Mean daily water intake from fluids (WATER-FL) has proven to be difficult to measure because of a range of nonvalidated data collection techniques. Few questionnaires have been validated to estimate WATER-FL against self-reported diaries or urinary hydration markers, which may limit their objectivity. The goals of this investigation were ) to assess the validity of a 7-d fluid record (7dFLR) to measure WATER-FL (WATER-FL-7dFLR) through comparison with WATER-FL as calculated by measuring deuterium oxide (DO) disappearance (WATER-FL-DO), and ) to evaluate the reliability of the 7dFLR in measuring WATER-FL. Participants [ = 96; 51% female; mean ± SD age: 41 ± 14 y; mean ± SD body mass index (in kg/m): 26.2 ± 5.1] completed body water turnover analysis over 3 consecutive weeks. They completed the 7dFLR and food diaries during weeks 2 and 4 of the observation. The records were entered into nutritional software to determine the water content of all foods and fluids consumed. WATER-FL-DO was calculated from water turnover (via the DO dilution method), minus water from food and metabolic water. The agreement between the 2 methods of determining WATER-FL were compared according to a Bland-Altman plot at week 2. The test-retest reliability of 7dFLR between weeks 2 and 4 was assessed via intraclass correlation (ICC). The mean ± SD difference between WATER-FL-7dFLR and WATER-FL-DO was -131 ± 845 mL/d. In addition, no bias was observed ( = 0.484; = 0.006; = 0.488). When comparing WATER-FL-7dFLR from weeks 2 and 4, no significant difference (mean ± SD difference: 71 ± 75 mL/d; = 0.954; = 0.343) and an ICC of 0.85 (95% CI: 0.77, 0.90) was observed. The main findings of this study were that the use of the 7dFLR is an effective and reliable method to estimate WATER-FL in adults. This style of questionnaire may be extremely helpful for collecting water intake data for large-scale epidemiologic studies.
Cancer cachexia (CC) results in impaired muscle function and quality of life and is the primary cause of death for ~20-30% of cancer patients. We demonstrated mitochondrial degeneration as a precursor to CC in male mice, however, if such alterations occur in females is currently unknown. The purpose of this study was to elucidate muscle alterations in CC development in female tumor-bearing mice. 60 female C57BL/6J mice were injected with PBS or Lewis Lung Carcinoma at 8-week age, and tumors developed for 1, 2, 3, or 4 weeks to assess the time course of cachectic development. In vivo muscle contractile function, protein fractional synthetic rate (FSR), protein turnover, and mitochondrial health were assessed. 3- and 4-week tumor-bearing mice displayed a dichotomy in tumor growth and were reassigned to High Tumor (HT) and Low Tumor (LT) groups. HT mice exhibited lower soleus, TA, and fat weights compared to PBS. HT mice showed lower peak isometric torque and slower one-half relaxation time compared to PBS. HT mice had lower FSR compared to PBS while E3 ubiquitin ligases were greater in HT compared to other groups. Bnip3 (mitophagy) and pMitoTimer red puncta (mitochondrial degeneration) were greater in HT while Pgc1α1 and Tfam (mitochondrial biogenesis) were lower in HT compared to PBS. We demonstrate alterations in female tumor-bearing mice where HT exhibited greater protein degradation, impaired muscle contractility, and mitochondrial degeneration compared to other groups. Our data provide novel evidence for a distinct cachectic development in tumor-bearing female mice compared to previous male studies.
Background Muscle atrophy is a common pathology associated with disuse, such as prolonged bed rest or spaceflight, and is associated with detrimental health outcomes. There is emerging evidence that disuse atrophy may differentially affect males and females. Cellular mechanisms contributing to the development and progression of disuse remain elusive, particularly protein turnover cascades. The purpose of this study was to investigate the initial development and progression of disuse muscle atrophy in male and female mice using the well‐established model of hindlimb unloading (HU). Methods One hundred C57BL/6J mice (50 male and 50 female) were hindlimb suspended for 0 (control), 24, 48, 72, or 168 h to induce disuse atrophy (10 animals per group). At designated time points, animals were euthanized, and tissues (extensor digitorum longus, gastrocnemius, and soleus for mRNA analysis, gastrocnemius and extensor digitorum longus for protein synthesis rates, and tibialis anterior for histology) were collected for analysis of protein turnover mechanisms (protein anabolism and catabolism). Results Both males and females lost ~30% of tibialis anterior cross‐sectional area after 168 h of disuse. Males had no statistical difference in MHCIIB fibre area, whereas unloaded females had ~33% lower MHCIIB cross‐sectional area by 168 h of unloading. Both males and females had lower fractional protein synthesis rates (FSRs) within 24–48 h of HU, and females appeared to have a greater reduction compared with males within 24 h of HU (~23% lower FSRs in males vs. 40% lower FSRs in females). Males and females exhibited differential patterns and responses in multiple markers of protein anabolism, catabolism, and myogenic capacity during the development and progression of disuse atrophy. Specifically, females had greater mRNA inductions of catabolic factors Ubc and Gadd45a (~4‐fold greater content in females compared with ~2‐fold greater content in males) and greater inductions of anabolic inhibitors Redd1 and Deptor with disuse across multiple muscle tissues exhibiting different fibre phenotypes. Conclusions These results suggest that the aetiology of disuse muscle atrophy is more complicated and nuanced than previously thought, with different responses based on muscle phenotypes and between males and females, with females having greater inductions of atrophic markers early in the development of disuse atrophy.
Metabolic efficiency was improved in BRJ. Paradoxically, body temperatures rose more. This was not due to gut permeability. Therefore, we speculate that based on elimination of other possibilities, blood redistribution from skin to skeletal muscle may have contributed to impaired heat exchange.
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