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  • American Physiological Society  (4)
  • Biology  (4)
  • 1
    Online Resource
    Online Resource
    Cardiovascular dynamics in healthy subjects with differing heart rate responses to tilt
    American Physiological Society ; 2008
    In:  Journal of Applied Physiology Vol. 105, No. 5 ( 2008-11), p. 1448-1453
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 105, No. 5 ( 2008-11), p. 1448-1453
    Abstract: Orthostatic stress such as head-up tilt (HUT) elicits a wide range of heart rate (HR) and arterial pressure (AP) responses among healthy individuals. In this study, we evaluated cardiovascular dynamics in healthy subjects with different HR responses to HUT, but without autonomic dysfunction. We measured AP (brachial artery) and HR (ECG) during 5 min of 60° HUT in 76 healthy normotensive individuals. We then chose individuals on the basis of the extremes of HR responses to HUT (high = ΔHR ≥ 20 beats/min, and low = ΔHR ≤ 10 beats/min; n = 15 per group). Peak HR during HUT was 87 ± 10 beats/min in the high and 69 ± 14 beats/min in the low group ( P 〈 0.05). High HR responders had lower systolic pressure at baseline (121 ± 9 vs. 129 ± 11 mmHg, P 〈 0.05) and during HUT (120 ± 10 vs. 131 ± 13 mmHg, P 〈 0.05), and higher plasma norepinephrine (NE) response to HUT (ΔNE: 156.9 ± 17.8 vs. 89.0 ± 17.2 pg/ml; P 〈 0.05). ΔNE during HUT was also significantly correlated with ΔHR when all 76 subjects were included in a regression analysis ( r = 0.39; P 〈 0.001). Pulse pressure was lower during HUT in high HR responders compared with low HR responders (45 ± 1 vs. 55 ± 2 mmHg, P 〈 0.05). High HR responders also had larger fluctuations in systolic and pulse pressure during HUT (coefficient of variation = 10.7 ± 0.7 vs. 5.7 ± 0.3%; 7.9 ± 0.5 vs. 4.1 ± 0.4%, respectively, P 〈 0.05). Sex distribution was different between groups (high: 5 women, 10 men; low: 10 women, 5 men). Higher HR with lower AP during HUT is consistent with normal baroreflex mechanisms of integration. Although interindividual variability appears to be a fundamental part of cardiovascular regulation, the mechanisms of these differences and the sex discrepancy requires further investigation.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.90796.2008
    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
    Location Call Number Limitation Availability
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  • 2
    Online Resource
    Online Resource
    Effect of aerobic exercise on tumor physiology in an animal model of human breast cancer
    American Physiological Society ; 2010
    In:  Journal of Applied Physiology Vol. 108, No. 2 ( 2010-02), p. 343-348
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 108, No. 2 ( 2010-02), p. 343-348
    Abstract: Recent epidemiologic studies report that regular exercise may be associated with substantial reductions in cancer-specific and all-cause mortality following a breast cancer diagnosis. The mechanisms underlying this relationship have not been identified. We investigated the effects of long-term voluntary wheel running on growth and progression using an animal model of human breast cancer. We also examined effects on the central features of tumor physiology, including markers of tumor blood perfusion/vascularization, hypoxia, angiogenesis, and metabolism. Athymic female mice fed a high-fat diet were orthotopically (direct into the mammary fat pad) implanted with human breast cancer cells (MDA-MB-231 at 1 × 10 6 ) into the right dorsal mammary fat pad and randomly assigned (1:1) to voluntary wheel running ( n = 25) or a nonintervention (sedentary) control group ( n = 25). Tumor volume was measured every three days using digital calipers. All experimental animals were killed when tumor volume reached ≥1,500 mm 3 . Kaplan-Meier (KM) analysis indicated that tumor growth (survival) was comparable between the experimental groups (exercise 44 days vs. control 48 days; KM proportional hazard ratio = 1.41, 95% confidence interval, 0.77–2.58, P = 0.14). However, tumors from exercising animals had significantly improved blood perfusion/vascularization relative to the sedentary control group ( P 〈 0.05). Histological analyses indicated that intratumoral hypoxia levels (as assessed by hypoxia-inducible factor 1) were significantly higher in the exercise group relative to sedentary control ( P 〈 0.05). Aerobic exercise can significantly increase intratumoral vascularization, leading to “normalization” of the tissue microenvironment in human breast tumors. Such findings may have important implications for inhibiting tumor metastasis and improving the efficacy of conventional cancer therapies.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00424.2009
    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
    Location Call Number Limitation Availability
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  • 3
    Online Resource
    Online Resource
    Treatment with oxandrolone and the durability of effects in older men
    American Physiological Society ; 2004
    In:  Journal of Applied Physiology Vol. 96, No. 3 ( 2004-03), p. 1055-1062
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 96, No. 3 ( 2004-03), p. 1055-1062
    Abstract: We investigated the effects of the anabolic androgen, oxandrolone, on lean body mass (LBM), muscle size, fat, and maximum voluntary muscle strength, and we determined the durability of effects after treatment was stopped. Thirty-two healthy 60- to 87-yr-old men were randomized to receive 20 mg oxandrolone/day ( n = 20) or placebo ( n = 12) for 12 wk. Body composition [dual-energy X-ray absorptiometry (DEXA), magnetic resonance imaging, and 2 H 2 O dilution] and muscle strength [1 repetition maximum (1 RM)] were evaluated at baseline and after 12 wk of treatment; body composition (DEXA) and 1-RM strength were then assessed 12 wk after treatment was discontinued ( week 24). At week 12, oxandrolone increased LBM by 3.0 ± 1.5 kg ( P 〈 0.001), total body water by 2.9 ± 3.7 kg ( P = 0.002), and proximal thigh muscle area by 12.4 ± 8.4 cm 2 ( P 〈 0.001); these increases were greater ( P 〈 0.003) than in the placebo group. Oxandrolone increased 1-RM strength for leg press by 6.7 ± 6.4% ( P 〈 0.001), leg flexion by 7.0 ± 7.8% ( P 〈 0.001), chest press by 9.3 ± 6.7% ( P 〈 0.001), and latissimus pull-down exercises by 5.1 ± 9.1% ( P = 0.02); these increases were greater than placebo. Oxandrolone reduced total (-1.9 ± 1.0 kg) and trunk fat (-1.3 ± 0.6 kg; P 〈 0.001), and these decreases were greater ( P 〈 0.001) than placebo. Twelve weeks after oxandrolone was discontinued ( week 24), the increments in LBM and muscle strength were no longer different from baseline ( P 〉 0.15). However, the decreases in total and trunk fat were sustained (-1.5 ± 1.8, P = 0.001 and -1.0 ± 1.1 kg, P 〈 0.001, respectively). Thus oxandrolone induced short-term improvements in LBM, muscle area, and strength, while reducing whole body and trunk adiposity. Anabolic improvements were lost 12 wk after discontinuing oxandrolone, whereas improvements in fat mass were largely sustained.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00808.2003
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2004
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
    Location Call Number Limitation Availability
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    Online Resource
  • 4
    Online Resource
    Online Resource
    Role of blood and vascular smooth muscle in the vasoactivity of nitrite
    American Physiological Society ; 2014
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 307, No. 7 ( 2014-10-01), p. H976-H986
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 307, No. 7 ( 2014-10-01), p. H976-H986
    Abstract: Recent evidence from humans and rats indicates that nitrite is a vasodilator under hypoxic conditions by reacting with metal-containing proteins to produce nitric oxide (NO). We tested the hypothesis that near-physiological concentrations of nitrite would produce vasodilation in a hypoxia- and concentration-dependent manner in the hind limb of sheep. Anesthetized sheep were instrumented to measure arterial blood pressure and femoral blood flows continuously in both hind limbs. Nitrite was infused into one femoral artery to raise the nitrite concentration in the femoral vein by 10 to 15-fold while the sheep breathed 50%, 14% or 12% oxygen in inspired air. In contrast to reports in humans and rats, the nitrite infusion had no measurable effect on mean femoral blood flows or vascular conductances, regardless of inspired O 2 levels. In vitro experiments showed no significant difference in the release of NO from nitrite in sheep and human red blood cells. Further experiments demonstrated nitrite is converted to NO in rat artery homogenates faster than sheep arteries, and that this source of NO production is attenuated in the presence of a heme oxidizer. Finally, western blots indicate that concentrations of the heme-containing protein cytoglobin, but not myoglobin, are markedly lower in sheep arteries compared with rats. Overall, the results demonstrate that nitrite is not a physiological vasodilator in sheep. This is likely due to a lack of conversion of nitrite to NO within the vascular smooth muscle, perhaps due to deficient amounts of the heme-containing protein cytoglobin.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00138.2014
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2014
    detail.hit.zdb_id: 1477308-9
    SSG: 12
    Location Call Number Limitation Availability
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