercise-induced protection of skeletal muscle fibers is commonly termed "exercise preconditioning". This review will discuss the biochemical mechanisms responsible for exercise-induced protection of skeletal muscle fibers against these harmful events. The first segment of this report highlights the evidence that endurance exercise training provides cytoprotection to skeletal muscle fibers against several potentially damaging insults. The second and third sections of the review will discuss the cellular adaptations responsible for exercise-induced protection of skeletal muscle fibers against doxorubicin-provoked damage and inactivity-induced fiber atrophy, respectively. Importantly, we also identify gaps in our understanding of exercise preconditioning in hopes of stimulating future research.

Redox Control of Proteolysis During Inactivity-Induced Skeletal Muscle Atrophy.

Significance: Skeletal muscles play essential roles in key body functions including breathing, locomotion, and glucose homeostasis; therefore, maintaining healthy skeletal muscles is important. Prolonged periods of muscle inactivity (e.g., bed rest, mechanical ventilation, or limb immobilization) result in skeletal muscle atrophy and weakness. Recent Advances: Disuse skeletal muscle atrophy occurs due to both accelerated proteolysis and decreased protein synthesis with proteolysis playing a leading role in some types of inactivity-induced atrophy. Although all major proteolytic systems are involved in inactivity-induced proteolysis in skeletal muscles, growing evidence indicates that both calpain and autophagy play an important role. Regulation of proteolysis in skeletal muscle is under complex control, but it is established that activation of both calpain and autophagy is directly linked to oxidative stress. Critical Issues: In this review, we highlight the experimental evidence that supports a cause and effect link between reactive oxygen species (ROS) and activation of both calpain and autophagy in skeletal muscle fibers during prolonged inactivity. We also review the sources of oxidant production in muscle fibers during inactivity-induced atrophy, and provide a detailed discussion on how ROS activates both calpain and autophagy during disuse muscle wasting. Future Directions: Future studies are required to delineate the specific mechanisms by which ROS activates both calpain and autophagy in skeletal muscles during prolonged periods of contractile inactivity. This knowledge is essential to develop the most effective strategies to protect against disuse muscle atrophy. Antioxid. Redox Signal. 33, 559-569.

Disturbances in Calcium Homeostasis Promotes Skeletal Muscle Atrophy: Lessons From Ventilator-Induced Diaphragm Wasting.

Mechanical ventilation (MV) is often a life-saving intervention for patients in respiratory failure. Unfortunately, a common and undesired consequence of prolonged MV is the development of diaphragmatic atrophy and contractile dysfunction. This MV-induced diaphragmatic weakness is commonly labeled "ventilator-induced diaphragm dysfunction" (VIDD). VIDD is an important clinical problem because diaphragmatic weakness is a major risk factor for the failure to wean patients from MV; this inability to remove patients from ventilator support results in prolonged hospitalization and increased morbidity and mortality. Although several processes contribute to the development of VIDD, it is clear that oxidative stress leading to the rapid activation of proteases is a primary contributor. While all major proteolytic systems likely contribute to VIDD, emerging evidence reveals that activation of the calcium-activated protease calpain plays a required role. This review highlights the signaling pathways leading to VIDD with a focus on the cellular events that promote increased cytosolic calcium levels and the subsequent activation of calpain within diaphragm muscle fibers. In particular, we discuss the emerging evidence that increased mitochondrial production of reactive oxygen species promotes oxidation of the ryanodine receptor/calcium release channel, resulting in calcium release from the sarcoplasmic reticulum, accelerated proteolysis, and VIDD. We conclude with a discussion of important and unanswered questions associated with disturbances in calcium homeostasis in diaphragm muscle fibers during prolonged MV.

Body Composition and Perceived Stress through a Calendar Year in NCAA I Female Volleyball Players.

The aim of the study was to track changes of perceived stress and body composition across an entire calendar year in National Collegiate Athletic Association (NCAA) division I female volleyball players. We hypothesized that perceived stress and body composition would vary between the competitive season and off-season, with the largest changes occurring during time points prior to the onset and after the end of the competitive season. Eight female volleyball players participated in a longitudinal study. Body mass, body mass index (BMI), percent body fat, fat mass, and fat free mass were obtained during the early, mid, late, and off season and during the pre, early, mid, and late competitive season. The perceived stress scale-10 was used to appraise stress levels. BMI and body mass were significantly higher in pre-season compared to early-offseason. Changes in BMI between these points were due to increase in fat mass. Fat mass and percent body fat were significantly higher in pre-season compared to late off-season, mid-season, and late season. Perceived stress was significantly higher at the mid-season compared to early offseason. A significant positive correlation existed between BMI and body fat (p<0.05, r=0.69), while a significant negative correlation existed between percent body fat and perceived stress (p<0.05, r=0.34). Tracking body composition and perceived stress in collegiate female volleyball players can provide informative feedback on the training status and well-being of female collegiate athletes. Interestingly, it appears stress in these athletes may be more dependent upon the school session rather than participation in competitive sports.

Effects of a Sprint Interval and Resistance Concurrent Exercise Training Program on Aerobic Capacity of Inactive Adult Women.

Salom Huffman, L, Wadsworth, DD, McDonald, JR, Foote, SJ, Hyatt, H, and Pascoe, DD. Effects of a sprint interval and resistance concurrent exercise training program on aerobic capacity of inactive adult women. J Strength Cond Res 33(6): 1641-1648, 2019-The purpose of this investigation was to examine the effects of high-intensity concurrent exercise training (CET) consisting of sprint intervals (sprint interval training [SIT]) and resistance exercise (RET) protocols on aerobic capacity in recreationally active, adult women. A total of 53 participants were pair-matched according to preliminary maximal aerobic capacity (VO2max) Bruce protocol assessment into level-grade (SIT0) or 6% incline (SIT6) groups. This 12-week intervention consisted of 3 CET sessions per week. Sprint interval protocol consisted of 2 (weeks 1-6) then 3 (weeks 7-12) sets of three 40-second sprints at specific intensities to evoke responses equivalent to 95% of age-predicted maximal heart rate interspersed with 20 seconds of rest; with 1 minute of passive recovery between sets. An undulating periodization model consisting of lifts such as the back squat and bench press constituted the RET component. Protocol order alternated each session. Posttraining revealed significant improvements in both SIT0 and SIT6 (p ≤ 0.05) for VO2max (2.11 ± 0.390 to 2.29 ± 0.382 L·min; 2.03 ± 0.382 to 2.09 ± 0.561 L·min), Tmax (490.5 ± 102.3 to 542.7 ± 81.5 seconds; 503.2 ± 75.4 to 541.8 ± 77.0 seconds), and Vmax (5.1 ± 0.92 miles per hour [MPH] to 5.9 ± 0.90 MPH; 4.3 ± 0.68 MPH to 4.9 ± 0.64 MPH), respectively. No significant between-group interactions were detected for any of the variables. Our SIT-based CET intervention represents an effective strategy to induce significant cardiovascular adaptations in older women as evident by aerobic capacity improvements, beneficial to overall health and critical for functionality into old age; an important concern for aging women.

Changes in Metabolism, Mitochondrial Function, and Oxidative Stress Between Female Rats Under Nonreproductive and 3 Reproductive Conditions.

Women who do not lactate display increased incidence of obesity, type II diabetes, and cancer. Stuebe and Rich-Edwards proposed that these effects occur because physiological changes that ensue during pregnancy are not reversed without lactation. To empirically test this hypothesis, we compared markers of metabolism, mitochondrial function, and oxidative stress between 4 groups of Sprague-Dawley rats: (1) nonreproductive (NR) rats, (2) rats killed at day 20 of gestation, (3) rats that gave birth but were not allowed to suckle their pups (nonlactating), and (4) rats that suckled their young for 14 days. Nonlactating females displayed higher body fat compared to all other groups. Peroxisome proliferator-activated receptor δ (PPARδ) in skeletal muscle and white adipose tissue of nonlactating rats was lower than the other groups. The PPARδ is associated with lipid metabolism suggesting that the higher fat mass in nonlactating females was not associated with the retention of a physiological state that was set during pregnancy but instead an independent drop in PPARδ. Relative mitochondrial respiratory function and complex activity in the liver and skeletal muscle of nonlactating mice were not predictive of higher body mass, and measures of oxidative stress displayed minimal variation between groups.

Endurance exercise protects skeletal muscle against both doxorubicin-induced and inactivity-induced muscle wasting.

Repeated bouts of endurance exercise promotes numerous biochemical adaptations in skeletal muscle fibers resulting in a muscle phenotype that is protected against a variety of homeostatic challenges; these exercise-induced changes in muscle phenotype are often referred to as "exercise preconditioning." Importantly, exercise preconditioning provides protection against several threats to skeletal muscle health including cancer chemotherapy (e.g., doxorubicin) and prolonged muscle inactivity. This review summarizes our current understanding of the mechanisms responsible for exercise-induced protection of skeletal muscle fibers against both doxorubicin-induced muscle wasting and a unique form of inactivity-induced muscle atrophy (i.e., ventilator-induced diaphragm atrophy). Specifically, the first section of this article will highlight the potential mechanisms responsible for exercise-induced protection of skeletal muscle fibers against doxorubicin-induced fiber atrophy. The second segment will discuss the biochemical changes that are responsible for endurance exercise-mediated protection of diaphragm muscle against ventilator-induced diaphragm wasting. In each section, we highlight gaps in our knowledge in hopes of stimulating future research in this evolving field of investigation.