Biomedical subjects

K C Westerlind

Publications and source records attributed to K C Westerlind.

22 records · Page 2Linked to original sources

PubMed1994

The effect of long-term ovarian hormone deficiency on transforming growth factor-beta and bone matrix protein mRNA expression in rat femora.

Estrogen deficiency results in increased bone turnover and osteopenia. Decreased transforming growth factor beta (TGF-beta) has been implicated as having a role in ovariectomy (OVX)-induced bone loss; however the decrease in TGF-beta mRNA may simply be due to the reduction in cancellous bone volume that occurs following OVX. This investigation characterized the effect of long-term OVX (11.5 months) on mRNA levels for TGF-beta, osteocalcin (OC), and type I collagen (TYPE I) and expressed these data relative to the amount of cancellous bone surface. Additionally, the short-term effect of estrogen administration on TGF-beta, OC, and TYPE I mRNA was evaluated. OVX resulted in a 56% loss of bone surface. At the tissue level, TGF-beta was reduced, OC was increased, and TYPE I was unchanged. Expressed relative to bone surface, TGF-beta was unchanged and OC and TYPE I were significantly elevated. Four hours after estrogen administration, TGF-beta mRNA was unchanged compared to vehicle-treated controls. The data suggest that bone turnover is elevated after long-term OVX, but do not suggest a direct role of TGF-beta in OVX-induced bone loss.

Aging↗

PubMed1994

Alterations in oxygen consumption during and between bouts of level and downhill running.

Since the etiology of the drift in VO2 during downhill running is unclear, this study was designed to assess the contribution of heart rate (HR), ventilation (VE), blood lactate, rectal temperature (RT), muscle damage, and several variables that have not previously been included in VO2 drift research: muscle temperature (MT), and stride rate (SR) and length (SL), to the drift in VO2. Six subjects participated in a 45-min level run (LEVEL) and two 45-min downhill runs (DOWN1 and DOWN2) at 50% VO2max. Although VO2 increased significantly over time for all bouts, the magnitude [4.3% (LEVEL), 5.4% (DOWN1), and 8.1% (DOWN2)] did not differ between bouts (P > 0.05). VO2 was significantly lower during DOWN2 than during LEVEL and DOWN1 (P < 0.05). MT increased during the three bouts (P < 0.05) but the change over time was not different between bouts. SR and SL did not change over time within each bout nor between the two downhill runs. Muscle damage, as indicated by serum creatine kinase levels and perceived soreness, was less following LEVEL and DOWN2 than DOWN1 (P < 0.05). HR and RT increased over time (P < 0.05) but did not differ between bouts. VE and blood lactate did not differ over time or between bouts. VO2 drift during the three bouts paralleled changes in RT, MT, and HR but appears unrelated to muscle damage or biomechanical factors.

Adult↗

PubMed1993

Estrogen does not increase bone formation in growing rats.

The purpose of these experiments was to test the hypothesis that estrogen has an anabolic effect on cancellous bone formation in long bones of growing rats. In the present studies, estrogen decreased measurements related to cancellous bone formation, including osteoblast number, fluorochrome-labeled bone perimeter, and incorporation of [3H]proline into osteoid. Steady state mRNA levels for bone matrix proteins and mineral apposition rate were unchanged or reduced. The [3H]thymidine labeling index for osteoblasts was very low and was reduced by estrogen treatment. Finally, estrogen decreased the rate of removal of tetracycline previously incorporated into cancellous bone as well as the growth-dependent decrease in cancellous bone area, indicating that hormone treatment reduced net bone resorption. In summary, no evidence was secured to support the hypothesis that estrogen has an anabolic action on bone formation; the results obtained in these studies consistently demonstrated a pronounced inhibitory action of the hormone on bone turnover.

Animals↗

PubMed1992

A comparison of the oxygen drift in downhill vs. level running.

This investigation explored the recent theory that muscle damage causes the drift in oxygen consumption (VO2) during low-intensity downhill running. Seven subjects participated in a maximal VO2 (VO2max) test and three submaximal bouts [one level (Level) and two downhill runs (Down 1, Down 2) at 40% peak VO2]. Two downhill runs (30 min at -10% grade) were performed to vary the extent of muscle damage. Creatine kinase (CK) increased more after Down 1 (61%) than after Down 2 (11%), as did soreness ratings, indicating reduced muscle damage during Down 2. Significantly greater increases in VO2 over time were noted for Down 1 (15.6%) and Down 2 (14.7%) than for Level (1.2%). Heart rate increased 8 beats/min for Level but 29 and 25 beats/min for Down 1 and Down 2, respectively. Expired ventilation increased more for Down 1 (20.5%) and Down 2 (24%) than for Level (3.5%). Rectal temperature increased approximately 0.8 degree C for all bouts. Because the magnitude of the drift was similar in the two downhill bouts, the findings suggest that muscle damage does not cause the drift in VO2 during low-intensity downhill running.

Adult↗