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Premenstrual Syndrome (PMS) is a complex physiological and psychological condition that affects a significant number of women during their reproductive years. Although the exact etiology of PMS remains unclear, its symptoms, including mood swings, bloating, irritability, and fatigue, can significantly impair the quality of life for affected individuals. The management of PMS traditionally involves pharmacological interventions; however, emerging evidence suggests that exercise may offer a valuable non-pharmacological approach to alleviate PMS symptoms. This narrative review aims to explore the proposed etiology, prevalence, and impact PMS has on women as well as examine the literature through which exercise can positively influence PMS symptoms. While the existing literature on exercise and PMS is limited and inconclusive, several studies have reported promising results. Regular exercise has been associated with a reduction in physical and psychological symptoms of PMS including pain, fatigue, mood disturbances, and water retention. Furthermore, exercise has demonstrated its potential to enhance overall well-being and mitigate the negative effects of PMS on daily functioning. Further research is warranted to elucidate the optimal exercise prescription, duration, and intensity required to maximize the benefits and improve the understanding of exercise mechanisms on PMS symptomatology.

Adults with Down syndrome are an underserved population at high risk for a host of different pathologies from aging and lack of activity.PurposeTo examine the effects of a 10-week resistance training program on measures of motor behavior, cognitive function, mood, and physical fitness.MethodsParticipants (n = 11) were men and women clinically diagnosed with Down syndrome (age: 25.8 ± 6.4 years; height: 151.5 ± 8.3 cm; weight: 67.5 ± 13.0 kg; IQ: 58.3 ± 19.7 units). After familiarization of testing procedures, subjects performed The Arizona Cognitive Test Battery for Down Syndrome, TGMD-2, lower and upper body strength assessments, and body composition via DXA testing, while parental guardians completed cognitive and mood survey assessments (Cognitive Scale for Down Syndrome, Behavioral Rating Inventory of Executive Function, NiSonger Child Behavior Rating Form, Scales of Independent Behavior-Revised, Child Eating Behavior Questionnaire, Social Communication Questionnaire, and Mood and Feelings Questionnaire) at pre and post 10 weeks of periodized resistance training.ResultsSignificant (P ≤ 0.05) improvements in locomotor skills and object control skills were observed post-training. Both locomotor skills (e.g., sprint, gallop, leaping, broad jump) and object control skills (e.g., baseball catch, underhand roll, basketball dribble) were all significantly improved. Facets of cognitive performance significantly improved, specifically executive function and visuospatial working memory capacity, and frontal lobe activity. Mood disturbances significantly decrease. All aspects of physical strength and endurance were improved, i.e., leg press, bench press, sit-ups, push-ups, and chair sit-to-stand post-training. Lean tissue mass was significantly increased post-training.ConclusionThis study dramatically demonstrates that life enhancements for individuals with Down syndrome are achievable with a properly designed resistance training program.

Brain-Derived Neurotropic Factor (BDNF) expression is decreased in conditions associated with cognitive decline as well as metabolic diseases. One potential strategy to improve metabolic health and elevate BDNF is by increasing circulating ketones. Beta-Hydroxybutyrate (BHB) stimulates BDNF expression, but the association of circulating BHB and plasma BDNF in humans has not been widely studied. Here, we present results from three studies that evaluated how various methods of inducing ketosis influenced plasma BDNF in humans. Study 1 determined BDNF responses to a single bout of high-intensity cycling after ingestion of a dose of ketone salts in a group of healthy adults who were habitually consuming either a mixed diet or a ketogenic diet. Study 2 compared how a ketogenic diet versus a mixed diet impacts BDNF levels during a 12-week resistance training program in healthy adults. Study 3 examined the effects of a controlled hypocaloric ketogenic diet, with and without daily use of a ketone-salt, on BDNF levels in overweight/obese adults. We found that (1) fasting plasma BDNF concentrations were lower in keto-adapted versus non keto-adapted individuals, (2) intense cycling exercise was a strong stimulus to rapidly increase plasma BDNF independent of ketosis, and (3) clinically significant weight loss was a strong stimulus to decrease fasting plasma BDNF independent of diet composition or level of ketosis. These results highlight the plasticity of plasma BDNF in response to lifestyle factors but does not support a strong association with temporally matched BHB concentrations.

Objective The aim of this study was to investigate changes in trunk muscle strength 12 months after lumbar spine fusion (LSF) compared to preoperative strength. Methods A total of 194 patients (mean±standard deviation [SD] age, 61±21 years) who underwent LSF participated in this prospective longitudinal study. Physical measurements of the participants were made before surgery and 12 months postoperatively. Isometric trunk extension and flexion strength was measured using a strain-gauge dynamometer in the standing position. Strength changes were calculated. Regression analysis was performed to explore which factors predicted strength levels at 12 months postoperatively. Results The preoperative mean±SD extension strength was 205±144 N, which increased to 258±142 N (p

Background: Ketogenic diets (KDs) that elevate beta-hydroxybutyrate (BHB) promote weight and fat loss. Exogenous ketones, such as ketone salts (KS), also elevate BHB concentrations with the potential to protect against muscle loss during caloric restriction. Whether augmenting ketosis with KS impacts body composition responses to a well-formulated KD remains unknown.Purpose: To explore the effects of energy-matched, hypocaloric KD feeding (1.0 mM capillary BHB) throughout the study (p < 0.001), with higher fasting concentrations observed in KD + KS than KD + PL for the first 2 weeks (p < 0.05). There were decreases in body mass, whole body fat and lean mass, mid-thigh muscle cross-sectional area, and both visceral and subcutaneous adipose tissues (p < 0.001), but no group differences between the two KDs or with the LFD. Urine nitrogen excretion was significantly higher in KD + PL than LFD (p < 0.01) and trended higher in KD + PL compared to KD + KS (p = 0.076), whereas the nitrogen excretion during KD + KS was similar to LFD (p > 0.05).Conclusion: Energy-matched hypocaloric ketogenic diets favorably affected body composition but were not further impacted by administration of an exogenous BHB-salt that augmented ketosis. The trend for less nitrogen loss with the BHB-salt, if manifested over a longer period of time, may contribute to preserved lean mass.

Whereas composition studies tends to use ethics and morality interchangeably, these terms may work better when explicitly distinguished, rearticulated as a topic, and kept in heuristic conflict. The more the tension between them is exploited, the closer our approach to a pedagogy not so much ethical as just.

Purpose: To determine if acute resistance exercise-induced increases in growth hormone (GH) and insulin-like growth factor-I (IGF-I) were differentially responsive for one or more molecular weight (MW) isoforms and if these responses were sex-dependent.Methods: College-aged men (n = 10) and women (n = 10) performed an acute resistance exercise test (ARET; 6 sets, 10 repetition maximum (10-RM) squat, 2-min inter-set rest). Serum aliquots from blood drawn Pre-, Mid-, and Post-ARET (0, +15, and +30-min post) were processed using High Performance Liquid Chromatography (HPLC) fractionation and pooled into 3 MW fractions (Fr.A: >60; Fr.B: 30–60; Fr.C: Fr.A > Fr.B, p ≤ 0.03). Sex × time interactions indicated that women experienced earlier and augmented increases in all serum GH MW isoform fraction pools (p < 0.05); however, men demonstrated delayed and sustained GH elevations (p < 0.01) in all fractions through +30-min of recovery. Similarly, we observed a sex-independent hierarchy among IGF-I MW fraction pools (Fr.A > Fr.B > Fr.C, p ≤ 0.01). Furthermore, we observed increases in IGF-I Fr. A (ternary complexes) in men only (p ≤ 0.05), and increases in Fr.C (free/unbound IGF-I) in women only (p ≤ 0.05) vs. baseline, respectively.Conclusions: These data indicate that the processing of GH and IGF-I isoforms from the somatotrophs and hepatocytes are differential in their response to strenuous resistance exercise and reflect both temporal and sex-related differences.

Isolated ginsenoside metabolites such as Compound K (CK) are of increasing interest to consumer and clinical populations as safe and non-pharmacological means to enhance psychomotor performance constitutively and in response to physical or cognitive stress. Nevertheless, the influence of CK on behavioral performance and EEG measures of cortical activity in humans is undetermined. In this double-blinded, placebo-controlled, counterbalanced within-group study, dose-dependent responses to CK (placebo, 160 and 960 mg) were assessed after 2 weeks of supplementation in nineteen healthy men and women (age: 39.9 ± 7.9 year, height 170.2 ± 8.6 cm, weight 79.7 ± 11.9 kg). Performance on upper- and lower-body choice reaction tests (CRTs) was tested before and after intense lower-body anaerobic exercise. Treatment- and stress-related changes in brain activity were measured with high-density EEG based on event-related potentials, oscillations, and source activity. Upper- (−12.3 ± 3.5 ms, p = 0.002) and lower-body (−12.3 ± 4.9 ms, p = 0.021) response times improved after exercise, with no difference between treatments (upper: p = 0.354; lower: p = 0.926). Analysis of cortical activity in sensor and source space revealed global increases in cortical arousal after exercise. CK increased activity in cortical regions responsible for sustained attention and mitigated exercise-induced increases in arousal. Responses to exercise varied depending on task, but CK appeared to reduce sensory interference from lower-body exercise during an upper-body CRT and improve the general maintenance of task-relevant sensory processes.

Hormones are largely responsible for the integrated communication of several physiological systems responsible for modulating cellular growth and development. Although the specific hormonal influence must be considered within the context of the entire endocrine system and its relationship with other physiological systems, three key hormones are considered the “anabolic giants” in cellular growth and repair: testosterone, the growth hormone superfamily, and the insulin-like growth factor (IGF) superfamily. In addition to these anabolic hormones, glucocorticoids, mainly cortisol must also be considered because of their profound opposing influence on human skeletal muscle anabolism in many instances. This review presents emerging research on: (1) Testosterone signaling pathways, responses, and adaptations to resistance training; (2) Growth hormone: presents new complexity with exercise stress; (3) Current perspectives on IGF-I and physiological adaptations and complexity these hormones as related to training; and (4) Glucocorticoid roles in integrated communication for anabolic/catabolic signaling. Specifically, the review describes (1) Testosterone as the primary anabolic hormone, with an anabolic influence largely dictated primarily by genomic and possible non-genomic signaling, satellite cell activation, interaction with other anabolic signaling pathways, upregulation or downregulation of the androgen receptor, and potential roles in co-activators and transcriptional activity; (2) Differential influences of growth hormones depending on the “type” of the hormone being assayed and the magnitude of the physiological stress; (3) The exquisite regulation of IGF-1 by a family of binding proteins (IGFBPs 1–6), which can either stimulate or inhibit biological action depending on binding; and (4) Circadian patterning and newly discovered variants of glucocorticoid isoforms largely dictating glucocorticoid sensitivity and catabolic, muscle sparing, or pathological influence. The downstream integrated anabolic and catabolic mechanisms of these hormones not only affect the ability of skeletal muscle to generate force; they also have implications for pharmaceutical treatments, aging, and prevalent chronic conditions such as metabolic syndrome, insulin resistance, and hypertension. Thus, advances in our understanding of hormones that impact anabolic: catabolic processes have relevance for athletes and the general population, alike.

This study examined the associations between asymmetric handgrip strength (HGS) and multimorbidity in American adults. Secondary analyses of data from persons aged at least 40 years from the 2011–2012 and 2013–2014 waves of the National Health and Nutrition Examination Survey were conducted. A handheld dynamometer collected HGS on each hand and persons with a strength imbalance >10% between hands were classified as having asymmetric HGS. Adults with the presence of ≥2 of the following conditions had multimorbidity: cardiovascular disease, chronic obstructive pulmonary disease, chronic kidney disease, asthma, arthritis, cancer, obesity, stroke, hypertension, high cholesterol, and diabetes. Of the n = 3483 participants included, n = 2700 (77.5%) had multimorbidity. A greater proportion of adults with multimorbidity had HGS asymmetry (n = 1234 (45.7%)), compared to persons living without multimorbidity (n = 314 (40.1%); p < 0.05). Relative to individuals without asymmetry, adults with asymmetric HGS had 1.31 (95% confidence interval (CI): 1.03–1.67) greater odds for multimorbidity. Moreover, persons with HGS asymmetry had 1.22 (CI: 1.04–1.44) greater odds for accumulating morbidities. Asymmetric strength, as another indicator of diminished muscle function, is linked to chronic morbidity status. Healthcare providers should recommend healthy behaviors for reducing asymmetries to improve muscle function and mitigate morbidity risk after completing asymmetry screenings.

Background. Foods rich in saturated fatty acids (SFAs) have been discouraged by virtue of their cholesterol-raising potential, but this effect is modulated by the food source and background level of carbohydrate. Objective. We aimed to compare the consumption of palm stearin (PS) versus butter on circulating cholesterol responses in the setting of both a low-carbohydrate/high-fat (LC/HF) and high-carbohydrate/low-fat (HC/LF) diet in healthy subjects. We also explored effects on plasma lipoprotein particle distribution and fatty acid composition. Methods. We performed a randomized, controlled-feeding, cross-over study that compared a PS- versus a Butter-based diet in a group of normocholesterolemic, non-obese adults. A controlled canola oil-based ‘Run-In’ diet preceded the experimental PS and Butter diets. All diets were eucaloric, provided for 3-weeks, and had the same macronutrient distribution but varied in primary fat source (40% of the total fat). The same Run-In and cross-over experiments were done in two separate groups who self-selected to either a LC/HF (n = 12) or a HC/LF (n = 12) diet track. The primary outcomes were low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein (HDL)-C, triglycerides, and LDL particle distribution. Results. Compared to PS, Butter resulted in higher LDL-C in both the LC/HF (13.4%, p = 0.003) and HC/LF (10.8%, p = 0.002) groups, which was primarily attributed to large LDL I and LDL IIa particles. There were no differences between PS and Butter in HDL-C, triglycerides, or small LDL particles. Oxidized LDL was lower after PS than Butter in LC/HF (p = 0.011), but not the HC/LF group. Conclusions. These results demonstrate that Butter raises LDL-C relative to PS in healthy normocholesterolemic adults regardless of background variations in carbohydrate and fat, an effect primarily attributed to larger cholesterol-rich LDL particles.

ABSTRACT Hypoxia is linked to therapeutic resistance and poor clinical prognosis for many tumor entities, including human papillomavirus (HPV)-positive cancers. Notably, HPV-positive cancer cells can induce a dormant state under hypoxia, characterized by a reversible growth arrest and strong repression of viral E6/E7 oncogene expression, which could contribute to therapy resistance, immune evasion and tumor recurrence. The present work aimed to gain mechanistic insights into the pathway(s) underlying HPV oncogene repression under hypoxia. We show that E6/E7 downregulation is mediated by hypoxia-induced stimulation of AKT signaling. Ablating AKT function in hypoxic HPV-positive cancer cells by using chemical inhibitors efficiently counteracts E6/E7 repression. Isoform-specific activation or downregulation of AKT1 and AKT2 reveals that both AKT isoforms contribute to hypoxic E6/E7 repression and act in a functionally redundant manner. Hypoxic AKT activation and consecutive E6/E7 repression is dependent on the activities of the canonical upstream AKT regulators phosphoinositide 3-kinase (PI3K) and mechanistic target of rapamycin (mTOR) complex 2 (mTORC2). Hypoxic downregulation of E6/E7 occurs, at least in part, at the transcriptional level. Modulation of E6/E7 expression by the PI3K/mTORC2/AKT cascade is hypoxia specific and not observed in normoxic HPV-positive cancer cells. Quantitative proteome analyses identify additional factors as candidates to be involved in hypoxia-induced activation of the PI3K/mTORC2/AKT signaling cascade and in the AKT-dependent repression of the E6/E7 oncogenes under hypoxia. Collectively, these data uncover a functional key role of the PI3K/mTORC2/AKT signaling cascade for viral oncogene repression in hypoxic HPV-positive cancer cells and provide new insights into the poorly understood cross talk between oncogenic HPVs and their host cells under hypoxia. IMPORTANCE Oncogenic HPV types are major human carcinogens. Under hypoxia, HPV-positive cancer cells can repress the viral E6/E7 oncogenes and induce a reversible growth arrest. This response could contribute to therapy resistance, immune evasion, and tumor recurrence upon reoxygenation. Here, we uncover evidence that HPV oncogene repression is mediated by hypoxia-induced activation of canonical PI3K/mTORC2/AKT signaling. AKT-dependent downregulation of E6/E7 is only observed under hypoxia and occurs, at least in part, at the transcriptional level. Quantitative proteome analyses identify additional factors as candidates to be involved in AKT-dependent E6/E7 repression and/or hypoxic PI3K/mTORC2/AKT activation. These results connect PI3K/mTORC2/AKT signaling with HPV oncogene regulation, providing new mechanistic insights into the cross talk between oncogenic HPVs and their host cells.

Objective A growing number of ultra-endurance athletes have switched to a very low-carbohydrate/high-fat eating pattern. We compared markers of cholesterol and the lipoprotein profile in a group of elite ultra-runners consuming a high-carbohydrate (HC) or low-carbohydrate (LC) diet.Methods Fasting blood was obtained from competitive male ultra-endurance runners habitually consuming a very low-carbohydrate (LC; n=10) or high-carbohydrate (HC; n=10) diet to determine blood cholesterol profile, lipoprotein particle distribution and sterol biomarkers of cholesterol balance.Results Plasma total cholesterol, low-density lipoprotein (LDL-C) and high-density lipoprotein (HDL-C) cholesterol were all significantly greater (p

Ketogenic diets (KDs) often contain high levels of saturated fat, which may increase liver fat, but the lower carbohydrate intake may have the opposite effect. Using a controlled feeding design, we compared liver fat responses to a hypocaloric KD with a placebo (PL) versus an energy-matched low-fat diet (LFD) in overweight adults. We also examined the added effect of a ketone supplement (KS). Overweight adults were randomized to a 6-week KD (KD + PL) or a KD with KS (KD + KS); an LFD group was recruited separately. All diets were estimated to provide 75% of energy expenditure. Weight loss was similar between groups (p > 0.05). Liver fat assessed by magnetic resonance imaging decreased after 6 week (p = 0.004) with no group differences (p > 0.05). A subset with nonalcoholic fatty liver disease (NAFLD) (liver fat > 5%, n = 12) showed a greater reduction in liver fat, but no group differences. In KD participants with NAFLD, 92% of the variability in change in liver fat was explained by baseline liver fat (p < 0.001). A short-term hypocaloric KD high in saturated fat does not adversely impact liver health and is not impacted by exogenous ketones. Hypocaloric low-fat and KDs can both be used in the short-term to significantly reduce liver fat in individuals with NAFLD.

Clenbuterol (CB) is one of the β2-adrenergic receptor agonists with powerful muscle anabolic and lipolytic effects, and is prohibited as a doping drug for athletes. However, it is one of the candidate countermeasures for aging-related diseases. Previously we reported that CB induced muscular hypertrophy, but inhibited the longitudinal growth of bones in young male rats. However, the mechanism of the inhibitory effect on bone growth is not yet clear. CB is manufactured as a 1:1 racemic mixture of 2 isomers of (-)-R and (+)-S enantiomers, and only the (-)-R enantiomer may have pharmacological activity. We examined the effects of two CB enantiomers, (+)-S-CB and (-)-R-CB, on growth of striated muscle and bone in young male rats. Eighteen male Sprague-Dawley rats (8-wk-old) were randomly assigned to a control (CONT, n = 6) and two CB enantiomers groups ((+)-S-CLEB: n=6, (-)-R-CLEB: n=6). Each CB enantiomer of 2 mg/kg body weight was daily administered subcutaneously for 2 weeks. After treatment, heart and the slow-twitch soleus (SOL) and fast-twitch extensor digitorum longus (EDL) muscles and bones were analyzed. The muscle wet weights of SOL and EDL muscles significantly increased in (+)-S-CLEB (HEART: +28%, SOL: +25%, EDL: +28%) and (-)-R-CLEB (HEART: +27%, SOL: +29%, EDL: +35%). Both (+)-S-CB and (-)-R-CB induced striated muscle hypertrophy (heart, SOL, and EDL). Concerning bones, (+)-S-CB induced decreased tibia length (-1.2%) and decreased femur BMD (-5.8%), and (-)-R-CB induced decreased femur BMD (-8.2%). These results show that (+)-S-CB and (-)-R-CB might work differently at times.