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  • 1
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    Determination of production of nitric oxide by lower airways of humans—theory
    American Physiological Society ; 1997
    In:  Journal of Applied Physiology Vol. 82, No. 4 ( 1997-04-01), p. 1290-1296
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 82, No. 4 ( 1997-04-01), p. 1290-1296
    Abstract: Hyde, Richard W., Edgar J. Geigel, Albert J. Olszowka, John A. Krasney, Robert E. Forster II, Mark J. Utell, and Mark W. Frampton.Determination of production of nitric oxide by the lower airways of humans—theory. J. Appl. Physiol.82(4): 1290–1296, 1997.—Exercise and inflammatory lung disorders such as asthma and acute lung injury increase exhaled nitric oxide (NO). This finding is interpreted as a rise in production of NO by the lungs (V˙no) but fails to take into account the diffusing capacity for NO (Dno) that carries NO into the pulmonary capillary blood. We have derived equations to measureV˙no from the following rates, which determine NO tension in the lungs (Pl) at any moment from 1) production (V˙no); 2) diffusion, where Dno(Pl) = rate of removal by lung capillary blood; and 3) ventilation, whereV˙a(Pl)/(Pb− 47) = the rate of NO removal by alveolar ventilation (V˙a) and Pb is barometric pressure. During open-circuit breathing when Pl is not in equilibrium, d/d tPl[V l / (Pb − 47)] (where V l is volume of NO in the lower airways) =V˙no− Dno(Pl) −V˙a(Pl)/(Pb− 47). When Pl reaches a steady state so that d/d t = 0 andV˙a is eliminated by rebreathing or breath holding, then Pl =V˙no/Dno. Pl can be interpreted as NO production per unit of Dno. This equation predicts that diseases that diminish Dno but do not alterV˙no will increase expired NO levels. These equations permit precise measurements of V˙no that can be applied to determining factors controlling NO production by the lungs.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1997.82.4.1290
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1997
    detail.hit.zdb_id: 1404365-8
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  • 2
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    Effect of carbohydrate or carbohydrate plus medium-chain triglyceride ingestion on cycling time trial performance
    American Physiological Society ; 2000
    In:  Journal of Applied Physiology Vol. 88, No. 1 ( 2000-01-01), p. 113-119
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 88, No. 1 ( 2000-01-01), p. 113-119
    Abstract: This study examined the effectiveness of ingesting a carbohydrate or carbohydrate + medium-chain triglycerides (MCT) on metabolism and cycling performance. Eight endurance-trained men [peak O 2 uptake = 4.71 ± 0.09 (SE) l/min] completed 35 kJ/kg as quickly as possible [time trial (TT)] while consuming 250 ml/15 min of either a 6% (wt/vol) carbohydrate solution (C), a 6% carbohydrate + 4.2% MCT solution (C+M), or a sweet placebo (P). Time to complete the set amount of work was reduced in both C and C+M compared with P by 7 and 5%, respectively (C: 166 ± 7 min; C+M: 169 ± 7 min; P: 178 ± 11 min; P 〈 0.01). Plasma glucose concentration was maintained at or above resting values throughout both C and C+M trials but decreased ( P 〈 0.05) below resting values in P at the completion of the TT. The estimated rate of carbohydrate oxidation was not different during the first 90 min of exercise but thereafter was reduced ( P 〈 0.05) in P and was maintained in both C and C+M. These data demonstrate that carbohydrate ingestion during exercise improves 100-km TT performance compared with a sweet placebo, but the addition of MCT does not provide any further performance enhancement.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.2000.88.1.113
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    detail.hit.zdb_id: 1404365-8
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  • 3
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    Age-related slowing of myosin actin cross-bridge kinetics is sex specific and predicts decrements in whole skeletal muscle performance in humans
    American Physiological Society ; 2013
    In:  Journal of Applied Physiology Vol. 115, No. 7 ( 2013-10-01), p. 1004-1014
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 115, No. 7 ( 2013-10-01), p. 1004-1014
    Abstract: We hypothesize that age-related skeletal muscle dysfunction and physical disability may be partially explained by alterations in the function of the myosin molecule. To test this hypothesis, skeletal muscle function at the whole muscle, single fiber, and molecular levels was measured in young (21–35 yr) and older (65–75 yr) male and female volunteers with similar physical activity levels. After adjusting for muscle size, older adults had similar knee extensor isometric torque values compared with young, but had lower isokinetic power, most notably in women. At the single-fiber and molecular levels, aging was associated with increased isometric tension, slowed myosin actin cross-bridge kinetics (longer myosin attachment times and reduced rates of myosin force production), greater myofilament lattice stiffness, and reduced phosphorylation of the fast myosin regulatory light chain; however, the age effect was driven primarily by women (i.e., age-by-sex interaction effects). In myosin heavy chain IIA fibers, single-fiber isometric tension and molecular level mechanical and kinetic indexes were correlated with whole muscle isokinetic power output. Collectively, considering that contractile dysfunction scales up through various anatomical levels, our results suggest a potential sex-specific molecular mechanism, reduced cross-bridge kinetics, contributes to the reduced physical capacity with aging in women. Thus these results support our hypothesis that age-related alterations in the myosin molecule contribute to skeletal muscle dysfunction and physical disability and indicate that this effect is stronger in women.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00563.2013
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2013
    detail.hit.zdb_id: 1404365-8
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  • 4
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    The role of myostatin and activin receptor IIB in the regulation of unloading-induced myofiber type-specific skeletal muscle atrophy
    American Physiological Society ; 2015
    In:  Journal of Applied Physiology Vol. 119, No. 6 ( 2015-09-15), p. 633-642
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 119, No. 6 ( 2015-09-15), p. 633-642
    Abstract: Chronic unloading induces decrements in muscle size and strength. This adaptation is governed by a number of molecular factors including myostatin, a potent negative regulator of muscle mass. Myostatin must first be secreted into the circulation and then bind to the membrane-bound activin receptor IIB (actRIIB) to exert its atrophic action. Therefore, we hypothesized that myofiber type-specific atrophy observed after hindlimb suspension (HLS) would be related to myofiber type-specific expression of myostatin and/or actRIIB. Wistar rats underwent HLS for 10 days, after which the tibialis anterior was harvested for frozen cross sectioning. Simultaneous multichannel immunofluorescent staining combined with differential interference contrast imaging was employed to analyze myofiber type-specific expression of myostatin and actRIIB and myofiber type cross-sectional area (CSA) across fiber types, myonuclei, and satellite cells. Hindlimb suspension (HLS) induced significant myofiber type-specific atrophy in myosin heavy chain (MHC) IIx ( P 〈 0.05) and MHC IIb myofibers ( P 〈 0.05). Myostatin staining associated with myonuclei was less in HLS rats compared with controls, while satellite cell staining for myostatin remained unchanged. In contrast, the total number myonuclei and satellite cells per myofiber was reduced in HLS compared with ambulatory control rats ( P 〈 0.01). Sarcoplasmic actRIIB staining differed between myofiber types (I 〈 IIa 〈 IIx 〈 IIb) independent of loading conditions. Myofiber types exhibiting the greatest cytoplasmic staining of actRIIB corresponded to those exhibiting the greatest degree of atrophy following HLS. Our data suggest that differential expression of actRIIB may be responsible for myostatin-induced myofiber type-selective atrophy observed during chronic unloading.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00762.2014
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2015
    detail.hit.zdb_id: 1404365-8
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    SSG: 31
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  • 5
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    Effect of heat stress on glucose kinetics during exercise
    American Physiological Society ; 1996
    In:  Journal of Applied Physiology Vol. 81, No. 4 ( 1996-10-01), p. 1594-1597
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 81, No. 4 ( 1996-10-01), p. 1594-1597
    Abstract: Hargreaves, Mark, Damien Angus, Kirsten Howlett, Nelly Marmy Conus, and Mark Febbraio. Effect of heat stress on glucose kinetics during exercise. J. Appl. Physiol. 81(4): 1594–1597, 1996.—To identify the mechanism underlying the exaggerated hyperglycemia during exercise in the heat, six trained men were studied during 40 min of cycling exercise at a workload requiring 65% peak pulmonary oxygen uptake (V˙o 2 peak ) on two occasions at least 1 wk apart. On one occasion, the ambient temperature was 20°C [control (Con)], whereas on the other, it was 40°C [high temperature (HT)] . Rates of glucose appearance and disappearance were measured by using a primed continuous infusion of [6,6- 2 H]glucose. No differences in oxygen uptake during exercise were observed between trials. After 40 min of exercise, heart rate, rectal temperature, respiratory exchange ratio, and plasma lactate were all higher in HT compared with Con ( P 〈 0.05). Plasma glucose levels were similar at rest (Con, 4.54 ± 0.19 mmol/l; HT, 4.81 ± 0.19 mmol/l) but increased to a greater extent during exercise in HT (6.96 ± 0.16) compared with Con (5.45 ± 0.18; P 〈 0.05). This was the result of a higher glucose rate of appearance in HT during the last 30 min of exercise. In contrast, the glucose rate of disappearance and metabolic clearance rate were not different at any time point during exercise. Plasma catecholamines were higher after 10 and 40 min of exercise in HT compared with Con ( P 〈 0.05), whereas plasma glucagon, cortisol, and growth hormone were higher in HT after 40 min. These results indicate that the hyperglycemia observed during exercise in the heat is caused by an increase in liver glucose output without any change in whole body glucose utilization.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1996.81.4.1594
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1996
    detail.hit.zdb_id: 1404365-8
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    SSG: 31
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  • 6
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    Rate of nitric oxide production by lower alveolar airways of human lungs
    American Physiological Society ; 1999
    In:  Journal of Applied Physiology Vol. 86, No. 1 ( 1999-01-01), p. 211-221
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 86, No. 1 ( 1999-01-01), p. 211-221
    Abstract: This report describes methods for measuring nitric oxide production by the lungs’ lower alveolar airways (V˙no), defined as those alveoli and bronchioles well perfused by the pulmonary circulation. Breath holding or vigorous rebreathing for 15–20 s minimizes removal of NO from the lower airways and results in a constant partial pressure of NO in the lower airways (Pl). Then the amount of NO diffusing into the perfusing blood will be the pulmonary diffusing capacity for NO (Dno) multiplied by Pl and by mass balance equalsV˙no, or V˙no = Dno(Pl). To measure Pl, 10 normal subjects breath held for 20 s followed by exhalation at a constant flow rate of 0.83 ± 0.14 (SD) l/s or rebreathed at 59 ± 15 l/min for 20 s while NO was continuously measured at the mouth. Dno was estimated to equal five times the single-breath carbon monoxide diffusing capacity. By using breath holding, Pl equaled 2.9 ± 0.8 mmHg × 10 −6 and V˙noequaled 0.39 ± 0.12 μl/min. During rebreathing Pl equaled 2.3 ± 0.6 mmHg × 10 −6 andV˙no equaled 0.29 ± 0.11 μl/min. Measurements of NO at the mouth during rapid, constant exhalation after breath holding for 20 s or during rebreathing provide reproducible methods for measuringV˙no in humans.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1999.86.1.211
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1404365-8
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    SSG: 31
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  • 7
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    Using molecular classification to predict gains in maximal aerobic capacity following endurance exercise training in humans
    American Physiological Society ; 2010
    In:  Journal of Applied Physiology Vol. 108, No. 6 ( 2010-06), p. 1487-1496
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 108, No. 6 ( 2010-06), p. 1487-1496
    Abstract: A low maximal oxygen consumption (V̇o 2max ) is a strong risk factor for premature mortality. Supervised endurance exercise training increases V̇o 2max with a very wide range of effectiveness in humans. Discovering the DNA variants that contribute to this heterogeneity typically requires substantial sample sizes. In the present study, we first use RNA expression profiling to produce a molecular classifier that predicts V̇o 2max training response. We then hypothesized that the classifier genes would harbor DNA variants that contributed to the heterogeneous V̇o 2max response. Two independent preintervention RNA expression data sets were generated ( n = 41 gene chips) from subjects that underwent supervised endurance training: one identified and the second blindly validated an RNA expression signature that predicted change in V̇o 2max (“predictor” genes). The HERITAGE Family Study ( n = 473) was used for genotyping. We discovered a 29-RNA signature that predicted V̇o 2max training response on a continuous scale; these genes contained ∼6 new single-nucleotide polymorphisms associated with gains in V̇o 2max in the HERITAGE Family Study. Three of four novel candidate genes from the HERITAGE Family Study were confirmed as RNA predictor genes (i.e., “reciprocal” RNA validation of a quantitative trait locus genotype), enhancing the performance of the 29-RNA-based predictor. Notably, RNA abundance for the predictor genes was unchanged by exercise training, supporting the idea that expression was preset by genetic variation. Regression analysis yielded a model where 11 single-nucleotide polymorphisms explained 23% of the variance in gains in V̇o 2max , corresponding to ∼50% of the estimated genetic variance for V̇o 2max . In conclusion, combining RNA profiling with single-gene DNA marker association analysis yields a strongly validated molecular predictor with meaningful explanatory power. V̇o 2max responses to endurance training can be predicted by measuring a ∼30-gene RNA expression signature in muscle prior to training. The general approach taken could accelerate the discovery of genetic biomarkers, sufficiently discrete for diagnostic purposes, for a range of physiological and pharmacological phenotypes in humans.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.01295.2009
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2010
    detail.hit.zdb_id: 1404365-8
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    SSG: 31
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  • 8
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    Simultaneous measurement of nitric oxide production by conducting and alveolar airways of humans
    American Physiological Society ; 1999
    In:  Journal of Applied Physiology Vol. 87, No. 4 ( 1999-10-01), p. 1532-1542
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 87, No. 4 ( 1999-10-01), p. 1532-1542
    Abstract: Human airways produce nitric oxide (NO), and exhaled NO increases as expiratory flow rates fall. We show that mixing during exhalation between the NO produced by the lower, alveolar airways (V˙l NO ) and the upper conducting airways (V˙u NO ) explains this phenomenon and permits measurement ofV˙l NO ,V˙u NO , and the NO diffusing capacity of the conducting airways (Du NO ). After breath holding for 10–15 s the partial pressure of alveolar NO (Pa) becomes constant, and during a subsequent exhalation at a constant expiratory flow rate the alveoli will deliver a stable amount of NO to the conducting airways. The conducting airways secrete NO into the lumen (V˙u NO ), which mixes with Pa during exhalation, resulting in the observed expiratory concentration of NO (Pe). At fast exhalations, Pa makes a large contribution to Pe, and, at slow exhalations, NO from the conducting airways predominates. Simple equations describing this mixing, combined with measurements of Pe at several different expiratory flow rates, permit calculation of Pa,V˙u NO , and Du NO .V˙l NO is the product of Pa and the alveolar airway diffusion capacity for NO. In seven normal subjects, Pa = 1.6 ± 0.7 × 10 −6 (SD) Torr,V˙l NO = 0.19 ± 0.07 μl/min,V˙u NO = 0.08 ± 0.05 μl/min, and Du NO = 0.4 ± 0.4 ml ⋅ min −1 ⋅ Torr −1 . These quantitative measurements ofV˙l NO andV˙u NO are suitable for exploring alterations in NO production at these sites by diseases and physiological stresses.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1999.87.4.1532
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1404365-8
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  • 9
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    Effect of carbohydrate ingestion on glucose kinetics during exercise in the heat
    American Physiological Society ; 2001
    In:  Journal of Applied Physiology Vol. 90, No. 2 ( 2001-02-01), p. 601-605
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 90, No. 2 ( 2001-02-01), p. 601-605
    Abstract: Six endurance-trained men [peak oxygen uptake (V˙o 2 ) = 4.58 ± 0.50 (SE) l/min] completed 60 min of exercise at a workload requiring 68 ± 2% peak V˙o 2 in an environmental chamber maintained at 35°C ( 〈 50% relative humidity) on two occasions, separated by at least 1 wk. Subjects ingested either a 6% glucose solution containing 1 μCi [3- 3 H]glucose/g glucose (CHO trial) or a sweet placebo (Con trial) during the trials. Rates of hepatic glucose production [HGP = glucose rate of appearance (R a ) in Con trial] and glucose disappearance (R d ), were measured using a primed, continuous infusion of [6,6- 2 H]glucose, corrected for gut-derived glucose (gut R a ) in the CHO trial. No differences in heart rate, V˙o 2 , respiratory exchange ratio, or rectal temperature were observed between trials. Plasma glucose concentrations were similar at rest but increased ( P 〈 0.05) to a greater extent in the CHO trial compared with the Con trial. This was due to the absorption of ingested glucose in the CHO trial, because gut R a after 30 and 50 min (16 ± 5 μmol · kg −1 · min −1 ) was higher ( P 〈 0.05) compared with rest, whereas HGP during exercise was not different between trials. Glucose R d was higher ( P 〈 0.05) in the CHO trial after 30 and 50 min (48.0 ± 6.3 vs 34.6 ± 3.8 μmol · kg −1 · min −1 , CHO vs. Con, respectively). These results indicate that ingestion of carbohydrate, at a rate of ∼1.0 g/min, increases glucose R d but does not blunt the rise in HGP during exercise in the heat.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.2001.90.2.601
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 1404365-8
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  • 10
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    Circadian variation in swim performance
    American Physiological Society ; 2007
    In:  Journal of Applied Physiology Vol. 102, No. 2 ( 2007-02), p. 641-649
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 102, No. 2 ( 2007-02), p. 641-649
    Abstract: Previous findings of time-of-day differences in athletic performance could be confounded by diurnal fluctuations in environmental and behavioral “masking” factors (e.g., sleep, ambient temperature, and energy intake). The purpose of this study was to examine whether there is a circadian rhythm in swim performance that is independent of these masking factors. Experienced swimmers ( n = 25) were assessed for 50–55 consecutive hours in the laboratory. The swimmers followed a 3-h “ultra-short” sleep-wake cycle, involving 1 h of sleep in darkness and 2 h of wakefulness in dim light, that was repeated throughout the observation. The protocol distributes behavioral and environmental masking factors equally across the 24-h period. Each swimmer was scheduled to perform six maximal-effort 200-m swim trials that were distributed equally across eight times of day ( n = 147 trials). Each trial was separated by 9 h. A cosine fit of intra-aural temperature data established the time of the lowest body temperature (T min ). Swim performances were z-transformed and compared across the eight times of day and across twelve 2-h intervals relative to T min . Analysis of covariance, controlling for trial number, revealed a significant ( P 〈 0.001) pattern in swim performance relative to environmental and circadian times of day. Performance peaked 5–7 h before T min (∼2300) and was worst from 1 h before to 1 h after T min (∼0500). Mean swim performance was 169.5 s; circadian variation from peak to worst performance was 5.8 s. These data suggest a circadian rhythm in athletic performance independent of environmental and behavioral masking effects.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00910.2006
    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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