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  • 1
    Online Resource
    Online Resource
    Carotid distensibility characterized via the isometric exercise pressor response
    American Physiological Society ; 2002
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 283, No. 6 ( 2002-12-01), p. H2592-H2598
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 283, No. 6 ( 2002-12-01), p. H2592-H2598
    Abstract: Distensibility of the large elastic arteries is a key index for cardiovascular health. Distensibility, usually estimated from resting values in humans, is not a static characteristic but a negative curvilinear function of pressure. We hypothesized that differences in vascular function with gender and age may only be recognized if distensibility is quantified over a range of pressures. We used isometric handgrip exercise to induce progressive increases in pressures and carotid diameters, thereby enhancing the characterization of distensibility. In 30 volunteers, evenly distributed by gender and age across the third to fifth decades of life, we derived pulsatile distensibility slopes as a function of arterial pressure for a dynamic distensibility index and compared it with a traditional static index at a reference pressure of 95 mmHg. We also assessed intima-media thickness (IMT). We found that women had greater distensibility slopes within each decade, despite comparable IMT. Furthermore, declines in distensibility slope with increasing age were correlated to increased IMT. The static distensibility index failed to show gender-related differences in distensibility but did show age-related differences. Our results indicate that gender- and age-related differences can be manifest even in young, healthy adults and may only be identified with techniques that assess carotid distensibility across a range of pressures.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00309.2002
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2002
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Low-frequency arterial pressure fluctuations do not reflect sympathetic outflow: gender and age differences
    American Physiological Society ; 1998
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 274, No. 4 ( 1998-04-01), p. H1194-H1201
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 274, No. 4 ( 1998-04-01), p. H1194-H1201
    Abstract: Low-frequency arterial pressure oscillations (Mayer waves) have been proposed as an index of vascular sympathetic outflow. However, cross-sectional differences in these pressure oscillations may not reflect different levels of sympathetic nervous outflow in humans. Three groups of healthy subjects with characteristically different sympathetic nervous outflow were studied: young females ( n = 10, 18–28 yr), young males ( n = 11, 18–29 yr), and older males ( n = 13, 60–72 yr). Average R-R interval, arterial pressures, and systolic pressure variability at the Mayer wave frequency (0.05–0.15 Hz) did not differ among the three groups. Diastolic pressure Mayer wave variability was similar in young females vs. young males (39 ± 10 vs. 34 ± 5 mmHg 2 ) and lower in older males vs. young males (14 ± 2 mmHg 2 ; P 〈 0.05). In contrast, muscle sympathetic activity was lowest in young females (892 ± 249 total activity/min) and highest in older males (3,616 ± 528 total activity/min; both P 〈 0.05 vs. young males: 2,505 ± 285 total activity/min). Across the three groups, arterial pressure Mayer wave variability did not correlate with any index of sympathetic activity. Our results demonstrate that arterial pressure Mayer wave amplitude is not a surrogate measure of vascular sympathetic outflow.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.1998.274.4.H1194
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1998
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Metabolic physiology and skeletal muscle phenotypes in male and female myoglobin knockout mice
    American Physiological Society ; 2021
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 321, No. 1 ( 2021-07-01), p. E63-E79
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 321, No. 1 ( 2021-07-01), p. E63-E79
    Abstract: Myoglobin (Mb) is a regulator of O 2 bioavailability in type I muscle and heart, at least when tissue O 2 levels drop. Mb also plays a role in regulating cellular nitric oxide (NO) pools. Robust binding of long-chain fatty acids and long-chain acylcarnitines to Mb, and enhanced glucose metabolism in hearts of Mb knockout (KO) mice, suggest additional roles in muscle intermediary metabolism and fuel selection. To evaluate this hypothesis, we measured energy expenditure (EE), respiratory exchange ratio (RER), body weight gain and adiposity, glucose tolerance, and insulin sensitivity in Mb knockout (Mb −/− ) and wild-type (WT) mice challenged with a high-fat diet (HFD, 45% of calories). In males ( n = 10/genotype) and females ( n = 9/genotype) tested at 5–6, 11–12, and 17–18 wk, there were no genotype effects on RER, EE, or food intake. RER and EE during cold (10°C, 72 h), and glucose and insulin tolerance, were not different compared with within-sex WT controls. At ∼18 and ∼19 wk of age, female Mb −/− adiposity was ∼42%–48% higher versus WT females ( P = 0.1). Transcriptomics analyses (whole gastrocnemius, soleus) revealed few consistent changes, with the notable exception of a 20% drop in soleus transferrin receptor (Tfrc) mRNA. Capillarity indices were significantly increased in Mb −/− , specifically in Mb-rich soleus and deep gastrocnemius. The results indicate that Mb loss does not have a major impact on whole body glucose homeostasis, EE, RER, or response to a cold challenge in mice. However, the greater adiposity in female Mb −/− mice indicates a sex-specific effect of Mb KO on fat storage and feed efficiency. NEW & NOTEWORTHY The roles of myoglobin remain to be elaborated. We address sexual dimorphism in terms of outcomes in response to the loss of myoglobin in knockout mice and perform, for the first time, a series of comprehensive metabolic studies under conditions in which fat is mobilized (high-fat diet, cold). The results highlight that myoglobin is not necessary and sufficient for maintaining oxidative metabolism and point to alternative roles for this protein in muscle and heart.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.00624.2020
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2021
    detail.hit.zdb_id: 1477331-4
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  • 4
    Online Resource
    Online Resource
    Coupling of energy intake and energy expenditure across a temperature spectrum: impact of diet-induced obesity in mice
    American Physiological Society ; 2020
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 319, No. 3 ( 2020-09-01), p. E472-E484
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 319, No. 3 ( 2020-09-01), p. E472-E484
    Abstract: Obesity and its metabolic sequelae are implicated in dysfunction of the somatosensory, sympathetic, and hypothalamic systems. Because these systems contribute to integrative regulation of energy expenditure (EE) and energy intake (EI) in response to ambient temperature (T a ) changes, we hypothesized that diet-induced obesity (DIO) disrupts T a -associated EE-EI coupling. C57BL/6N male mice were fed a high-fat diet (HFD; 45% kcal) or low-fat diet (LFD; 10% kcal) for ∼9.5 wk; HFD mice were then split into body weight (BWT) quartiles ( n = 8 each) to study DIO-low gainers (Q1) versus -high gainers (Q4). EI and indirect calorimetry (IC) were measured over 3 days each at 10°C, 20°C, and 30°C. Responses did not differ between LFD, Q1, and Q4; EI and BWT-adjusted EE increased rapidly when transitioning toward 20°C and 10°C. In all groups, EI at 30°C was not reduced despite lower EE, resulting in positive energy balance and respiratory exchange ratios consistent with increased de novo lipogenesis, energy storage, and relative hyperphagia. We conclude that 1) systems controlling T a -dependent acute EI/EE coupling remained intact in obese mice and 2) rapid coupling of EI/EE at cooler temperatures is an important adaptation to maintain energy stores and defend body temperature, but less critical at thermoneutrality. A post hoc analysis using digestible EI plus IC-calculated EE suggests that standard IC assumptions for EE calculation require further validation in the setting of DIO. The experimental paradigm provides a platform to query the hypothalamic, somatosensory, and sympathetic mechanisms that drive T a -associated EI/EE coupling.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.00041.2020
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2020
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    Diet-induced obesity causes innate airway hyperresponsiveness to methacholine and enhances ozone-induced pulmonary inflammation
    American Physiological Society ; 2008
    In:  Journal of Applied Physiology Vol. 104, No. 6 ( 2008-06), p. 1727-1735
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 104, No. 6 ( 2008-06), p. 1727-1735
    Abstract: We previously reported that genetically obese mice exhibit innate airway hyperresponsiveness (AHR) and enhanced ozone (O 3 )-induced pulmonary inflammation. Such genetic deficiencies in mice are rare in humans, and they may not be representative of human obesity. Thus the purpose of this study was to determine the pulmonary phenotype of mice with diet-induced obesity (DIO), which more closely mimics the cause of human obesity. Therefore, wild-type C57BL/6 mice were reared from the time of weaning until at least 30 wk of age on diets in which either 10 or 60% of the calories are derived from fat in the form of lard. Body mass was ∼40% greater in mice fed 60 vs. 10% fat diets. Baseline airway responsiveness to intravenous methacholine, measured by forced oscillation, was greater in mice fed 60 vs. 10% fat diets. We also examined lung permeability and inflammation after exposure to room air or O 3 (2 parts/million for 3 h), an asthma trigger. Four hours after the exposure ended, O 3 -induced increases in bronchoalveolar lavage fluid protein, interleukin-6, KC, macrophage inflammatory protein-2, interferon-γ-inducible protein-10, and eotaxin were greater in mice fed 60 vs. 10% fat diets. Innate AHR and augmented responses to O 3 were not observed in mice raised from weaning until 20–22 wk of age on a 60% fat diet. These results indicate that mice with DIO exhibit innate AHR and enhanced O 3 -induced pulmonary inflammation, similar to genetically obese mice. However, mice with DIO must remain obese for an extended period of time before this pulmonary phenotype is observed.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00075.2008
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2008
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 6
    Online Resource
    Online Resource
    Human soleus and vastus lateralis muscle protein metabolism with an amino acid infusion
    American Physiological Society ; 2005
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 288, No. 3 ( 2005-03), p. E479-E485
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 288, No. 3 ( 2005-03), p. E479-E485
    Abstract: The calf muscles, compared with the thigh, are less responsive to resistance exercise in ambulatory and bed-rested individuals, apparently due to muscle-specific differences in protein metabolism. We chose to evaluate the efficacy of using amino acids to elevate protein synthesis in the soleus, because amino acids have been shown to have a potent anabolic effect in the vastus lateralis. Mixed muscle protein synthesis in the soleus and vastus lateralis was measured before and after infusion of mixed amino acids in 10 individuals (28 ± 1 yr). Phosphorylation of ribosomal protein p70 S6 kinase (p70 S6K ; Thr 389 ) and eukaryotic initiation factor 4E-binding protein-1 (4E-BP1; Thr 37/46 ) was also evaluated at rest and after 3 h of amino acid infusion. Basal protein synthesis was similar ( P = 0.126), and amino acids stimulated protein synthesis to a similar extent ( P = 0.004) in the vastus lateralis (0.043 ± 0.011%/h) and soleus (0.032 ± 0.017%/h). Phosphorylation of p70 S6K ( P = 0.443) and 4E-BP1 ( P = 0.192) was not increased in either muscle; however, the soleus contained more total ( P = 0.002) and phosphorylated ( P = 0.013) 4E-BP1 than the vastus lateralis. These data support the need for further study of amino acid supplementation as a means to compensate for the reduced effectiveness of calf resistance exercise in ambulatory individuals and those exposed to extended periods of unloading. The greater 4E-BP1 in the soleus suggests that there is a muscle-specific distribution of general translational initiation machinery in human skeletal muscle.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.00393.2004
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2005
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Pulmonary responses to acute ozone exposure in fasted mice: effect of leptin administration
    American Physiological Society ; 2007
    In:  Journal of Applied Physiology Vol. 102, No. 1 ( 2007-01), p. 149-156
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 102, No. 1 ( 2007-01), p. 149-156
    Abstract: Leptin is a satiety hormone that also has proinflammatory effects, including augmentation of ozone-induced pulmonary inflammation. The purpose of this study was to determine whether reductions in endogenous levels of leptin can attenuate pulmonary responses to ozone. To reduce serum leptin, we fasted mice overnight before ozone exposure. Fasting caused a marked reduction in serum leptin to approximately one-sixth the levels observed in fed mice, and continuous infusion of leptin via Alzet micro-osmotic pumps restored serum leptin to, but not above, fed levels. Ozone exposure (2 ppm for 3 h) caused a significant, ∼40% increase in pulmonary resistance ( P 〈 0.01) and increased airway responsiveness in fasted but not in fed mice. The increased effect of ozone on pulmonary mechanics and airway responsiveness in fasted mice was not observed when leptin was restored via continuous infusion. Ozone exposure caused pulmonary inflammation, as evident by increases in bronchoalveolar lavage cells, protein, and soluble tumor necrosis factor receptors. There was no effect of fasting status on ozone-induced changes in the bronchoalveolar lavage inflammatory profile, and leptin treatment did not alter these responses. Our results indicate that fasting augments ozone-induced changes in pulmonary mechanics and airway responsiveness in mice. These effects of fasting are the result of declines in serum leptin. The mechanistic basis for this protective effect of leptin in fasted mice remains to be determined but is not related to effects on ozone-induced inflammation.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00300.2006
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2007
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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