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Effects of hydration state on plasma testosterone, cortisol and catecholamine concentrations before and during mild exercise at elevated temperature (1994)

Hoffman, J. R. ; Maresh, C. M. ; Armstrong, L. E. ; [et al.]

Springer

European journal of applied physiology 69 (1994), S. 294-300

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ISSN: 1439-6327

Keywords: Dehydration ; Fluid intake ; Testosterone ; Cortisol ; Catecholamines

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Abstract This investigation examined the influence of pre-exercise hydration status, and water intake during low intensity exercise (5.6 km · h−1 at 5% gradient) in the heat (33° C), on plasma testosterone (TEST), cortisol (CORT), adrenaline (A), and noradrenaline (NA) concentrations at baseline (BL), pre-exercise (PRE), and immediately (IP), 24 h (24 P), and 48 h postexercise (48 P). Ten active men participated in four experimental treatments. These treatments differed in preexercise hydration status [euhydrated or hypohydrated (HY, −3.8 (SD 0.7)% body mass)] and water intake during exercise (water ad libitum or no water intake during exercise, NW). There were no significant changes in TEST, CORT, or A concentrations with time (BL, PRE, IP, 24 P, and 48 P), or among treatments. However, significant increases from BL and PRE plasma NA concentrations were observed at IP during all four treatment conditions. In addition, HY + NW resulted in significantly higher plasma NA concentrations at IP compared to all other treatments. These results suggest that moderate levels of hypohydration during prolonged, low intensity exercise in the heat do not influence plasma TEST, CORT, or A concentrations. However, plasma NA appears to respond in a sensitive manner to these hydration and exercise stresses.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF00392033

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Selective reduction of anaphase B in quinacrine-treated PtK1 cells (1989)

Armstrong, L. ; Snyder, Judith A.

New York, NY : Wiley-Blackwell

Cell Motility and the Cytoskeleton 14 (1989), S. 220-229

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ISSN: 0886-1544

Keywords: microtubules ; mitosis ; kinetochore ; Life and Medical Sciences ; Cell & Developmental Biology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology , Medicine

Notes: Quinacrine, an acridine derivative which competitively binds to ATP binding sites, has previously been shown to cause the reorganization of metaphase spindle microtubules (MTs) due to changes in interactions of non-kinetochore microtubules (nkMTs) of opposite polarity (Armstrong and Snyder: Cell Motil. Cytoskeleton 7:10-19, 1987). In the study presented here, mitotic PtK1 cells were treated in early anaphase with concentrations of quinacrine ranging from 2 to 12 μM to determine energy requirements for chromosome motion. The rate and extent of chromosome-to-pole movements (anaphase A) were not affected by these quinacrine treatments. The extent of anaphase B (kinetochore-kinetochore separation) was reduced with increasing concentrations of quinacrine. Five micromolar quinacrine reduced the extent of kinetochore-kinetochore separation by 20%, and addition of 12 μM quinacrine reduced the kinetochore-kinetochore separation by 40%. To determine the role of nkMTs in anaphase spindle elongationquinacrine-treated metaphase cells were treated with hyperosmotic sucrose concentrations, and spindle elongation was measured (Snyder et al.: Eur J. Cell Biol. 39:373-379, 1985). Metaphase cells treated with 2-10 μM concentrations of quinacrine for 2-5 min reduced spindle lengths by 10-50% prior to 0.5 M sucrose treatment for 5 min. This treatment showed a significant reduction in the ability of sucrose to induce spindle elongation in cells pretreated with quinacrine. As spindle length and birefringence was reduced by quinacrine treatment, sucrose-induced elongation was concomitantly diminished. These data suggest that quinacrine-sensitive linkages are necessary for anaphase B motions. Reduction in these linkages and/or MT length in the nkMT continuum may reduce the ability of the nkMTs to hold compression at metaphase. This form of energy is thought to drive a significant proportion of normal anaphase B in PtK1 cells and sucrose-induced metaphase spindle elongation.

Additional Material: 11 Ill.