R. C. Hickson

Interference of Strength Development by Simultaneously Training for Strength and Endurance

SummaryThe 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, an 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, VO2 max 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 VO2 max 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 VO2 max.

Uniqueness of interval and continuous training at the same maintained exercise intensity

SummaryThe present study sought to evaluate the inconsistencies previously observed regarding the predominance of continuous or interval training for improving fitness. The experimental design initially equated and subsequently maintained the same relative exercise intensity by both groups throughout the program. Twelve subjects were equally divided into continuous (CT, exercise at 50% maximal work) or interval (IT, 30 s work, 30 s rest at 100% maximal work) training groups that cycled 30 min day−1, 3 days week−1, for 8 weeks. Following training, aerobic power (VO2max), exercising work rates, and peak power output were all higher (9–16%) after IT than after CT (5–7%). Vastus lateralis muscle citrate synthase activity increased 25% after CT but not after IT. A consistent increase in adenylate kinase activity (25%) was observed only after IT. During continuous cycling testing the CT group had reduced blood lactate (1ab) levels and respiratory quotient at both the same absolute and relative (70% VO2max) work rates after training, while the IT group displayed similar changes only at the same absolute work rates. By contrast, both groups responded similarly during intermittent cycling testing with lower 1ab concentrations seen only at absolute work rates. These results show that, of the two types of training programs currently employed, IT produces higher increases in VO2max and in maximal exercise capacity. Nevertheless, CT is more effective at increasing muscle oxidative capacity and delaying the accumulation of 1ab during continuous exercise.

Glucocorticoid antagonism by exercise and androgenic-anabolic steroids

This work evaluated the anticatabolic capacity of androgenic-anabolic steroids and exercise (contractile activity) in inhibiting skeletal muscle atrophy associated with excessive levels of circulating glucocorticoids. With androgenic-anabolic steroids, most binding studies indicate that they have very low binding specificity for the glucocorticoid receptor. Androgens may interact through their own receptor to interfere with glucocorticoid functioning at the gene level, but this remains unproven. Current literature suggests that androgens do not prevent atrophy but may retard growth suppression accompanying glucocorticoid treatment. With exercise, functional overload, resistance, and endurance types of training are capable of preventing muscle atrophy from glucocorticoids. Androgen and glucocorticoid-receptor binding and glucocorticoid-receptor activation studies have, thus far, not established that atrophy prevention is mediated through the receptor. In conclusion, the role of androgenic-anabolic steroids as glucocorticoid antagonists requires further study. Study of the effects of exercise on muscle gene expression of glucocorticoid-inducible proteins is needed to gain additional understanding of this mechanism of atrophy prevention.

Adverse Effects of Anabolic Steroids

SummaryAnabolic steroids are used therapeutically for various disorders and as ergogenic aids by athletes to augment strength, muscular development, and to enhance performance. There is a wide range of concomitant temporary and permanent adverse effects with steroid administration. Several well-documented adverse actions of these hormones may develop rapidly within several weeks or less (i.e. altered reproductive function) or require up to several years of steroid intake (i.e. liver carcinoma). More recent studies indicate that glucose intolerance, insulin resistance, increased cardiovascular disease risk profiles, cerebral dangers, musculoskeletal injuries, prostate cancer, psychosis and schizophrenic episodes, among others, accompany anabolic steroid intake. There is, at present, no evidence to support the claim that athletes are less susceptible to adverse effects than those individuals receiving hormone treatment in a clinical setting. Based on the available information which has accumulated primarily from cross-sectional, short term longitudinal, and case studies, there is a need: (a) to develop a comprehensive battery of specific and sensitive markers of adverse effects, particularly those that would be able to detect the onset of adverse actions; and (b) to conduct controlled long term longitudinal studies in order to fully understand the extensiveness and mechanisms involved in the occurrence of adverse effects.

Skeletal muscle fiber type, resistance training, and strength-related performance

The research goal was to attempt to clarify the consequences of increased strength on performance at submaximal exercise intensities. Eight subjects (4 males, 4 females) completed a 3-d.wk-1, 16-wk resistance training regimen. After training, upper (bench press, BP) and lower (parallel squat, PS) extremity strength were increased by 23% and 37%, respectively. Performance at the same absolute work rates as before training was increased by 30-159% following training depending on intensity and type of exercise. Performance at the same relative work rates (80%, 60%, 40%) remained unchanged by the training for both exercises. Prior to training, PS repetitions at 40% were correlated (r = 0.69, P < 0.05) with the percentage of slow-twitch (ST) fibers in the vastus lateralis muscle. There were similar relationships at 40% (r = 0.73) and at 60% (r = 0.83) for the PS exercise after training. However, the resistance program did not result in greater relative submaximal performance in individuals with a higher percentage of ST fibers. We conclude that strength improvement of up to 40% does not produce a strength-related performance deficit, when training and testing procedures are identical. Yet, these data do not rule out the potential of a strength-related repetition performance deficit. When subjects were equally divided by strength levels, those tested at the highest absolute resistance had significantly lower bench press repetition performance at 60% and 40% of the 1-RM than the subjects tested at the lowest absolute resistance.

Fatty Acid Binding Proteins in the Three Types of Rat Skeletal Muscle

Abstract By means of Sephadex G-50 column chromatography, a M r 12,000 fatty acid binding protein (FABP) was found to be present in all three types of skeletal muscle. FABP concentrations in muscle cytosols (105,000g supernatant) were fiber type specific with binding levels (expressed as pmole [14C]oleate bound/mg protein) of 70 ± 7 in fast-twitch white (FTW) (heart FABP = 469 ± 33). Cytosols from all three fiber types cross-reacted with antibody to pure heart FABP on Ouchterlony immunodiffusion analysis. FABP content, determined by radial immunodiffusion, followed the same pattern in the muscle types as that in the binding assay. The values (in μg/mg protein) were 3.3 ± 0.1 in FTW, 17.0 ± 0.4 in FTR, and 31.7 ± 1.4 in STR fibers (heart = 55). Disc gel electrophoresis revealed a protein band in each fiber type that had migration identical to that of pure heart FABP and was proportional to the amounts determined by Sephadex G-50 chromatography and immunoassay. In addition, Western blots of tissue cytosols, using antibody to heart FABP, detected single protein bands identical in size to pure heart FABP in all three types of skeletal muscle. These results show the presence of a FABP in all skeletal muscle types with an immunologic and electrophoretic characterization identical to that of heart FABP.

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.

Exercise interrupts ongoing glucocorticoid-induced muscle atrophy and glutamine synthetase induction

This study was undertaken to determine whether regular endurance exercise is a deterrent to a developing state of muscle atrophy from glucocorticoids and to evaluate whether the contractile activity antagonizes the hormonal actions on glutamine synthetase, alanine aminotransferase, and cytosolic aspartate aminotransferase (cAspAT). Adult female rats were administered cortisol acetate (CA, 100 mg/kg body wt) or an equal volume of the vehicle solution for up to 15 days. Exercise (treadmill running at 31 m/min, 10% grade, 90 min/day) was introduced after 4 days of CA treatment, at which time plantaris and quadriceps muscle mass had been reduced to 90% of control levels. Running for 11 consecutive days prevented 40 mg of the 90-mg loss and 227 mg of the 808-mg loss that were subsequently observed in plantaris and quadriceps muscles, respectively, in the sedentary animals. Glutamine synthetase mRNA and enzyme activity were elevated threefold by glucocorticoid treatment in the deep quadriceps (fast-twitch red) muscles after 4 days. Initiating exercise completely interfered with the further hormonal induction (to approximately 5-fold) of this enzyme and, after 11 consecutive days of the exercise regimen, glutamine synthetase mRNA and enzyme activity were 58 and 68% of values from CA-treated sedentary animals. In vehicle-treated groups, basal levels of glutamine synthetase expression were also diminished by exercise to approximately 40% of the values in sedentary controls. Hormone treatment did not alter either aminotransferase enzyme activity but reduced cAspAT mRNA in fast-twitch red muscles by 50%. Exercise abolished the glucocorticoid effect on cAspAT mRNA.(ABSTRACT TRUNCATED AT 250 WORDS)

Protective Effect of Glutamine from Glucocorticoid-Induced Muscle Atrophy Occurs without Alterations in Circulating Insulin-Like Growth Factor (IGF)-I and IGF-Binding Protein Levels

Abstract We investigated whether the prevention of glucocorticoid-induced muscle atrophy by glutamine infusion is associated with alterations in serum levels of insulin-like growth factor (IGF)-I and its binding proteins (IGFBPs). Hormone (cortisol acetate [CAI, 100 mg/kg body wt/day) and vehicle (carboxymethyl cellulose [CMC])-treated female rats were infused with either saline or glutamine (240 mM, 0.75 ml/hr) for a 7-day period. Glutamine infusion prevented over 70% of the skeletal muscle mass loss due to the glucocorticoid injections. Serum IGF-I concentrations, which were measured by radioimmunoassay (RIA) after acid solid-phase extraction of IGFBPs, were not significantly different among groups (range of means: 373-395 ng/ml). Saline/CA treatment resulted in a 2-fold increase in circulating levels of IGFBP-3 (38- to 50-kDa bands from ligand blotting measurements) versus the saline/CMC group. Levels of 30-to 32-kDa bands were increased by ∼3-fold in the CA-treated rats. lmmunoprecipitation studies suggested that the increase in the 30- to 32-kDa binding proteins were not due to elevated levels of IGFBP-1, −2, or −5. None of the treatments significantly modified circulating levels of IGFBP-4 (24 kDa). Glutamine infusion did not reverse the effects of glucocorticoids on circulating levels of 38- to 50- and 30- to 32-kDa IGFBPs. We conclude that the attenuation of glucocorticoid-induced muscle atrophy by glutamine infusion is not associated with changes in circulating levels of IGF-I or IGFBPs.

Specificity of activated glucorticoid receptor expression in heart and skeletal muscle types

Muscle metabolic responses to glucocorticoids are specific to fiber type. The present study revealed that a definite pattern exists in the formation of the two thermally activated glucocorticoid receptor complexes among the different types of muscle. Fiber types that enlarge from glucocorticoids (heart) contained the highest relative distribution of binder II and lowest content of binder IB. Fibers that atrophy from glucocorticoids (white muscle) contained negligible content of binder II and the highest appearance of binder IB. The formation of binder IB could not be explained by differences in proteolysis among the cell types. These results are consistent with the hypothesis that specific receptor forms may regulate the glucocorticoid induction of muscle hypertrophy and atrophy.