Search PubMed⌕ Search

Biomedical subjects

A H Goldfarb

Publications and source records attributed to A H Goldfarb.

33 records · Page 2Linked to original sources

Beta-endorphin time course response to intensity of exercise: effect of training status.

The concentration of beta-endorphin (B-EP) was measured in 6 trained and 6 untrained cyclists during three intensities of exercise to determine the time course changes of B-EP. B-EP was determined by radioimmunoassay with less than 5% cross reactivity with beta-lipotrophin. A counter-balanced design was used to avoid an order effect from exercise intensity. Resting B-EP values were similar across visits. There were no differences in resting B-EP values comparing the trained (4.61 +/- 0.25 pmol.l-1) to the untrained (4.03 +/- 0.23 pmol.l-1) group. Cycling at 60% VO2max did not increase B-EP in either group at any time measured. Cycling at 70% VO2max increased B-EP by 10 min in both groups p less than 0.05. The rate and magnitude of increase of B-EP were similar for both groups. B-EP changes at 80% VO2max were significantly greater that at 70% VO2max and were identical for the two groups. Both groups demonstrated increases by 5 min and further increases at 30 min of exercise p less than 0.01. These changes occurred despite the fact that lactate levels were lower in the trained group at both 70 and 80% VO2max intensities. It is concluded that the time course change for B-EP is similar for trained and untrained individuals working at the same relative intensity of exercise and does not seem to be related to plasma lactate concentrations.

Adult↗

Endurance training, not acute exercise, differentially alters beta-receptors and cyclase in skeletal fiber types.

beta-Adrenergic receptor binding characteristics and adenylate cyclase activity were examined in rat skeletal muscle membranes to determine if acute exercise or endurance training altered beta-receptors or adenylate cyclase activity in different muscle fiber types. Binding characteristics and adenylate cyclase activity were examined in type IIA [red fast-twitch, red vastus (RV)], type IIB [white fast-twitch, white vastus (WV)], and type I [red slow-twitch, soleus (S)] muscles. Acute exercise involved a 20-min run on a treadmill at 20 m/min and did not alter beta-receptor density or adenylate cyclase activity in any of the fiber types examined. Endurance training consisted of a progressive treadmill protocol that involved increasing intensity and duration of exercise for 18 wk. beta-Adrenergic receptor density increased in skeletal muscle fiber types primarily recruited during submaximal training (types I and IIA), whereas nonreceptor-mediated adenylate cyclase activity was altered in the three fiber types. Endurance training significantly increased beta-receptor density in RV by 25% and in S by 19% (P less than 0.05), whereas in WV beta-receptor density was not altered. Basal adenylate cyclase activity in RV was increased approximately 2.5 fold by endurance training. Nonreceptor-mediated adenylate cyclase activity, stimulated by NaF and forskolin, increased by approximately twofold in both RV and WV as a result of endurance training. The data support and extend previous observations to show greater effects of endurance training in types I and IIA fibers with respect to alterations in beta-receptor density and alterations in adenylate cyclase activity in each fiber type. Acute exercise did not alter these parameters either in trained or untrained rats.

Adenylyl Cyclases↗

Plasma beta-endorphin concentration: response to intensity and duration of exercise.

Twelve college-age men exercised on a bicycle ergometer to VO2max and at 60, 70, and 80% VO2max for 30 min to determine the effects of exercise intensity on plasma beta-endorphin (B-EP). The time course for alterations in B-EP and the relationship to lactate were also examined. Following the VO2max test, the three submaximal intensities were completed on separate days using a counter-balanced design. Blood was sampled from an indwelling venous catheter at rest during exercise and recovery to assess the time course response. B-EP content was determined by radioimmunoassay (Immunonuclear) with less than 5% cross-reactivity to B-LPH. At rest, B-EP content was similar across visits, 4.34 +/- 0.36 pmol.l-1. The 60% intensity did not elevate B-EP at any time measured. B-EP content increased by 15 min at 70% VO2max with a further increase at 30 min. B-EP remained elevated during the 20 min recovery. At 80% VO2max B-EP content increased by 5 min. B-EP continued to increase during the exercise and peaked at 21.91 +/- 2.03 pmol.l-1 5 min into the recovery. Lactate showed a mild correlation with B-EP (r = 0.43) at 80% VO2max. A significant correlation (r = 0.78) between lactate and B-EP did occur with the VO2max test. It is concluded that an exercise intensity of at least 70% VO2max for 15 min is needed to increase plasma B-EP. Furthermore, the higher the exercise intensity the more rapid the onset for increases in plasma B-EP.

Adult↗

The effect of training on the norepinephrine response at rest and during exercise in 5 degrees and 20 degrees C environments.

Eleven males were examined at rest and during submaximal exercise in 5 degrees C and 20 degrees C environments to determine if the norepinephrine (NE) and other physiological responses in the cold would be altered by eight weeks of training. Blood samples were obtained at the end of 15 minutes of rest and submaximal exercise, and were assayed for NE. Pretraining resting NE levels in the 5 degrees C condition were significantly higher than those found in the 20 degrees C environment (684 +/- 89 vs 491 +/- 48 pg/ml). A significant training effect reduced resting NE levels in the 5 degrees C (502 +/- 77 pg/ml) but not the 20 degrees C (392 +/- 45 pg/ml) condition. Pre and posttraining exercise NE levels were elevated above resting in both the 5 degrees C (1477 +/- 136 vs 1559 +/- 208) and the 20 degrees C environments (1623 +/- 176 pg/ml vs 1444 +/- 224 pg/ml), but were not significantly different between conditions. Skin temperatures were significantly lower, and resting blood pressure was significantly higher in the 5 degrees C condition. These data suggest that both cold and exercise act as stimulators of NE release, but an additive effect on NE of cold and exercise does not occur. The resting NE levels pre and posttraining in the 5 degrees C condition suggest that a cross tolerance to cold stress was present.

Adaptation, Physiological↗

Intensity and duration of exercise effects on skeletal muscle cAMP, phosphorylase, and glycogen.

To gain further insights into the mechanisms regulating skeletal muscle glycogenolysis during exercise, glycogen, phosphorylase, and adenosine 3',5'-cyclic monophosphate (cAMP) were determined in fast-twitch white (FTW) and fast-twitch red (FTR) muscle from groups of rats that ran for 0, 5, 10, 15, or 30 min at either 15 or 30 m/min. Glycogen degradation demonstrated an intensity and duration response in both fiber types. cAMP increased in both fiber types by 5 min and remained elevated at all times measured. FTW muscle cAMP levels were independent of both intensity and duration of exercise. FTR muscle cAMP levels were higher from 10 to 30 min at the 30-m/min intensity compared with the 15-m/min intensity. The ratio of the activity of phosphorylase in the presence of 2 mM AMP X 100 (phosphorylase a%) remained elevated at 20-22% independent of intensity and duration in FTW muscle; however, phosphorylase a% demonstrated an intensity and duration effect in FTR muscle. Glycogenolytic rates decreased with time, even though both cAMP and phosphorylase a% remained elevated in both fiber types. These data suggest that cAMP and phosphorylase a activation can be maintained during exercise in skeletal muscle but indicate a dissociation of these factors from glycogenolysis.

Animals↗

Increased training intensity effects on plasma lactate, ventilatory threshold, and endurance.

The purpose of this study was to determine the effects of increased training intensity (ITI) on VO2max, plasma lactate accumulation, ventilatory threshold (VT), and performance in trained distance runners. Seven trained male distance runners increased their training intensity three d.wk-1 at 90-95% HRmax for eight wk. ITI did not alter VO2max (65.3 +/- 2.3 vs 65.8 +/- 2.4 ml.kg-1.min-1) but improved 10 km race time (means = 63 s decrease) and increased run time to exhaustion on the treadmill at the same speed and grade (means = 3.88 min). Significant decreases in plasma lactate concentration at 85 and 90% of VO2max were observed after ITI. No differences were found in plasma lactate at 65, 70, 75 or 80% of VO2max or VT following ITI. Significant correlations were obtained between 10 km race times and changes in plasma lactate at 85 and 90% of VO2max (r = 0.69 and 0.73, respectively). Lactate accumulation at both 2.5 and 4.0 mM were at a significantly greater percent of VO2max after ITI. Additionally, the changes in plasma lactate were dissociated from alterations in VT after ITI. These data indicate that previously trained runners can increase training intensity to improve endurance performance by lowering lactate at the intensity at which they trained despite no changes in VO2max and VT.

Adult↗

MDA content increases in fast- and slow-twitch skeletal muscle with intensity of exercise in a rat.

Previous work has shown that high-intensity (HI) exercise results in total body increased production of lipid peroxidation. These results suggest that exercise induces a higher level of oxidative stress in muscles leading to the production of various peroxides and aldehydes that are potentially toxic to cells. However, these past studies were carried out only with subjects that were exercised to exhaustion or at a very high intensity. In this paper, we report how a moderate-intensity (MI) exercise, which is more normally experienced, as well as a HI acute bout of exercise influenced oxidative stress-related reactions by measuring malonaldehyde (MDA) and lipid hydroperoxides (LH) in red vastus, white vastus, and soleus muscle. The muscles from untrained male Sprague-Dawley rats were removed immediately after either a HI 1-min run at 45 m/min (n = 8) or a 20-min MI run at 20 m/min (n = 8) and compared with a control group that did not run. MI exercise resulted in a 90% increase in MDA in white vastus and a 62% increase in red vastus muscle (P less than 0.05). HI exercise resulted in a 157, 167, and 83% increase in MDA in white vastus, red vastus, and soleus muscle, respectively. LH values in red and white vastus after HI exercise increased an average of 33%, but this proved not to be statistically significant. These results confirm earlier studies that HI exercise does increase MDA in skeletal muscle, and when intensity of exercise is considerably lowered, elevated MDA is still found but at a relatively lesser amount.

Animals↗

Lipid peroxidation and scavenger enzymes during exercise: adaptive response to training.

This study was designed to determine whether endurance training would influence the production of lipid peroxidation (LI-POX) by-products as indicated by malondialdehyde (MDA) at rest and after an acute exercise run. Additionally, the scavenger enzymes catalase (CAT) and superoxide dismutase (SOD) were examined to determine whether changes in LIPOX are associated with alterations in enzyme activity both at rest and after exercise. Male Sprague-Dawley rats (n = 32) were randomly assigned to either trained or sedentary groups and were killed either at rest or after 20 min of treadmill running. The training program increased oxidative capacity 64% in leg muscle. After exercise, the sedentary group demonstrated increased LIPOX levels in liver and white skeletal muscle, whereas the endurance-trained group did not show increases in LIPOX after exercise. CAT activity was higher in both red and white muscle after exercise in the trained animals. Total SOD activity was unaffected by either acute or chronic exercise. These data suggest that endurance training can result in a reduction in LIPOX levels as indicated by MDA during moderate-intensity exercise. It is possible that activation of the enzyme catalase and the increase in respiratory capacity were contributory factors responsible for regulating LIPOX after training during exercise.

Acclimatization↗

Serum beta-endorphin and affective responses to graded exercise in young and elderly men.

Nine young (26.1 +/- 2.52 years) (M +/- SD) and seven elderly (66.0 +/- 5.85 years) untrained men performed a graded exercise to peak VO2 to compare whether serum beta-endorphin (B-EP) would respond similarly with age. B-EP levels were not different at rest (31.8 +/- 3.3 and 25.3 +/- 4.1 pg/ml in the old and young groups, respectively), and both groups displayed similar responses to exercise. Specifically, we noted no change in B-EP during the final stage of exercise followed by a significant rise for the recovery period (40.0 +/- 3.7 and 38.1 +/- 5.0 pg/ml in the aged and young groups, respectively). Post-exercise reports of anxiety and depression were unchanged in either group, and only minor changes in hostility were noted, as measured by the Multiple Affect Adjective Checklist. These results demonstrate a similar serum B-EP response in older men compared to young men following graded maximal exercise and support the contention that circulatory changes in B-EP may not be related to changes in specific affective states.

Adult↗

Serum beta-endorphin levels during a graded exercise test to exhaustion.

Serum beta-endorphin levels during a graded exercise test to exhaustion. Med. Sci. Sports Exerc., Vol. 19, No. 2, pp. 78-82, 1987. Nine untrained college age males completed a graded exercise protocol to maximal capacity on a bicycle ergometer to determine if there was a relationship between intensity of exercise and serum beta-endorphin (beta-EP) levels. Subjects fasted for 12 h and abstained from physical activity at least 24 h prior to testing. Subjects completed the Multiple Affect Adjective Check List prior to and following exercise to ascertain if psychological state would be associated with beta-EP levels. The initial workload was 150 kilopond meters and was increased 150 kilopond meters every 3 min until VO2max or leg fatigue occurred. Expired gases were continuously analyzed, and a venous blood sample was drawn from an indwelling catheter during the final 30 s of each stage and 5-min post-exercise. beta-EP levels were determined from serum using a radioimmunoassay technique and corrected for cross-reactivity with beta-lipotropin using affinity chromatography. Resting beta-EP levels were 25.3 +/- 4.1 pg X ml-1 and did not demonstrate significant changes during any stage of exercise. A correlation analysis (r = 0.30) revealed no significant relationship between exercise intensity and beta-EP levels. Following exercise, beta-EP levels were significantly increased compared to resting values (38.8 +/- 4.8 pg X ml-1). In addition, psychological state was unaffected by exercise despite significant increases in recovery beta-EP levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Age-associated blood glucose levels during exercise in female swimmers.

The purpose of this study was to determine whether age-associated alterations in blood glucose levels occur during exercise. In addition, blood lactate and fitness levels (VO2max) were examined to ascertain if these factors influenced the age-related responses. Sixty-four female masters swimmers (25-75 years) were classified into either a well trained (WT) or recreational trained (RT) group and exercised on a treadmill to VO2max X VO2max data confirmed our classification of WT and RT swimmers based on activity levels. There were no differences in post-absorptive blood glucose and lactate levels across age and fitness. Significant age-related effects on blood glucose levels during exercise (p less than 0.01) but no fitness effect were revealed by ANOVA. Within the first or second exercise stage all age groups demonstrated a significant decline in blood glucose (6.3 to 14.1%). A hyperglycemic response was observed during recovery in all age groups with the exception of the over 60 (60+) group. The 60+ group exhibited lower blood glucose levels compared to all other age groups during exercise commencing with the second exercise stage. There were no significant differences in glucose levels among any of the other age groups during exercise or recovery. There were no age-related differences in maximal or recovery lactates. These data indicate that there is an alteration of blood glucose homeostasis during exercise in females over 60 years of age.

Adult↗

Intensity and duration effects of exercise on heart cAMP, phosphorylase, and glycogen.

Glycogen, phosphorylase, and adenosine 3',5'-cyclic monophosphate (cAMP) were determined in rat heart following an acute exercise bout. Intensity and duration of exercise were varied to gain further insights into the mechanism regulating myocardial glycogenolysis during exercise. Groups of rats were run at either 15 or 30 m/min for 0, 5, 10, 15, or 30 min and immediately killed. Heart glycogen degradation was influenced by intensity and duration of exercise and was independent of cAMP levels and activation of phosphorylase to its a form. cAMP levels were increased in the heart, dependent on intensity and duration of exercise. Phosphorylase in the a form increased at the onset of exercise, independent of intensity, and remained elevated throughout the exercise despite little or no glycogenolysis. Absolute phosphorylase a activity was also increased with exercise and was independent of intensity of exercise. Compared with resting levels, total phosphorylase activity was decreased at all times at the lower exercise intensity, whereas total phosphorylase activity declined at the higher intensity only after glycogenolysis had occurred. These data suggest that myocardial glycogen degradation during exercise can occur independently of cAMP and that the percentage of phosphorylase in the a form is not a good indicator of glycogenolytic rate.

Animals↗

Specificity of cardiac glycoside binding to membrane filters.

Two cardiac glycosides, with different physiochemical properties, were investigated to assess their binding characteristics to filters. The lipophilic cardiac glycoside, digoxin, demonstrated significant (10%) retention to certain cellulose filters. There were considerable differences in the amount of digoxin retained among the cellulose type filters. The polycarbonate type filter (10 microns thick) demonstrated less than 2% retention. This was similar in magnitude to the cellulose-acetate-nitrate ester filters (100 microns thick) which demonstrated less than 1% retention. Ouabain, the polar cardiac glycoside, appeared to have minimal (2%) retention on all filter types tested. Increasing the size of the pore from .4 microM to .8 microM resulted in a minimal decrease in retention for the Amicon filters, whereas the nucleopore polycarbonate filters demonstrated a significant reduction in retention of the lipophilic cardiac glycoside. A comparison of the 100 micron thick filters with the 10 micron thick filters suggests that there is no correlation with the thickness of the filter and the retention of the drug bound by that filter. These studies suggest that lipophilic drugs are retained on membrane filters depending on the filter's composition and that caution should be utilized with the filtration technique.

Cardiac Glycosides↗

Effect of an exercise run to exhaustion on cAMP in the rat heart.

The purpose of this investigation was to determine whether adenosine 3',5'-cyclic monophosphate (cAMP) content is increased in vivo in the heart as a result of exercise at a time when there is rapid cardiac glycogen utilization. Rats were run to exhaustion on a treadmill for a period of 164.5 +/- 9.5 min. Blood norepinephrine and epinephrine were significantly elevated approximately 2.5-fold above resting levels at the end of the treadmill run. Myocardial glycogen was reduced by 54.7% at exhaustion compared with control values. Myocardial cAMP was significantly elevated 88% above control levels as a result of the run. Associated with the depletion of myocardial glycogen and the elevation of cAMP was an activation of phosphorylase to its a form. These data suggest that myocardial glycogen metabolism during exercise is, in part, mediated by hormonal influences that are associated with increases in cAMP.

Animals↗