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  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 1987
    In:  Journal of Applied Physiology Vol. 63, No. 3 ( 1987-09-01), p. 1107-1113
    In: Journal of Applied Physiology, American Physiological Society, Vol. 63, No. 3 ( 1987-09-01), p. 1107-1113
    Abstract: Hormonal and substrate influences on in vivo cellular membrane function were evaluated in 15 healthy male volunteers. Each subject underwent serial evaluations of membrane function in the anterior tibialis muscle, as assessed by transcutaneous measurement of resting membrane potential (Em). Group A subjects (n = 9) underwent measurement of resting Em in the basal state and again during the 10th day of intravenous feeding (IVF). Group B subjects (n = 6) underwent measurement of resting Em in the basal state during epinephrine infusion and again during epinephrine infusion on the 7th day of IVF. Percutaneous needle biopsy of the vastus lateralis muscle permitted calculation of transmembrane electrolyte distribution from the Nernst equation, using the measured Em and the chloride space method. Hospitalization with intake of a defined-formula enteral diet for 3 days resulted in depolarization (P less than 0.05) of resting Em (-75.3 +/- 1.6 mV) compared with normal (-79.8 +/- 0.9 mV). Despite 10 days of subsequent IVF, further depolarization (P less than 0.05) of resting Em (-71.2 +/- 1.2 mV) was observed. In the dual presence of IVF and exogenous epinephrine infusion, there was an increase (P less than 0.05) in intracellular potassium concentration and repolarization of resting Em (-80.6 +/- 0.8 mV) to normal levels. These data indicate that hormonal background and substrate availability contribute to the in vivo modulation of cellular membrane function in human skeletal muscle, possibly through facilitation of sodium-dependent amino acid transport across the cell membrane.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
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    Language: English
    Publisher: American Physiological Society
    Publication Date: 1987
    detail.hit.zdb_id: 1404365-8
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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 1978
    In:  Journal of Applied Physiology Vol. 44, No. 1 ( 1978-01-01), p. 85-89
    In: Journal of Applied Physiology, American Physiological Society, Vol. 44, No. 1 ( 1978-01-01), p. 85-89
    Abstract: The purpose of this study was to assess cardiac adaptation to endurance training in rats. After 11 wk of progressive treadmill exercise (1 h/day), gastrocnemius cytochrome c oxidase activity was 38% higher (P less than 0.01) in the trained (n = 20) as compared to control (n = 20) rats. Cardiac Mg2+-stimulated myofibril ATPase activity (0.308 +/- 0.012 vs. 0.324 +/- 0.006 micrometer.mg-1.min-1) did not change nor was there any change in myofibril protein concentration (60.0 +/- 1.12 vs. 59.9 +/- 0.85 mg.g-1). The isolated left ventricular papillary muscle showed no significant change in time-to-peak tension (TPT) or half-relaxation time. Tension output, however, was significantly increased with training, 2.2 +/- 0.3 vs. 1.5 +/- 0.1 g.mm-2 (P less than 0.025). Furthermore, when the papillary preparations were perfused with 0.5 mM lanthanum (La3+) to displace membrane-bound Ca2+, the time course for tension decay was significantly prolonged in the trained muscles (P less than 0.001). We conclude that endurance running of this type does not necessarily increase myofibril ATPase activity or the time course of the isometric twitch of rat papillary muscle. However, tension output per unit area does increase and this appears to be due to a greater amount of Ca2+ being made available to the contractile apparatus.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1978
    detail.hit.zdb_id: 1404365-8
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    SSG: 31
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  • 3
    Online Resource
    Online Resource
    American Physiological Society ; 1993
    In:  Journal of Applied Physiology Vol. 74, No. 1 ( 1993-01-01), p. 460-465
    In: Journal of Applied Physiology, American Physiological Society, Vol. 74, No. 1 ( 1993-01-01), p. 460-465
    Abstract: The effects of 8-epi-prostaglandin (PG) F2 alpha, a recently discovered noncyclooxygenase free radical-catalyzed product of arachidonic acid, on pulmonary vascular and airway tone, its potency, and its mechanism of action were studied. Progressively increasing bolus doses (1.0, 5.0, 10.0, and 20.0 micrograms) of 8-epi-PGF2 alpha were injected into the pulmonary artery catheter of 18 isolated rat lungs, and a single dose (40.0 micrograms) was injected into 7 additional rat lungs. The lungs were perfused with Krebs-Henseleit buffer solution containing 3% bovine serum albumin at 50 ml.kg-1.min-1 during ventilation with 21% O2–5% CO2–74% N2. 8-Epi-PGF2 alpha caused rapid pulmonary vascular and airway constrictor responses, which were followed by a gradual return over 10 min to baseline levels. Double vascular occlusion at peak rise in pulmonary arterial pressure (Ppa) revealed a 28% increase in arterial resistance. The rise in Ppa with 20 micrograms of 8-epi-PGF2 alpha was approximately twofold greater than with 20 micrograms of the cyclooxygenase-derived prostaglandin PGF2 alpha. The addition of 100 microM N-nitro-L-arginine, a blocker of endothelium-derived relaxing factor, in the perfusate potentiated the rise in Ppa by 244%. Injection of 40 micrograms of rat atrial natriuretic factor at peak response to 20 micrograms of 8-epi-PGF2 alpha accelerated the return to baseline Ppa, resistance to airflow across the lung, and dynamic lung compliance values.(ABSTRACT TRUNCATED AT 250 WORDS)
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1993
    detail.hit.zdb_id: 1404365-8
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  • 4
    In: Journal of Applied Physiology, American Physiological Society, Vol. 127, No. 6 ( 2019-12-01), p. 1622-1631
    Abstract: Arterial oxygen tension and oxyhemoglobin saturation ([Formula: see text] ) decrease in parallel during hypoxia. Distinguishing between changes in oxygen tension and oxygen content as the relevant physiological stimulus for cardiorespiratory alterations remains challenging. To overcome this, we recruited nine individuals with hemoglobinopathy manifesting as high-affinity hemoglobin [HAH; partial pressure at 50% [Formula: see text] (P 50 ) = 16 ± 0.4 mmHg] causing greater [Formula: see text] at a given oxygen partial pressure compared with control subjects ( n = 12, P 50  = 26 ± 0.4 mmHg). We assessed ventilatory and cardiovascular responses to acute isocapnic hypoxia, iso-oxic hypercapnia, and 20 min of isocapnic hypoxia (arterial Po 2  = 50 mmHg). Blood gas alterations were achieved with dynamic end-tidal forcing. When expressed as a function of the logarithm of oxygen partial pressure, ventilatory sensitivity to hypoxia was not different between groups. However, there was a significant difference when expressed as a function of [Formula: see text]. Conversely, the rise in heart rate was blunted in HAH subjects when expressed as a function of partial pressure but similar when expressed as a function of [Formula: see text] . Ventilatory sensitivity to hypercapnia was not different between groups. During sustained isocapnic hypoxia, the rise in minute ventilation was similar between groups; however, heart rate was significantly greater in the controls during 3 to 9 min of exposure. Our results support the notion that oxygen tension, not content, alters cellular Po 2 in the chemosensors and drives the hypoxic ventilatory response. Our study suggests that in addition to oxygen partial pressure, oxygen content may also influence the heart rate response to hypoxia. NEW & NOTEWORTHY We dissociated the effects of oxygen content and pressure of cardiorespiratory regulation studying individuals with high-affinity hemoglobin (HAH). During hypoxia, the ventilatory response, expressed as a function of oxygen tension, was similar between HAH variants and controls; however, the rise in heart rate was blunted in the variants. Our work supports the notion that the hypoxic ventilatory response is regulated by oxygen tension, whereas cardiovascular regulation may be influenced by arterial oxygen content and tension.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
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    Language: English
    Publisher: American Physiological Society
    Publication Date: 2019
    detail.hit.zdb_id: 1404365-8
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    SSG: 31
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  • 5
    Online Resource
    Online Resource
    American Physiological Society ; 1981
    In:  Journal of Applied Physiology Vol. 51, No. 2 ( 1981-08-01), p. 485-493
    In: Journal of Applied Physiology, American Physiological Society, Vol. 51, No. 2 ( 1981-08-01), p. 485-493
    Abstract: Bradykinin stimulates the afferent vagal endings of bronchial C-fibers but has little effect on other pulmonary vagal afferents. In anesthetized dogs with open chest, we recorded transverse tension in the posterior wall (trachealis muscle) of an upper cervical tracheal segment and stimulated bronchial C-fibers selectively by injecting bradykinin (19 ng-3 microgram) into a bronchial artery. The recurrent and pararecurrent laryngeal nerves were cut so that the superior laryngeal nerves provided the motor supply to the segment. Bradykinin caused a dose-dependent increase in tracheal muscle tension and often a conspicuous decrease in heart rate, which were abolished by vagotomy or administration of atropine. Injection of bradykinin still evoked tracheal contraction when myelinated lung afferents were blocked by cooling the midcervical vagi to 7 degrees C, but contraction was abolished when unmyelinated lung afferents were blocked by cooling to 0-1 degrees C, the effects of cooling being reversible. Our results indicate that stimulation of bronchial C-fibers, like that of pulmonary C-fibers, evokes reflux contraction of airway smooth muscle and reflex cardiac slowing.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1981
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 6
    Online Resource
    Online Resource
    American Physiological Society ; 1992
    In:  Journal of Applied Physiology Vol. 72, No. 1 ( 1992-01-01), p. 219-225
    In: Journal of Applied Physiology, American Physiological Society, Vol. 72, No. 1 ( 1992-01-01), p. 219-225
    Abstract: Biomechanical changes in airway cartilage could influence the mechanics of maximal expiratory flow and cough and the degree of shortening of activated airway smooth muscle. We examined the tensile stiffness of small samples of human tracheal cartilage rings in specimens obtained at autopsy from 10 individuals who ranged in age from 17 to 81 yr. The tensile properties of the cartilage were compared with its content of water (%water), glycosaminoglycans (chondroitin sulfate equivalents, mg/mg dry wt), and hydroxyproline content (mg hydroxyproline/mg dry weight). The average values for tensile stiffness ranged between 1 and 15 MPa and increased significantly with increasing age [tensile stiffness = 0.19 x (age in yr) + 2.02; r = 0.83, P less than 0.05]. The outermost layer of cartilage was the most stiff in all individuals, and the deeper layers were progressively less stiff. Water content and hydroxyproline content both decreased with increasing age. Thus tensile stiffness correlated inversely with water content and hydroxyproline content [tensile stiffness = -0.83 x (%water) + 16.4; r = 0.82, P less than .05 and tensile stiffness = -342 x (hydroxyproline content) + 25; r = 0.87, P less than 0.05] . Total tissue content of glycosaminoglycans did not change with age, although changes in glycosaminoglycan type and proteoglycan structure with increasing age have been described. We conclude that there are age-related changes in the biomechanical properties and biochemical composition of airway cartilage that could influence airway dynamics.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1992
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 7
    Online Resource
    Online Resource
    American Physiological Society ; 1974
    In:  Journal of Applied Physiology Vol. 37, No. 4 ( 1974-10), p. 515-520
    In: Journal of Applied Physiology, American Physiological Society, Vol. 37, No. 4 ( 1974-10), p. 515-520
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1974
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 8
    Online Resource
    Online Resource
    American Physiological Society ; 1998
    In:  Journal of Applied Physiology Vol. 84, No. 4 ( 1998-04-01), p. 1311-1315
    In: Journal of Applied Physiology, American Physiological Society, Vol. 84, No. 4 ( 1998-04-01), p. 1311-1315
    Abstract: This study was designed to examine the effects of a high-fat refined-sugar (HFS) or a low-fat complex-carbohydrate (LFCC) diet on insulin-stimulated skeletal muscle glucose transport, plasma insulin, blood pressure, plasma triglycerides, plasma glycerol, body weight, and body fat in female Fischer rats. Insulin-stimulated glucose transport was significantly reduced in the HFS group at 2 wk, 2 mo, and 2 yr, whereas serum insulin was significantly elevated at all time points. Blood pressure was not significantly elevated in the HFS group until 12 mo, and all HFS animals were hypertensive by 18 mo. Glycerol, triglycerides, and abdominal fat cell size were not significantly different at 2 wk but were significantly elevated in the HFS rats at 2 and 6 mo. Body weight was similar in both groups until 20 wk on the diet, when the HFS rats started to gain more weight. These results demonstrate that insulin resistance and hyperinsulinemia occur before the other manifestations of the metabolic syndrome and that diet, not obesity, is the underlying cause.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
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    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1998
    detail.hit.zdb_id: 1404365-8
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    SSG: 31
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  • 9
    In: Journal of Applied Physiology, American Physiological Society, Vol. 127, No. 1 ( 2019-07-01), p. 254-263
    Abstract: Effective treatments preventing brain neuroinflammatory diseases are lacking. Resistance-exercise training (RT) ameliorates mild cognitive impairment (MCI), a forerunner to neuroinflammatory diseases. However, few studies have addressed the molecular basis by which RT abates MCI. Thus experiments were performed to identify some molecular changes occurring in response to RT in young, female Wistar rats. To induce MCI, intraventricular lipopolysaccharide (LPS) injections were used to increase dentate gyrus inflammation, reflected by significantly increased TNF-α (~400%) and IL-1β (~1,500%) mRNA ( P 〈 0.0001) after 6 wk. Five days after LPS injections, half of LPS-injected rats performed RT by ladder climbing for 6 wk, 3 days/wk, whereas half remained without ladders. RT for 6 wk increased lean body mass percentage ( P 〈 0.05), individual muscle masses (gastrocnemius and tibialis anterior) ( P 〈 0.05), and maximum lifting capacity ( P 〈 0.001). The RT group, compared with sedentary controls, had 1) ameliorated spatial learning deficits ( P 〈 0.05), 2) increased dentate gyrus phosphorylation of IGF-1R, protein kinase B, and GSK-3β proteins ( P 〈 0.05), components of downstream IGF-1 signaling, and 3) increased dentate gyrus synaptic plasticity marker synapsin protein ( P 〈 0.05). Two follow-up experiments (without LPS) characterized dentate gyrus signaling during short-term RT. Twenty-four hours following the third workout in a 1-wk training duration, phosphorylation of ERK1/2 and GSK-3β proteins, as well as proliferation marker protein, PCNA, were significantly increased ( P 〈 0.05). Similar changes did not occur in a separate group of rats following a single RT workout. Taken together, these data indicate that RT ameliorates LPS-induced MCI after RT, possibly mediated by increased IGF-1 signaling pathway components within the dentate gyrus. NEW & NOTEWORTHY The data suggest that resistance-exercise training restores cognitive deficits induced by lipopolysaccharides and can activate associated IGF-1 signaling in the dentate gyrus. Our data show, for the first time, that as few as three resistance-exercise workouts (spread over 1 wk) can activate IGF-1 downstream signaling and increase proliferation marker PCNA in the dentate gyrus.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2019
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 10
    In: Journal of Applied Physiology, American Physiological Society, Vol. 97, No. 5 ( 2004-11), p. 1978-1984
    Abstract: We tested the hypothesis that the oral α 1 -adrenergic agonist, midodrine, would limit the fall in arterial pressure observed during exercise in patients with pure autonomic failure (PAF). Fourteen subjects with PAF underwent a stand test, incremental supine cycling exercise (25, 50, and 75 W), and ischemic calf exercise, before (control) and 1 h after ingesting 10 mg midodrine. Heart rate (ECG), beat-to-beat blood pressure (MAP, arterial catheter), cardiac output (Q̇, open-circuit acetylene breathing), forearm blood flow (FBF, Doppler ultrasound), and calf blood flow (CBF, venous occlusion plethysmography) were measured. The fall in MAP after standing for 2 min was similar (∼60 mmHg; P = 0.62). Supine MAP immediately before cycling was greater after midodrine (124 ± 6 vs 117 ± 6 mmHg; P 〈 0.03), but cycling caused a workload-dependent hypotension ( P 〈 0.001), whereas increases in Q̇ were modest but similar. Midodrine increased MAP and total peripheral resistance (TPR) during exercise ( P 〈 0.04), but the exercise-induced fall in MAP and TPR were similar during control and midodrine ( P = 0.27 and 0.14). FBF during cycling was not significantly reduced by midodrine ( P 〉 0.2). By contrast, recovery of MAP after cycling was faster ( P 〈 0.04) after midodrine (∼25 mmHg higher after 5 min). Ischemic calf exercise evoked similar peak CBF in both trials, but midodrine reduced the hyperemic response over 5 min of recovery ( P 〈 0.02). We conclude midodrine improves blood pressure and TPR during exercise and dramatically improves the recovery of MAP after exercise.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2004
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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