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Biomedical subjects

J L Kilgore

Publications and source records attributed to J L Kilgore.

9 recordsLinked to original sources
PubMed2004

Severity of viral infection is promoted by hyperthermic pretreatment.

The aim of this study was to determine if prior heat shock and consequential heat shock protein (HSP) accumulation would inhibit viral infection. Confluent cultures of Madin-Darby bovine kidney cells were subjected to 30 mins of hyperthermia at 42 degrees C then allowed to recover at 37 micro C for six hrs. During the six hrs, HSP concentrations increased by 232% in heat-shocked cultures. Following the recovery period, six replicates of heat-shocked (HS) and six replicates of non-heat-shocked (CON) cultures were infected with Bovine Herpes virus 1. After 72 hours, severity of infection was assessed by counting formed viral plaques in cell cultures. CON cultures averaged 172.0+/-34.3 plaques per culture and HS cultures averaged 339.3+/-96.1 plaques per culture, representing a significant increase in infected cells (p=0.0044). These data provide evidence that physiological stressors related to extreme or exhaustive exercise, specifically hyperthermia, may increase risk of viral infection.

Animals↗
PubMed2000

Induction of mitochondrial stress proteins following treadmill running.

PURPOSE: The purpose of this investigation was to examine the relationship between the expression of HSP60 and GRP75 and the oxidative potential of skeletal muscle as assessed by the citrate synthase activity following endurance training to sedentary controls. METHODS: Female Wistar rats were assigned to one of two groups: sedentary controls (N = 8) or endurance trained (N = 9). Endurance trained rats were run 60 min x d(-1) at 27 m x min(-1) up a 10% incline 6 d x wk(-1) for 8 wk on a motor-driven treadmill. RESULTS: Training produced a 47% increase in citrate synthase activity along with a 103% increase in the expression of HSP60 and a 105% increase in the expression of GRP75 in plantaris muscle. In addition, there was a significant correlation between the citrate synthase activity and expression of HSP60 found in plantaris muscle. CONCLUSIONS: These findings are consistent with the hypothesis that the adaptive response to treadmill running may require elevations in the expression of HSP60 and GRP75 to support protein import and folding.

Animals↗
PubMed1998

Physical activity, muscle, and the HSP70 response.

Selye (1936) described how organisms react to various external stimuli (i.e., stressors). These reactions generally follow a programmed series of events and help the organism adapt to the imposed stress. The heat shock response is a common cellular reaction to external stressors, including physical activity. A characteristic set of proteins is synthesised shortly after the organism is exposed to stress. Researchers have not determined how heat shock proteins affect the exercise response. However, their role in adaptation to exercise and training might be inferred, since the synthetic patterns correlate well with the stress adaptation syndrome that Selye described. This review addresses the 70 kilodalton heat shock protein family (HSP70), the most strongly induced heat shock proteins. This paper provides an overview of the general heat shock response and a brief review of literature on HSP70 function, structure, regulation, and potential applications. Potential applications in health, exercise, and medicine are provided.

Amino Acid Sequence↗
PubMed1996

Effects of low-volume resistive exercise on beta-endorphin and cortisol concentrations.

It has been recently suggested that high and sustained lactate levels may elicit increases in peripheral B-EN concentrations (16). We have observed elevated and sustained lactate concentrations in response to a low-volume resistive exercise protocol (14) that were similar to those from other exercise protocols that produced elevated beta-endorphin (B-EN) concentrations. Thus, the purpose of the study was to determine the effects of a low-volume (21,700 J) resistive exercise repetition maximum (RM) protocol using weight machines on peripheral lactate, B-EN and cortisol concentrations. Subjects completed 3 sets of bench press, lat-pull, leg extension, and leg curl exercise at a 10-RM load. Blood samples were collected and rating of perceived exertion (RPE, 15-point Borg scale) was assessed before exercise (-40 and -10 min), after each exercise, and after the exercise session (+ 35 min); blood samples were collected at 7 additional post-exercise times. RPE increased significantly throughout the exercise. Lactate concentrations rose significantly to peak at 8.54 mM at LE. B-EN and cortisol concentrations (-10) of 4.63 +/- 0.54 pmol.l-1 and 12.09 +/- 1.44 micrograms.dl-1, respectively, were not significantly elevated over time. The data suggest that a low-volume resistive exercise protocol using weight machines elevates lactate concentrations without altering B-EN and cortisol concentrations.

Adult↗
PubMed1994

Stress protein induction in skeletal muscle: comparison of laboratory models to naturally occurring hypertrophy.

The purpose of the study was to compare stress protein [heat shock protein (HSP) 72] response in laboratory models of hypertrophy to naturally occurring work-induced hypertrophy. Two laboratory models of hypertrophy inducement, namely, compensatory hypertrophy and stretch hypertrophy, were compared with hypertrophy resulting from migratory flight in the blue-winged teal. We hypothesized that HSP 72 would be expressed more strongly in hypertrophied muscle than in control muscle. Furthermore, we hypothesized that changes occurring in laboratory models would also occur in work-induced enlargement. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blot analyses were used to assess HSP 72 levels in control and hypertrophied muscle. Laboratory models elicited similar responses, with increased HSP 72 content in hypertrophied muscle. Work-induced hypertrophy or disuse atrophy did not change the degree of HSP 72 expression in the blue-winged teal. The presence of HSP 72 in these conditions may indicate that stressors eliciting changes in muscle protein expression, including the loss of muscle mass, may elicit HSP 72 synthesis.

Adaptation, Physiological↗
PubMed1993

Plasma volume changes in response to resistive exercise.

The present study was designed to determine the cumulative effects of a series of four resistive exercises on intravascular plasma volume throughout one exercise session. Seven healthy males, mean (+/- SE) age 26.7 +/- 1.2 y, participated in the study. In two separate trials the subjects' one-repetition maximum (1-RM) and 10-RM were determined. In a third session, an IV catheter was inserted into a forearm vein at 0800 h and kept patent with a heparin lock. At 0940 h three sets of bench press (BP), lat pull (LP), leg extension (LE), and leg curl (LC) were executed at a 10-RM load for 10 repetitions or until failure. Blood samples were collected before (-30, 0), during (after BP, LP, LE, LC), and after [5 min, 15 min, and 25 min into recovery (R5, R15, R25)] the resistive exercise session. Plasma volume was reduced as much as -13.35% at LE and returned to normal after R15. We conclude that plasma volume is substantially reduced after performing a short session of upper and lower body resistive exercises. The findings demonstrate the magnitude of resistive-exercise-induced plasma volume loss and underscore the importance of accounting for plasma volume change when determining response of a particular blood parameter to resistive exercise.

Adult↗
PubMed1992

Growth hormone, IGF-I, and testosterone responses to resistive exercise.

It has been suggested that growth hormone (GH), testosterone (T), and insulin-like growth factor I (IGF-I) play large roles in muscle tissue growth; however, in only two investigations IGF-I responses to resistive exercise have been examined. Eight young males who had not weight trained for a minimum of 5 months participated in the study. Three sets of bench press (BP), lat-pull (LP), leg extension (LE), and leg curl (LC) exercises were performed at a 10-RM load for 10 repetitions or until failure. Blood samples were collected from an IV catheter before exercise (-30 min and -10 min), after each individual exercise (BP, LP, LE, LC), and after the exercise session (+5, +15, +25, +35, +95 min; +5:35, +22:30, and +23:30 h). GH, IGF-I, and T determinations were corrected for plasma volume change. GH significantly increased (P < 0.05), but IGF-I did not change. Correction for plasma volume accounted for significant increases in T, but did not account for GH and IGF-I results. These data suggest that moderate resistive exercise may increase GH concentrations, whereas elevated T levels can be accounted for by exercise-induced alteration of plasma volume.

Adult↗
PubMedDate not supplied

Regional distribution of HSP70 proteins after myocardial infarction.

Hypoxia and altered hemodynamic status, both components of myocardial infarction, have been shown to be potent inducers of the 70 kD family of heat shock proteins (HSP70). We hypothesized that after infarction, the surviving myocardium would synthesize HSP70 proteins in a temporally and regionally distinct pattern. We believed that there would be a lack of an HSP70 response in the infarcted area (I), reflecting the loss of viable cells. We further postulated that tissues bordering infarctions (M) would have a compromised HSP70 response. Conversely, we proposed that HSP70 would be induced in septal tissues (S) of the infarcted heart, as a hypertrophic adaptation. A rat model of myocardial infarction was used to examine the changes in relative concentration and distribution of three major HSP70 family proteins; cytoplasmic HSP72, mitochondrial HSP75, and endoplasmic reticular GRP78 (glucose regulated protein) during 21 days of recovery. While all three HSP70 family proteins investigated were detected in all hearts from all groups at all time periods, experimental treatment (infarction) induced changes in relative protein concentrations that varied with time and sample site location. Relative concentrations of HSP72 and GRP78 were unchanged in the 24 h following infarction while relative HSP75 concentrations were halved in M tissues during the same time period. Between days 5 and 7, several changes were noted. M samples displayed nearly twice the relative concentrations of HSP75 and GRP78 after infarction, but showed no change in HSP72. S tissues showed two-fold or larger increases in all three HSP70 family proteins. I samples showed unanticipated increases in HSP75 and GRP78 during this time period. After 14 to 21 days of recovery, HSP70 family protein concentration levels in M, S, and I tissues from infarcted hearts had returned to levels similar to those seen in control animals. We conclude that the myocardium is unable to, or does not, mount an immediate HSP70 response after infarction but does recover such activity by 5-7 days after infarction.

Animals↗