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  • 11
    Online Resource
    Online Resource
    Effects of “priming” exercise on pulmonary O 2 uptake and muscle deoxygenation kinetics during heavy-intensity cycle exercise in the supine and upright positions
    American Physiological Society ; 2006
    In:  Journal of Applied Physiology Vol. 101, No. 5 ( 2006-11), p. 1432-1441
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 101, No. 5 ( 2006-11), p. 1432-1441
    Abstract: We hypothesized that the performance of prior heavy exercise would speed the phase 2 oxygen consumption (V̇o 2 ) kinetics during subsequent heavy exercise in the supine position (where perfusion pressure might limit muscle O 2 supply) but not in the upright position. Eight healthy men (mean ± SD age 24 ± 7 yr; body mass 75.0 ± 5.8 kg) completed a double-step test protocol involving two bouts of 6 min of heavy cycle exercise, separated by a 10-min recovery period, on two occasions in each of the upright and supine positions. Pulmonary O 2 uptake was measured breath by breath and muscle oxygenation was assessed using near-infrared spectroscopy (NIRS). The NIRS data indicated that the performance of prior exercise resulted in hyperemia in both body positions. In the upright position, prior exercise had no significant effect on the time constant (τ) of the V̇o 2 response in phase 2 ( bout 1: 29 ± 10 vs. bout 2: 28 ± 4 s; P = 0.91) but reduced the amplitude of the V̇o 2 slow component ( bout 1: 0.45 ± 0.16 vs. bout 2: 0.22 ± 0.14 l/min; P = 0.006) during subsequent heavy exercise. In contrast, in the supine position, prior exercise resulted in a significant reduction in the phase 2 τ ( bout 1: 38 ± 18 vs. bout 2: 24 ± 9 s; P = 0.03) but did not alter the amplitude of the V̇o 2 slow component ( bout 1: 0.40 ± 0.29 vs. bout 2: 0.41 ± 0.20 l/min; P = 0.86). These results suggest that the performance of prior heavy exercise enables a speeding of phase 2 V̇o 2 kinetics during heavy exercise in the supine position, presumably by negating an O 2 delivery limitation that was extant in the control condition, but not during upright exercise, where muscle O 2 supply was probably not limiting.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00436.2006
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2006
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 12
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    Online Resource
    Activity level, apoptosis, and development of cachexia in Apc Min /+ mice
    American Physiological Society ; 2010
    In:  Journal of Applied Physiology Vol. 109, No. 4 ( 2010-10), p. 1155-1161
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 109, No. 4 ( 2010-10), p. 1155-1161
    Abstract: Criteria for diagnosing cachexia in adults include unintentional loss in body weight, decreased strength, fatigue, anorexia, and low muscle mass. Cachexia is also associated with systemic inflammation, altered metabolism, and anemia. The Apc Min/+ mouse is a model of cachexia directly related to intestinal tumor burden and subsequent chronic inflammation. These mice also demonstrate muscle weakness, fatigue, decreased volitional activity, and elevated circulating IL-6 levels. The purpose of this study was to determine the time course of changes in physical activity and their relationship to anemia, muscle apoptosis, and muscle mass and body mass loss during cachexia. A subset of male Apc Min/+ mice were given access to voluntary activity wheels from 5 to 26 wk of age, while sedentary male Apc Min/+ mice were housed in cages lacking wheels. At the study's end mice were stratified by cachectic symptoms. Severely cachectic mice had decreased wheel running performance at 15 wk of age, while anemia and body weight loss were not present until 18 wk of age. Severely cachectic mice had lower hemoglobin levels compared with mildly cachectic mice at 13, 18, and 22 wk of age. Severely cachectic mice also demonstrated threefold more BCL2-associated X protein (BAX) protein in the gastrocnemius muscle at 26 wk of age compared with mildly cachectic mice. In sedentary Apc Min/+ mice at 26 wk of age anemia was present, and markers of apoptosis were induced in severely cachectic muscle. Proapoptotic protein expression was induced in both red and white portions of gastrocnemius muscle as well as in soleus muscle of severely cachectic mice compared with mildly cachectic mice. These data demonstrate that decrements in wheel running performance precede loss of body mass and that inherent muscle oxidative capacity is not protective against muscle apoptosis.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00442.2010
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2010
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 13
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    Online Resource
    Measuring lung liquid volume and secretion using radioiodinated serum albumin and blue dextran
    American Physiological Society ; 2003
    In:  Journal of Applied Physiology Vol. 94, No. 3 ( 2003-03-01), p. 1293-1294
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 94, No. 3 ( 2003-03-01), p. 1293-1294
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.1152/japplphysiol.00872.2002
    DOI: 10.1152/japplphysiol.00872.2002
    DOI: 10.1152/japplphysiol.00872.2002
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2003
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 14
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    Online Resource
    Thermoregulation, metabolism, and stages of sleep in cold-exposed men
    American Physiological Society ; 1986
    In:  Journal of Applied Physiology Vol. 61, No. 3 ( 1986-09-01), p. 940-947
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 61, No. 3 ( 1986-09-01), p. 940-947
    Abstract: Four naked men, selected for their ability to sleep in the cold, were exposed to an ambient temperature (Ta) of 21 degrees C for five consecutive nights. Electrophysiological stages of sleep, O2 consumption (VO2), and skin (Tsk), rectal (Tre), and tympanic (Tty) temperatures were recorded. Compared with five nights at a thermoneutral Ta of 29 degrees C, cold induced increased wakefulness and decreased stage 2 sleep, without significantly affecting other stages. Tre and Tty declined during each condition. The decrease in Tre was greater at 21 degrees C than at 29 degrees C, whereas Tty did not differ significantly between conditions. Increases in Tty following REM sleep onset at 21 degrees C were negatively correlated with absolute Tty. VO2 and forehead Tsk also increased during REM sleep at both TaS, whereas Tsk of the limb extremities declined at 21 degrees C. Unsuppressed REM sleep in association with peripheral vasoconstriction and increased Tty and VO2 in cold-exposed humans, do not signify an inhibition of thermoregulation during this sleep stage as has been observed in other mammals.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1986.61.3.940
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1986
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 15
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    Online Resource
    Plasma Met-enkephalin and catecholamine responses to intense exercise in humans
    American Physiological Society ; 1992
    In:  Journal of Applied Physiology Vol. 73, No. 1 ( 1992-07-01), p. 388-392
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 73, No. 1 ( 1992-07-01), p. 388-392
    Abstract: Native and cryptic Met-enkephalin and catecholamines are coreleased in response to stress. However, it is not known whether Met-enkephalin and catecholamines exhibit concurrent temporal relationships in response to exercise. The purpose of this investigation was to examine the corelease of catecholamines and Met-enkephalin in endurance-trained (n = 6) and untrained (n = 6) male subjects during a 6-min bout of exercise: 4 min at 70% of maximal O2 uptake (VO2max) followed by 2 min at 120% VO2max. Peak catecholamine levels were found at 1 min of recovery. In trained subjects, native Met-enkephalin peaked during exercise at 70% VO2max, declined during exercise at 120% VO2max, and returned to basal levels by 1 min of recovery. In the untrained subjects, native Met-enkephalin peaked at 120% VO2max (6 min) and returned to baseline by 5 min of recovery. In both groups, cryptic Met-enkephalin peaked at 70% VO2max and returned to basal levels during exercise at 120% VO2max. These data demonstrate that during exercise there is a temporal dissociation in plasma levels of Met-enkephalin and catecholamines.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1992.73.1.388
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1992
    detail.hit.zdb_id: 1404365-8
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    SSG: 31
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  • 16
    Online Resource
    Online Resource
    Use of rubber membranes to improve sucrose-gap and other electrical recording techniques
    American Physiological Society ; 1969
    In:  Journal of Applied Physiology Vol. 26, No. 3 ( 1969-03-01), p. 378-382
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 26, No. 3 ( 1969-03-01), p. 378-382
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1969.26.3.378
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1969
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 17
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    Online Resource
    Three-dimensional alignment of the aggregated myocytes in the normal and hypertrophic murine heart
    American Physiological Society ; 2009
    In:  Journal of Applied Physiology Vol. 107, No. 3 ( 2009-09), p. 921-927
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 107, No. 3 ( 2009-09), p. 921-927
    Abstract: Several observations suggest that the transmission of myocardial forces is influenced in part by the spatial arrangement of the myocytes aggregated together within ventricular mass. Our aim was to assess, using diffusion tensor magnetic resonance imaging (DT-MRI), any differences in the three-dimensional arrangement of these myocytes in the normal heart compared with the hypertrophic murine myocardium. We induced ventricular hypertrophy in seven mice by infusion of angiotensin II through a subcutaneous pump, with seven other mice serving as controls. DT-MRI of explanted hearts was performed at 3.0 Tesla. We used the primary eigenvector in each voxel to determine the three-dimensional orientation of aggregated myocytes in respect to their helical angles and their transmural courses (intruding angles). Compared with controls, the hypertrophic hearts showed significant increases in myocardial mass and the outer radius of the left ventricular chamber ( P 〈 0.05). In both groups, a significant change was noted from positive intruding angles at the base to negative angles at the ventricular apex ( P 〈 0.01). Compared with controls, the hypertrophied hearts had significantly larger intruding angles of the aggregated myocytes, notably in the apical and basal slices ( P 〈 0.001). In both groups, the helical angles were greatest in midventricular sections, albeit with significantly smaller angles in the mice with hypertrophied myocardium ( P 〈 0.01). The use of DT-MRI revealed significant differences in helix and intruding angles of the myocytes in the mice with hypertrophied myocardium.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00275.2009
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2009
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 18
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    Online Resource
    Exercise intensity typical of mountain climbing does not exacerbate acute mountain sickness in normobaric hypoxia
    American Physiological Society ; 2012
    In:  Journal of Applied Physiology Vol. 113, No. 7 ( 2012-10-01), p. 1068-1074
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 113, No. 7 ( 2012-10-01), p. 1068-1074
    Abstract: Physical exertion is thought to exacerbate acute mountain sickness (AMS). In this prospective, randomized, crossover trial, we investigated whether moderate exercise worsens AMS in normobaric hypoxia (12% oxygen, equivalent to 4,500 m). Sixteen subjects were exposed to altitude twice: once with exercise [3 × 45 min within the first 4 h on a bicycle ergometer at 50% of their altitude-specific maximal workload (maximal oxygen uptake)], and once without. AMS was evaluated by the Lake Louise score and the AMS-C score of the Environmental Symptom Questionnaire. There was no significant difference in AMS between the exposures with and without exercise, neither after 5, 8, nor 18 h (incidence: 64 and 43%; LLS: 6.5 ± 0.7 and 5.1 ± 0.8; AMS-C score: 1.2 ± 0.3 and 1.1 ± 0.3 for exercise vs. rest at 18 h; all P 〉 0.05). Exercise decreased capillary Po 2 (from 36 ± 1 Torr at rest to 31 ± 1 Torr), capillary arterial oxygen saturation (from 72% at rest to 67 ± 2%), and cerebral oxygen saturation (from 49 ± 2% at rest to 42 ± 1%, as assessed by near-infrared spectroscopy; P 〈 0.05), and increased ventilation (capillary Pco 2 27 ± 1 Torr; P 〈 0.05). After exercise, the increase in ventilation persisted for several hours and was associated with similar levels of capillary and cerebral oxygenation at the exercise and rest day. We conclude that moderate exercise at ∼50% maximal oxygen uptake does not increase AMS in normobaric hypoxia. These data do not exclude that considerably higher exercise intensities exacerbate AMS.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00329.2012
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2012
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 19
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    Online Resource
    Remote ischemic preconditioning does not prevent acute mountain sickness after rapid ascent to 3,450 m
    American Physiological Society ; 2017
    In:  Journal of Applied Physiology Vol. 123, No. 5 ( 2017-11-01), p. 1228-1234
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 123, No. 5 ( 2017-11-01), p. 1228-1234
    Abstract: Remote ischemic preconditioning (RIPC) has been shown to protect remote organs, such as the brain and the lung, from damage induced by subsequent hypoxia or ischemia. Acute mountain sickness (AMS) is a syndrome of nonspecific neurologic symptoms and in high-altitude pulmonary edema excessive hypoxic pulmonary vasoconstriction (HPV) plays a pivotal role. We hypothesized that RIPC protects the brain from AMS and attenuates the magnitude of HPV after rapid ascent to 3,450 m. Forty nonacclimatized volunteers were randomized into two groups. At low altitude (750 m) the RIPC group ( n = 20) underwent 4 × 5 min of lower-limb ischemia (induced by inflation of bilateral thigh cuffs to 200 mmHg) followed by 5 min of reperfusion. The control group ( n = 20) underwent a sham protocol (4 × 5 min of bilateral thigh cuff inflation to 20 mmHg). Thereafter, participants ascended to 3,450 m by train over 2 h and stayed there for 48 h. AMS was evaluated by the Lake Louise score (LLS) and the AMS-C score. Systolic pulmonary artery pressure (SPAP) was assessed by transthoracic Doppler echocardiography. RIPC had no effect on the overall incidence (RIPC: 35%, control: 35%, P = 1.0) and severity (RIPC vs. control: P = 0.496 for LLS; P = 0.320 for AMS-C score) of AMS. RIPC also had no significant effect on SPAP [maximum after 10 h at high altitude; RIPC: 33 (SD 8) mmHg; controls: 37 (SD 7) mmHg; P = 0.19]. This study indicates that RIPC, performed immediately before passive ascent to 3,450 m, does not attenuate AMS and the magnitude of high-altitude pulmonary hypertension. NEW & NOTEWORTHY Remote ischemic preconditioning (RIPC) has been reported to improve neurologic and pulmonary outcome following an acute ischemic or hypoxic insult, yet the effect of RIPC for protecting from high-altitude diseases remains to be determined. The present study shows that RIPC, performed immediately before passive ascent to 3,450 m, does not attenuate acute mountain sickness and the degree of high-altitude pulmonary hypertension. Therefore, RIPC cannot be recommended for prevention of high-altitude diseases.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00505.2017
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2017
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 20
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    Online Resource
    Dimethylthiourea decreases acute lung edema in phorbol myristate acetate-treated rabbits
    American Physiological Society ; 1986
    In:  Journal of Applied Physiology Vol. 61, No. 1 ( 1986-07-01), p. 353-360
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 61, No. 1 ( 1986-07-01), p. 353-360
    Abstract: Treatment with dimethylthiourea (DMTU), a potent O2 metabolite scavenger, prevented neutrophil-mediated acute edema in lungs of rabbits given phorbol myristate acetate (PMA) and in isolated rabbit lungs perfused with neutrophils and PMA. DMTU-treated rabbits given PMA did not increase their lung weight-to-total body weight ratios (5.0 +/- 0.3) or lung lavage albumin concentrations (14 +/- 4.6 mg/dl) in comparison to untreated rabbits given PMA (6.6 +/- 0.5 and 60 +/- 10 mg/dl, respectively). Similarly, DMTU-treated isolated rabbit lungs perfused with neutrophils and PMA did not gain weight (0 g) or increase their lavage albumin concentrations (82 +/- 17 mg/dl) in comparison to untreated lungs perfused with neutrophils and PMA (71 +/- 3.1 g and 1,299 +/- 47 mg/dl, respectively). DMTU did not appear to decrease edema by preventing increases in pulmonary arterial pressures (PAP). First, treatment with DMTU did not decrease initial PAP increases in rabbits given PMA. Second, even though addition of DMTU attenuated PAP increases in isolated lungs perfused with neutrophils and PMA, DMTU-treated isolated lungs did not develop acute edema when subjected to mechanical increases in venous outflow pressures. The mechanism by which DMTU decreases lung edema is unclear but may involve scavenging of toxic O2 metabolites, since DMTU also decreased hydrogen peroxide (H2O2) and hydroxyl radical (OH) concentrations in in vitro mixtures containing neutrophils and PMA.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1986.61.1.353
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1986
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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