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Biomedical subjects

R C Hickson

Publications and source records attributed to R C Hickson.

At least 55 records · Page 3Linked to original sources
PubMed1984

Countereffects of compensatory overload and glucocorticoids in skeletal muscle: androgen and glucocorticoid cytosol receptor binding.

Male hypophysectomized rats were divided into a control group and a group that was subjected to compensatory overload of plantaris muscles for 7 days following surgical removal of synergistic musculature. These groups received daily subcutaneous injections of either cortisone acetate (CA) (100 mg/kg b.wt) or the vehicle for 7 days starting at the time the overload was initiated. Plantaris muscle weights were atrophied by 25% in CA-treated controls, were hypertrophied by 45% in the vehicle-treated overloaded group, and remained similar to vehicle-treated controls in the group receiving both treatments. Scatchard analyses of specific binding of [3H]methyltrienolone (R1881), a synthetic androgen that binds to androgen receptors, were non-linear in plantaris muscle cytosols of vehicle-treated control and overloaded groups and were resolved by a two-component binding model. The lower affinity component, which was attributed to binding of methyltrienolone to a glucocorticoid receptor, disappeared in glucocorticoid-treated rats as evidenced by linear Scatchard plots. Receptor concentrations of the androgenic component of [3H]methyltrienolone binding were unchanged by CA treatment and were significantly increased only in the vehicle-treated overloaded group. [3H]Dexamethasone cytosol binding was increased nearly 2-fold in plantaris muscles of vehicle-treated overloaded animals (64 +/- 3 fmol/mg protein) as compared to those in vehicle-treated controls (32 +/- 2 fmol/mg protein), but was decreased to 2 and 4 fmol/mg protein in the CA-treated controls and CA-treated overloaded groups respectively. These results show that overload and glucocorticoids have opposing actions skeletal muscle, but the overload in the presence of glucocorticoids did not stimulate an increase in androgen cytosol receptor binding.

Animals↗
PubMed1984

Androgen cytosol binding in exercise-induced sparing of muscle atrophy.

This study was undertaken to determine whether the exercise-induced sparing of glucocorticoid-induced muscle atrophy is related to increased androgen cytosol binding. Female rats were divided into a sedentary or an exercise group that was trained by treadmill running 100 min/day for 13-15 wk. During the last 12 days of training, each of these groups was further subdivided into groups that received daily subcutaneous injections of cortisone acetate (CA) (100 mg/kg body wt) or the vehicle 1% carboxymethyl cellulose. Exercise prevented 30-40% of the weight loss due to CA treatment in gastrocnemius and plantaris muscles. Scatchard analyses of specific binding of [3H]methyltrienolone (R1881), a synthetic androgen that binds to androgen receptors, were nonlinear in muscles from vehicle-treated sedentary and trained rats and were resolved by a two-component binding model. The lower affinity component, which was attributed to a glucocorticoid receptor, disappeared in muscles of glucocorticoid-treated animals as evidenced by linear Scatchard plots. Receptor concentrations of the androgenic component of [3H]methyltrienolone binding were similar in gastrocnemius and plantaris muscles in all treatment groups. In binding specificity studies of gastrocnemius muscles, the relatively high competition by various glucocorticoids and progesterone for [3H]methyltrienolone binding in the vehicle-treated groups was reduced by CA treatment. The lack of change in androgen cytosol receptor levels suggests that this is not a mechanism by which exercise protects against glucocorticoid-induced muscle atrophy.

Androgens↗
PubMed1984

Androgen and glucocorticoid mechanisms in exercise-induced cardiac hypertrophy.

Female rats were trained daily by means of two 2-h-long bouts of swimming separated by a 30- to 40-min rest period. Absolute ventricular weights of the swimmers were increased above sedentary control values by 6% after 2 days, 15% after 7 days, and 30% after 35 days of exercise. Resting levels of total and free serum testosterone and total 5 alpha-dihydrotestosterone were not altered by the training. Total serum corticosterone concentrations at rest were significantly lower in the 7-day (149 +/- 16 ng/ml) and 35-day (169 +/- 24) swimmers compared with the controls (293 +/- 26). However, free corticosterone was not significantly reduced from controls in any of the swimming groups. Ventricular muscle cytosol androgen receptor binding dissociation constants and receptor binding capacities, measured using [3H]methyltrienolone (R1881), were not significantly different from control values in the exercised groups. Glucocorticoid cytosol receptor binding capacity in ventricular tissue, determined using [3H]dexamethasone, was significantly increased as femtomoles per milligram protein (39.3 +/- 3.1 vs. 31.4 +/- 1.4) and femtomoles per milligram DNA (2,683 +/- 226 vs. 1,786 +/- 71). These findings show that glucocorticoids, rather than androgens, undergo adaptive changes in the circulation and in muscle during the development of exercise-induced cardiac hypertrophy.

Androgens↗
PubMed1984

Glucocorticoid-induced cardiac hypertrophy: additive effects of exercise.

Female rats were divided into a sedentary control and an exercise group that was trained by treadmill running 100 min/day for 13-15 wk. During the last 12 days of training, they were further subdivided into trained and sedentary groups that received either daily subcutaneous injections of cortisone acetate (CA) (100 mg/kg body wt) or the vehicle, 1% (wt/vol) carboxymethylcellulose. As a result of the exercise program, ventricular weights were 15% (P less than 0.01) heavier in the vehicle-treated runners than in the vehicle-treated controls, but there were no changes in cardiac androgen (methyltrienolone, R1881) or glucocorticoid (dexamethasone, DEX) cytosol-specific binding concentrations. Body weights were decreased by 11-12% in both CA-treated groups. Ventricular weights of the CA-treated controls were 11% (P less than 0.01) heavier than the weights of the vehicle-treated controls. The combination of exercise and glucocorticoid treatments resulted in ventricular weights that were 21% heavier than those in the vehicle-treated controls and 8 and 5% (P less than 0.05) greater than those resulting from CA and endurance training individually. Both R1881 and DEX binding were decreased in hearts of CA-treated animals from those of vehicle-treated animals, and exercise did not modify this response. These results show that glucocorticoid treatment can induce cardiac enlargement, and the combination of glucocorticoids and exercise can have additive effects on the growth, yet their mechanisms appear different.

Animals↗
PubMed1984

Reduced training frequency effects on aerobic power and muscle adaptations in rats.

Female rats were exercised by swimming up to 4 h/day either 2, 4, or 6 days/wk. After 7 wk they continued to train at these frequencies or had their training reduced from 6 to 4, 2, or 0 days/wk for an additional 9 wk. Ventricular weights and maximum O2 uptake (VO2max) were increased by 5-10% after training 2 days/wk, 15-17% after 4 days/wk, and 25-30% after 6 days/wk. Following reduced training, VO2max was similar when the 4- or 2-day/wk reduced training groups are compared with their 4- or 2-day/wk continued training counterparts. In contrast, VO2max was greater in the 0-day reduced than in the sedentary control group. No differences in mitochondrial markers or myoglobin content in red or mixed skeletal muscles were found between training 2 or 4 days/wk vs. reduced training at comparable frequencies. O2 uptake capacity of plantaris muscles and myoglobin concentration in fast-twitch red vastus lateralis muscles were greater in the 0-day reduced group than in the sedentary controls. These data show that VO2max and certain markers of aerobic metabolism in skeletal muscles of rats are lost at a slower rate than their rate of increase from the untrained state. However, a reduction of swimming frequency from 6 to 4 or 2 days/wk is not a sufficient stimulus to maintain VO2max, cardiac enlargement, or the increased aerobic potential of skeletal muscle at the 6-day/wk levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1983

Skeletal muscle cytosol [3H]methyltrienolone receptor binding and serum androgens: effects of hypertrophy and hormonal state.

Normal, castrated, and hypophysectomized male rats underwent compensatory hypertrophy of plantaris muscles following surgical removal of their synergistic gastrocnemius muscles. The increases in muscle wet weights above control values, determined when the muscles were in stable-state hypertrophy, were as follows: normal 50%, castrated 50%, and hypophysectomized 32%. There were marked differences in concentration of serum androgens between surgical groups, yet no increases in testosterone or 5 alpha-dihydrotestosterone were observed as a result of hypertrophy. The amount of testosterone binding to serum proteins (approx 94%) was reduced only in hypophysectomized animals that underwent muscle growth. Cytosol androgen receptor specific binding (fmol/mg protein), measured using saturating concentrations of [3H]methyltrienolone (R1881) at 4 degrees C for 20 h for exchange with endogenous steroid, was significantly increased in hypertrophied muscles of normal, (1.77 +/- 0.17 vs 1.16 +/- 0.21), castrated (2.27 +/- 0.20 vs 1.46 +/- 0.03) and hypophysectomized (6.23 +/- 0.56 vs 3.64 +/- 0.30) animals. Receptor dissociation constants (Kd) were approx 10(-10) M in all groups and were not altered by the hypertrophy. These findings show that a major adaptation to skeletal muscle enlargement is an augmentation of cytosol [3H]methyltrienolone receptor binding capacity. This effect occurs in a normal or androgen deficient state.

Androgens↗
PubMed1982

Reduced training duration effects on aerobic power, endurance, and cardiac growth.

Thirteen subjects participated in an exercise program of bicycling and running 40 min/day, 6 days/wk. After 10 wk they continued to train either 26 of 13 min/day for an additional 15 wk. Intensity and frequency for the additional 15 wk remained the same as the last 3 wk of training. This study was undertaken to gain further insights into whether the increases in maximum uptake (VO2 max), endurance, and cardiac size can be maintained with reduced training durations. The average increases in VO2 max in response to 10 wk training were between 10 and 20% during the bicycle and treadmill testing. After reduced training, VO2 max continued to remain at the training levels in both groups. Short-term endurance (approx 5 min) was also maintained by both groups. Long-term endurance (2 h or more) remained the same in the 26-min group but decreased significantly (10%, 139-123 min) in the 13-min group. Calculated left ventricular mass increased 15-20% after training and remained elevated after reduced training in both groups. We conclude that it is possible to maintain almost all of the performance increases with up to a two-thirds reduction of training duration. Nevertheless, the data provide initial evidence that all aspects of the endurance-trained state may not be regulated uniformly in reduced training, particularly since VO2 max and short-term endurance were maintained, but long-term endurance decreased in the 13-min group.

Adult↗
PubMed1981

Separate turnover of cytochrome c and myoglobin in the red types of skeletal muscle.

The purpose of this investigation was to determine whether cytochrome c and myoglobin have similar turnover rates in the three types of skeletal muscles. Exercise (endurance training) was used as an inducing stimulus to increase their concentrations. The half-lives (t 1/2) were subsequently estimated from the time course of return to base-line levels after cessation of exercise. When exercise was stopped, cytochrome c concentration returned rapidly to control levels; the lengths of t 1/2 were approximately 8 days in fast-twitch red, 5 days in slow-twitch red, and 9 days in mixed muscles. These findings confirm previous results of cytochrome c turnover. The concentration of myoglobin decreased at a slower rate than that observed for cytochrome c during detraining in fast-red slow-red, and plantaris muscles, and did not return to sedentary control levels throughout the 50-day detraining period. Myoglobin concentration in fast-twitch white muscle did not increase with the training. These results provide evidence that the degradation rate of myoglobin differs from that of cytochrome c in the red types of skeletal muscle. These elevated myoglobin levels may, in part, provide one explanation for the slow rate of decline in aerobic power that has been observed when individuals stop exercising.

Animals↗
PubMed1981

Partial prevention of glucocorticoid-induced muscle atrophy by endurance training.

Male rats were either sham-operated (N) or castrated (C) at 65 days of age. They were further subdivided into sedentary or exercise groups that were trained by treadmill running 5 days/wk for 12 wk. During the last 10 days of training, the animals received daily subcutaneous injections of cortisone acetate (CA) (100 mg/kg) or 1% carboxymethylcellulose. Body weight decreased approximately 25% in all groups that received CA. The fast-twitch plantaris and gastrocnemius muscle weights were approximately 35% lower in CA-treated versus cortisone-free N and C sedentary animals. Exercise prevented from one-fourth to one-half of the muscle weight loss in N and C runners when compared to their respective pair weight controls. Muscle weights of the CA-treated freely eating N controls were significantly less than that of N runners that received CA. In plantaris muscles of both N and C animals that received CA, total protein concentration and citrate synthase activity, a mitochondrial marker, remained constant, but their amounts per muscle decreased in proportion to the atrophy. However, myoglobin concentration increased in plantaris muscles of CA-treated animals, although total myoglobin per muscle was reduced slightly. Myoglobin levels were increased in plantaris muscles both as a result of training and CA, but citrate synthase activity was increased only as a result of the exercise. These results show that exercise can retard the glucocorticoid-induced muscle atrophy.

Animals↗
PubMed1981

Skeletal muscle cytochrome c and myoglobin, endurance, and frequency of training.

This study was undertaken to evaluate the effects of various training frequencies on performance capacity, the mitochondrial marker cytochrome c, and myoglobin, which is responsible for storage and transport of O2, in the three types of skeletal muscle. Female rats were trained by treadmill running up to 120 min/day, either 2, 4, or 6 days/wk for 14 wk. As a result of training, exercise time to exhaustion was increased in proportion to the number of training sessions per week. Cytochrome c concentration increased (range 20-90%) as a linear function of the number of exercises per week in the fast-twitch red vastus lateralis (FTR), the slow-twitch soleus (STR), and the mixed plantaris muscles. However, the concentration of cytochrome c in fast-twitch white vastus lateralis (FTW) muscles increased to approximately the same extent (40-50%) in all training groups. The increases in myoglobin concentration (13-45%) with training were significantly related to frequency in FTR muscle but not in STR muscle. Myoglobin levels in FTW muscle remained unchanged, regardless of training group. These results provide evidence that the capacity to perform endurance exercise and the mitochondrial content of the red skeletal muscle types are directly affected by training frequency.

Animals↗
PubMed1981

Reduced training frequencies and maintenance of increased aerobic power.

The purpose of this study was to obtain information regarding the minimum training frequency necessary to maintain the exercise-induced increase in maximum oxygen uptake (VO2max). Twelve subjects (average age = 23 yr) participated in an endurance exercise program of bicycling and running 40 min/d, 6 d/wk. After 10 wk, they continued to train either 4 d/wk or 2 d/wk for an additional 15 wk. Intensity and duration for the additional 15 wk remained the same as on the tenth week of training. The average increase of VO2max in response to 10 wk of training was 25% when measured during bicycle testing and 20% when measured during treadmill testing. VO2max in the 4 d/wk and 2 d/wk groups remained essentially the same as the trained levels when determined at 5-wk intervals of reduced training. These results provide evidence that more exercise is required to increase VO2max, than that required to maintain it at the trained level in young adults performing high-intensity exercise. Furthermore, it is possible to maintain the increased VO2max for at least 15 wk by training at high intensity for 2 d/wk or 4 d/wk.

Adult↗
PubMed1981

Time course of the adaptive responses of aerobic power and heart rate to training.

Nine subjects participated in an exercise program for 40 min/day, 6 days/wk. The training work rates were kept constant for the first 4 wk. The work rates were then increased to a higher level and kept constant for an additional 5 wk. During both training periods, maximum oxygen uptake (VO2max) increased for the first 3 wk and then remained constant. The half times (tl/2) of the increases in VO2max during the two periods were 10.3 and 10.8 days. These results provide evidence that the adaptation to endurance exercise of the system(s) that limit VO2max is rapid, with a tl/2 of less than 11 days. The total increase in VO2max in the 9 wk of training was 23%. The decreases in the heart rate and blood lactate responses to a standard submaximal exercise test also occurred within the first 2 to 3 wk of each training period. Our results show that unless the training stimulus is increased, a high intensity daily exercise program does not result in a further increase in VO2max or further decreases in the blood lactate or heart rate responses to submaximal exercise after 3 wk.

Adult↗
PubMed1980

Interference of strength development by simultaneously training for strength and endurance.

The purpose of this study was to determine how individuals adapt to a combination of strength and endurance training as compared to the adaptations produced by either strength or endurance training separately. There were three exercise groups: a strength group (S) that exercised 30--40 min . day-1, 5 days . week-1, and endurance group (E) that exercised 40 min . day-1, 6 days . week-1; and an S and E group that performed the same daily exercise regimens as the S and E groups. After 10 weeks of training, VO2max increased approx. 25% when measured during bicycle exercise and 20% when measured during treadmill exercise in both E, and S and E groups. No increase in VO2max was observed in the S group. There was a consistent rate of development of leg-strength by the S group throughout the training, whereas the E group did not show any appreciable gains in strength. The rate of strength improvement by the S and E group was similar to the S group for the first 7 weeks of training, but subsequently leveled off and declined during the 9th and 10th weeks. These findings demonstrate that simultaneously training for S and E will result in a reduced capacity to develop strength, but will not affect the magnitude of increase in VO2max.

Adaptation, Physiological↗
PubMed1980

Faster adjustment to and recovery from submaximal exercise in the trained state.

This study was undertaken to evaluate the effects of endurance exercise training on O2 deficit and O2 debt, and on the time courses of the adjustment to, and recovery from, submaximal exercise of oxygen uptake (VO2) carbon dioxide production (VCO2), minute ventilation (VE), and heart rate (HR). Eight subjects participated in a 9-wk-long exercise program that increased their VO2max by 24%. It was found that O2 deficit and O2 debt were lower at the same absolute work rate and not significantly different at the same relative work rate after training. The increases in VO2, VCO2, VE, and HR at the onset of constant load submaximal work, and the decreases in VO2, VCO2, VE, and HR in recovery were more rapid at both the same absolute and the same relative work rates after training. These results show that the adaptations to endurance exercise training enable an individual to adjust to the energy requirement of constant load submaximal work more rapidly, resulting in a smaller O2 deficit. The rate of recovery is also more rapid after training, resulting in a smaller O2 debt.

Adult↗
PubMed1980

Left ventricular responses to a program of lower-limb strength training.

Nine healthy male subjects ages 18-27 exercised five days per week. Three days per week they performed five repetitions of squats, leg extensions and leg flexions with maximal resistance for a total of 11 sets. On the other two days each week subjects performed five leg presses and 20 calf raises with maximal resistance. Resting echocardiograms and physiologic evaluations were made prior to starting the strength training and again after ten weeks of training. Resting heart rate +/- SEM before and after training was 65 +/- 2 and 58 +/- 1.7 beats/min (P < .001). Maximal O2 uptake did not change significantly. Left ventricular wall thickness +/- SEM before and after training increased from 0.76 +/- .02 to 0.85 +/- 0.04 cm (P < .05). Left ventricular mass +/- SEM increased from 81.9 +/- 5 to 92.3 +/- 3.7 g (P < .05). The percentage of left ventricular fractional shortening +/- SEM increased from 32 percent +/- 1.2 to 36 percent +/- .9 (P < .001). Lower limb strength training in normal subjects did not increase maximal O2 uptake, but did induce increases in left ventricular wall thickness similar to that seen in champion strength-trained athletes. In addition, improvement in left ventricular performance without significant changes in left ventricular volumes was also observed.

Adolescent↗
PubMed1980

Strength training effects on aerobic power and short-term endurance.

Nine men participated in an exercise program (five days a week for 10 weeks) that was designed to strengthen the quadriceps muscles. This study was undertaken to determine if heavy resistance training results in an increase in endurance, Vo2max and whether the differences that are normally observed during bicycle and treadmill Vo2max measurements in the same individuals are strength-related. Following training, endurance time to exhaustion significantly increased while cycling (47%) and while running (12%), when the subjects exercised at 100% of their pretraining Vo2max. There was a small increase in Vo2max (4%, P < 0.05) during bicycle exercise (3.40 l.min-1 to 3.54 l.min-1) after training, but no significant differences were observed when expressed in (ml.kg-1.min-1). Strength training had no effect on Vo2max when measured during treadmill exercise. Absolute differences between bicycle and treadmill Vo2max were essentially the same after training as before. Lactate concentration in blood after the bicycle and treadmill endurance tests were not elevated to a greater extent after training. Thigh girth increased significantly and muscle strength increased 40% with the training. These findings provide evidence that HRT is capable of dramatically increasing short-term endurance, when the muscles involved in the training are used almost exclusively during the testing without an accompanying increase in Vo2max. These data also suggest that the differences in Vo2max between bicycle and treadmill exercise are not the result of inadequate muscle strength.

Adolescent↗