Muscle Citrate Synthase Activity Research Articles

Lack of antioxidant adaptation to short-term aerobic training in human muscle.

The effects of 8 wk of 35 min of aerobic cycle training (3 times/wk) on indexes of male and female human vastus lateralis muscle antioxidant status were investigated. Training resulted in significant elevations in whole body maximal O2 consumption and muscle citrate synthase activity. Despite this, muscle superoxide dismutase, catalase, and glutathione peroxidase activities were not significantly altered by the training protocol. In addition, training did not affect muscle vitamin E (alpha- and gamma-tocopherol) concentrations. Glutathione status determined as the concentrations of reduced glutathione (GSH), oxidized glutathione (GSSG), total glutathione (GSH + 2 x GSSG), and GSH/GSSG ratio was unaffected by the training protocol. There were no significant differences between males and females in any indexes of muscle antioxidant status. These results indicate that the moderate aerobic training typically performed by regularly exercising humans did not positively alter endogenous antioxidant status. This suggests that short-term aerobic training increases capacity for flux through the citric acid cycle without necessarily increasing the ability to handle potential free radicals generated by the enhanced electron flux.

Tests of running performance do not predict subsequent spontaneous running in rats

Rats of similar mass and genetic stock have up to a 50-fold difference in spontaneous daily running distance. However, the reasons for this large variability in spontaneous running distance are not known. This study examined whether tests of running performance predict subsequent spontaneous running distance in rats housed in individual running wheel cages. Long-Evans rats ( n = 56) were randomly assigned to either a sedentary control group (C) or a group housed in specially designed wheel cages in which they were able to exercise spontaneously (ES). They then underwent a high-intensity running test (MAX), during which oxygen consumption was measured at a submaximal ( VO 2submax) and maximal workload ( VO 2max). The rats' submaximal running endurance (END) and maximal sprinting speed (SPRINT) were also tested on the treadmill. After 8 weeks the average spontaneous running distance of ES was 29.7 ± 3.7 km · wk −1 (mean ± SE), but ranged from 1.4 to 71.1 km · wk −1. Tests of running performance and oxygen consumption were repeated in both groups, followed by in situ measurements of muscle contractile properties and of citrate synthase activity in the skeletal muscle. None of the measurements of running performance or oxygen consumption during the initial tests conducted at the start of the experiment was related to subsequent average spontaneous running distance. After 8 weeks, the mean peak force generated by the electrically stimulated gastrocnemius/plantaris muscles was greater in ES than in C (746± 89 vs. 455 ± 28 mg, p < 0.005), but this difference was not related to spontaneous running distance. Conversely, citrate synthase activity of the soleus muscle after training was related to average spontaneous running distance ( r = 0.92, p < 0.0004). Average spontaneous running distance was also related to MAX ( r = 0.65, p < 0.002), END ( r = 0.59, p < 0.0009), and SPRINT ( r = 0.61, p < 0.0005) and was inversely related to running intensity ( r = −0.66, p < 0.002) after 8 weeks of training. It can be concluded from this study that 1) spontaneous running distance in rats cannot be predicted by pretraining tests of running performance. Hence, low levels of spontaneous running activity in some rats are not explained by skeletal muscular and cardiovascular factors thought to determine running capacity, and 2) posttraining tests of running performance were proportionally related to total spontaneous running distance and muscle oxidative enzyme changes but not to the in situ contractile properties of the muscles.

Effects of trandolapril and verapamil on glucose transport in insulin-resistant rat skeletal muscle

We have used an animal model of insulin resistance—the obese Zucker ( fa fa ) rat—to test whether oral administration of the non—sulfhydryl-containing angiotensin-converting enzyme (ACE) inhibitor, trandolapril, alone or in combination with the Ca 2+-channel blocker, verapamil, can induce a beneficial effect on insulin-stimulated glucose transport and metabolism in skeletal muscle. Insulin-stimulated 2-deoxyglucose (2-DG) uptake in the isolated epitrochlearis muscle was less than 50% as great in obese animals compared with lean ( Fa/-) controls ( P < .05), but was significantly improved in the obese group by both short-term (6 hours, +33%) and long-term (14 days, +70%) oral treatment with trandolapril. Verapamil treatment alone did not alter insulin-stimulated 2-DG uptake in muscle, but simultaneous administration of verapamil and trandolapril resulted in the most pronounced effect on insulin-stimulated 2-DG uptake (+106%). Long-term treatment with trandolapril alone and in combination with verapamil significantly increased muscle glycogen (+26% to 27%), glucose transporter GLUT-4 protein (+27% to 31%), and hexokinase activity (+21% to 49%), and decreased plasma insulin levels (−23% to −29%). Muscle citrate synthase activity was enhanced only when trandolapril and verapamil were administered in combination (+24%). We conclude that the long-acting, non—sulfhydryl-containing ACE inhibitor, trandolapril, alone and in combination with the Ca 2+-channel blocker, verapamil, can significantly improve insulin-stimulated glucose transport activity in skeletal muscle of the insulin-resistant obese Zucker rat, and that this improvement is associated with favorable adaptive responses in GLUT-4 protein levels, glycogen storage, and activities of relevant intracellular enzymes of glucose catabolism.

PRIOR TRAINING INCREASES COLLATERAL BLOOD FLOW IN RATS FOLLOWING ACUTE FEMORAL ARTERY LIGATION 1026

Endurance exercise training is know to increase vascular capacity and enhance vasoresponsiveness of feed arteries and large conduit vessels. We evaluated whether similar changes could modify pre-existing collateral vessels to improve collateral blood flow (BF) subsequent to acute femoral artery occlusion. Adult male Sprague-Dawley rats (-350 g) were trained (n=12) by treadmill running at 30 m/min, for 60 min/d, 5 d/wk for 6 wk, or limited to cage activity (sedentary; n=13). Training increased muscle citrate synthase activity (p<0.001). Collateral-dependent BFs were determined (85Sr& 141Ce μspheres) while running at 2 speeds (25 & 30 m/min) 4-6h following bilateral femoral artery ligation. Maximal collateral-dependent BFs were obtained, as calf muscle BFs were not further increased by the higher running speed. BFs were higher in the trained group (P<0.01; cf.Figure) even though aortic pressures were similar(150-160 mmHg). These data suggest that prior exercise training can`condition' (expand And/or better dilate?) pre-existing conduit vessels to optimize collateral-dependent BF immediately following obstruction of a primary distal artery.

Composition and size of type I, IIA, IID/X, and IIB fibers and citrate synthase activity of rat muscle

A population of muscle fibers containing a myosin heavy-chain isoform IId (or 2x) has recently been identified in rat muscle. The purpose of this study was to histochemically determine the relative population and size of muscle fibers composed of type IID/X fibers as well as type I, IIA, and IIB fibers to estimate the absolute mass of the different types of fibers in rat muscle. In addition, muscle citrate synthase activity was measured to determine the relationship between fiber composition and muscle oxidative capacity. Seventy-six muscles or muscle parts from the face, neck, shoulder, arm, trunk, hip, thigh, and leg of three adult (4.5-5 mo of age) male Sprague-Dawley rats were removed, weighed, and frozen for histochemical and biochemical analyses. The data demonstrated that type IIB fibers make up 71% of the total muscle mass, type IID/X fibers 18%, type IIA fibers 5%, and type I fibers 6%. The mean cross-sectional area across all muscles was 5,078 +/- 175 microns 2 for type IIB fibers, 3,078 +/- 105 microns2 for type IID/X fibers, 2,045 +/- 80 microns2 for type IIA fibers, and 1,898 +/- 90 microns2 for type I fibers. Citrate synthase activity, an indicator of muscle mitochondrial content, was most closely related to the population of type IIA fibers and was in the rank order of type IIA > I > IID/X > IIB. NADH-tetrazolium reductase staining intensity also confirmed this order. These data demonstrate that type IID/X fibers make up a significant portion of the adult rat muscle mass and are intermediate to type IIA and IIB fibers in regard to fiber size and oxidative potential.

Muscle blood flow during exercise in sedentary and trained hypothyroid rats

Hypothyroidism is characterized by exercise intolerance. We hypothesized that active muscle blood flow during in vivo exercise is inadequate in the hypothyroid state. Additionally, we hypothesized that endurance exercise training would restore normal blood flow during acute exercise. To test these hypotheses, rats were made hypothyroid (Hypo) over 3-4 mo with propylthiouracil. A subset of Hypo rats was trained (THypo) on a treadmill at 30 m/min (15% grade) for 60 min/day 5 days/wk over 10-15 wk. Hypothyroidism was evidenced by approximately 80% reductions in plasma triiodothyronine levels in Hypo and THypo and by 40-50% reductions in citrate synthase activities in high oxidative muscles in Hypo compared with euthyroid (Eut) rats. Training efficacy was indicated by increased (25-100%) citrate synthase activities in muscles of THypo vs. Hypo. Regional blood flows were determined by the radiolabeled microsphere method before exercise and at 1-2 min of treadmill running at 15 m/min (0% grade). Preexercise muscle blood flows were generally similar among groups. During exercise, however, flows were lower in Hypo than in Eut for high oxidative muscles such as the red section of vastus lateralis [277 +/- 24 and 153 +/- 13 (SE) ml.min-1.100 g-1 for Eut and Hypo, respectively; P < 0.01] and vastus intermedius (317 +/- 32 and 187 +/- 20 ml.min-1.100 g-1 for Eut and Hypo, respectively; P < 0.01) muscles. Training (THypo) did not normalize these flows (168 +/- 24 and 181 +/- 24 ml.min-1.100 g-1 for red section of vastus lateralis and vastus intermedius muscles, respectively). Blood flows to low oxidative muscle, such as the white section of vastus lateralis muscle, were similar among groups (21 +/- 5, 25 +/- 4, and 34 +/- 7 ml.min-1.100 g-1 for Eut, Hypo, and THypo, respectively; P = NS). These findings indicate that hypothyroidism is associated with reduced blood flow to skeletal muscle during exercise, suggesting that impaired delivery of nutrients to and/or removal of metabolites from skeletal muscle contributes to the poor exercise tolerance characteristic of hypothyroidism.

Growth Rate and Function of Skeletal Muscles in Japanese Quail Selected for Four-Week Body Mass

We compared growth and physiological function in pectoral and leg muscles of Japanese quail chicks from a line selected for 4-wk body mass (P line) and an unselected control (C) line. Growth rates of pectoral and, especially, leg muscles were higher in the P line than in the control line during the first week posthatching but not thereafter. Citrate synthase (CS) activity in pectoral muscle increased early in postnatal development but reached much higher levels in control chicks than in selected chicks; metabolic response to cold stress also was greater in C-line chicks than in P-line chicks. Pyruvate kinase (PK) activity and potassium concentration increased rapidly during the early postnatal development period and did not differ between lines except that the increase in PK in leg muscle was delayed in P-line chicks compared with C-line chicks. Exponential growth rates (EGR) of leg and pectoral muscles exhibited inverse relations to increasing PK activity that were indistinguishable between selected and control lines. Pyruate kinase activity was normalized to the peak value for each muscle mass within each line to establish an index to functional maturity (M) extending from 0 to 1. The negative relation between EGR and M did not differ significantly between type of muscle or between line. This result is consistent with the presence of a growth rate-functional maturity trade-off that governs the rate of growth of skeletal muscle during postnatal development. Accordingly, the growth response of leg muscles of selected chicks may be related to delayed maturation, as indicated by PK activity. In addition, although the growth rate of leg muscle in unselected chicks during the first week posthatch is less than expected from M, EGR values for leg muscles of selected quail are close to predicted values. Thus, the growth rate of the leg muscles possibly is down regulated in control lines but released in response to selection for rapid growth to realize more fully the growth potential of the muscle at a given state of maturity.

Fiber type-specific effects of clenbuterol and exercise training on insulin-resistant muscle

The interrelationships among glucose uptake, GLUT-4 protein, and citrate synthase activity in insulin-resistant skeletal muscle were investigated. Female obese (fa/fa) Zucker rats were randomly assigned to treadmill training, ingestion of the selective beta 2-adrenergic agonist clenbuterol, or sedentary control groups. After 7-8 wk of treatment, hindlimbs were perfused to determine maximal insulin-stimulated (10 mU/ml) 2-[3H]deoxy-D-glucose (2-DG) uptake. Exercise training significantly enhanced 2-DG uptake and GLUT-4 protein in red gastrocnemius and plantaris. Alternatively, 2-DG uptake was not altered in soleus after exercise training despite a 52% increase in GLUT-4 protein. The increases in GLUT-4 protein in red gastrocnemius, plantaris, and soleus of the trained rats were accompanied by increases in citrate synthase activity. In contrast to exercise training, clenbuterol administration decreased citrate synthase activity in red and white gastrocnemius, yet had no effect on GLUT-4 protein levels or maximal insulin-stimulated 2-DG uptake. Clenbuterol treatment did, however, increase citrate synthase activity and GLUT-4 protein in soleus. These findings indicate that total GLUT-4 protein largely determines the maximal rate of insulin-stimulated glucose uptake in fast-twitch muscle, whereas in slow-twitch muscle it does not. In addition, the results demonstrate that coordination of proteins governing glucose uptake and disposal may be disrupted in a fiber type-specific manner. Overall, the findings raise important questions as to whether regulation of proteins governing glucose uptake and disposal differs significantly among fiber types.

Role of beta-adrenergic mechanisms in exercise training-induced metabolic changes in respiratory and locomotor muscle.

To test the hypothesis that beta-adrenergic stimulation is required for the normal increase in oxidative capacity of respiratory and locomotor skeletal muscle in response to exercise training, we examined the effects of beta-blockade on muscle oxidative capacity in trained and sedentary rats. Thirty-four female adult Sprague-Dawley rats were randomly divided into four experimental groups: 1) trained+propranolol (TP); 2) trained + sham injection (TS); 3) sedentary + propranolol (SP); and 4) sedentary + sham injection (SS). Training increased (p < 0.05) citrate synthase (CS) activity in the plantaris (+29%) and costal diaphragm (+12%) of TS animals compared to SS animals. In contrast, training did not (p > 0.05) increase costal diaphragm CS activity in TP animals compared to the SS group. Further, although training increased (p < 0.05) plantaris CS activity in the TP group (+18%) compared to the SP group, the training-induced increase in muscle CS activity was 11% lower (p < 0.05) than observed in TS animals. Collectively, these results suggest that beta-adrenergic mechanisms may play a role in the normal training-induced increase in oxidative capacity in both respiratory and locomotor skeletal muscles.

Effects of hyperthyroidism on muscle blood flow during exercise in rats

Hyperthyroidism is associated with exercise intolerance. Previous research, however, has shown that cardiac output is either normal or enhanced during exercise in the hyperthyroid state. We therefore hypothesized that blood flow to working skeletal muscle is augmented in hyperthyroid animals during in vivo submaximal exercise and, consequently, that noncardiovascular factors are responsible for intolerance to exercise. To test this hypothesis, rats were made hyperthyroid (Hyper) over 6-12 wk with injections of triiodothyronine (300 micrograms/kg). Hyperthyroidism was evidenced by left ventricular hypertrophy [euthyroid (Eut), 2.12 +/- 0.05 mg/g body wt; Hyper, 2.78 +/- 0.06; P < 0.005], 25-60% increases in citrate synthase activities in Hyper hindlimb muscles over those of Eut rats, and higher preexercise heart rates (Eut, 415 +/- 18 beats/min; Hyper, 479 +/- 19; P < 0.025). Regional blood flows were determined by the radiolabeled microsphere method, preexercise, and at 1-2 min of treadmill running at 15 m/min (0% grade). Total hindlimb muscle blood flow preexercise was unaffected (Eut, 31 +/- 4 ml.min-1.(100) g-1, n = 11; Hyper, 40 +/- 6, n = 9; not significant) but was higher (P < 0.025) in Hyper (127 +/- 17, n = 9) compared with Eut (72 +/- 11, n = 9) during treadmill running. During exercise, flows to individual muscles and muscle sections were approximately 50-150% higher in Hyper compared with Eut rats. Visceral blood flows were largely similar between groups. These findings indicate that hyperthyroidism is associated with augmented blood flow to skeletal muscle during submaximal exercise. Thus hypoperfusion of skeletal muscle does not account for the poor exercise tolerance characteristic of hyperthyroidism.

Effect of exercise training on the onset of Type I diabetes in the BB/Wor rat

The effects of regular exercise training on the onset and/or severity of hyperglycemia were studied in female diabetes-prone Biobreeding/Worcester (DP BB/Wor) rats. At 38-39 d of age, animals were weight-matched and randomly assigned to exercise-trained (T) and untrained (Unt) groups. The T rats exercised on a rodent treadmill at a moderate workload, 5 successive days with the 6th day being one of rest. Training lasted 5-11 wk until rats became moribund. Red gastrocnemius muscle citrate synthase activity was significantly higher in T (54.2 +/- 4.7 mumol.g-1.min-1) compared with Unt (42.9 +/- 5.1). No significant difference was found between the T and Unt groups in the following: age at onset of hyperglycemia (T = 82.9 +/- 8.7 d; Unt = 82.0 +/- 13.5 d, mean +/- SD), ultimate level of hyperglycemia, age of death (T = 89.9 +/- 9.2 d; Unt = 89.4 +/- 13.9 d), number of days between onset of hyperglycemia and death, or body weights at the onset of hyperglycemia. No significant difference was found between groups in pancreatic insulin concentration (microgram.g-1 of protein), T = 0.22 +/- 0.04; Unt = 0.20 +/- 0.34. These data suggest that a program of regular exercise training may not delay the onset and/or reduce the severity of hyperglycemia in the DP BB/Wor rat. Regular exercise training had no beneficial or detrimental effect on pancreatic beta-cell destruction.

Exercise training does not alter cytochrome P-450 content and microsomal metabolism

The purpose of this investigation was to determine whether increased endurance exercise capacity alters total hepatic cytochrome P-450 content and cytochrome P-450 (CYP1A and CYP2B) mediated hepatic microsomal mixed-function oxidase drug metabolism. Twenty adult male Sprague-Dawley rats were randomly assigned to either a control (C) or an endurance trained group (ET). ET rats were progressively trained 5 d.wk-1 for 11 wk. Both C and ET rats were administered in random order single posttraining doses of probe drugs theophylline (probe for CYP1A) and antipyrine (probe for CYP2B). Soleus muscle citrate synthase activity of ET rats was significantly greater (P < 0.01) than for C rats (mean +/- SD; C, 26.4 +/- 1.3 mumol.g-1.min-1; ET, 46.1 +/- 2.7). In contrast, total liver cytochrome P-450 content was not significantly different (P > 0.01) among C and ET rats (mean +/- SD; C, 0.554 +/- 0.055 nmol.mg-1 liver protein; ET, 0.604 +/- 0.080). Likewise, the posttraining C and ET single-sample plasma clearances of theophylline (mean +/- SD; C, 1.89 +/- 0.360 1.h-1.kg-1 total liver weight; ET, 2.08 +/- 0.49) and antipyrine (mean +/- SD; C, 6.44 +/- 1.56 1.h-1.kg-1 total liver weight; ET, 6.51 +/- 1.02) were not significantly different (P > 0.01). Therefore, it was concluded that strenuous endurance training of 11 wk duration did not alter total hepatic cytochrome P-450 content or CYP1A or CYP2B activity.

Effects of exercise on iron status in mature female rats

Forty-eight female rats, age 6–8 months, were utilized in a six-week experiment to investigate the effect of exercise to exhaustion and iron intakes on several parameters of iron status. Animals were placed on diets of either 9 ppm or 40 ppm dietary iron and either subjected to exercise or remained sedentary to form the following experimental groups: 9-E, 9-S, 40-E, 40-S. Body weights and food intakes were not affected by iron intake or exercise. Animals that were exercised by swimming exhibited a training effect as measured by muscle citrate synthase activity. Weights of heart, liver, spleen and gastrocnemius muscle were not uniformly affected by exercise. Hemoglobin and hematocrit were significantly higher in the 40 ppm diet, but exercise did not affect either parameter. However, serum Fe and Total Iron Binding Capacity (TIBC) were significantly lowered (p<0.05) by exercise. Transferrin saturation was significantly lower in the 9-E groups. The tissue concentration of Fe was not uniformly altered by diet or exercise in heart, liver, spleen, and muscle. Iron positive bone marrow cells were lowered significantly (p<0.05) by exercise. A combination of low iron intake and exercise results in an obvious decline of iron status in the mature rat.

Canine cardiac sarcoplasmic reticulum is not altered with endurance exercise training

To investigate the effect of exercise training on calcium movements by isolated cardiac sarcoplasmic reticulum (SR), mongrel dogs either remained sedentary (S) or were exercise-trained (E) via running for a period of 8-10 wk. The trained state was confirmed by the increase in skeletal muscle citrate synthase activity and decreases in submaximal exercise heart rates in the E group but not in the S dogs. The properties of isolated cardiac SR were identical between the groups. The variables tested included ATP-dependent calcium transport and calcium-stimulated ATPase activity. Importantly, there was no difference in spontaneous calcium release which occurred after peak ATP-dependent calcium accumulation was reached. Calcium release from passively loaded vesicles induced by calcium and ionophore also did not differ in the SR isolated from the E dogs. The change in the affinity of the SR Ca ATPase for calcium after the addition of the polyanion, heparin, was similar in both groups, indicating that the regulation of calcium-stimulated ATPase activity by the SR protein, phospholamban, is not modified by exercise training. We conclude that exercise training of 8-10 wk duration does not alter the calcium handling properties of cardiac SR isolated from mongrel dogs.

Exercise training alters endothelium-dependent vasoreactivity of rat abdominal aorta.

We tested the hypothesis that adaptations in peripheral arterial vasoreactivity are induced by exercise training. Male rats were trained to run on a treadmill at 30 m/min (15 degrees incline) for 1 h/day 5 days/wk for 10-12 wk. Efficacy was indicated by a 51% increase (P < 0.05) in citrate synthase activity in soleus muscle of exercise-trained (ET) rats compared with that of sedentary (SED) control rats. Responses to vasoactive compounds were examined in vitro using rings of abdominal aorta. Maximal isometric contractile tension evoked by KCl, norepinephrine (NE), and phenylephrine were not different between groups; sensitivity to phenylephrine was also not different between groups. However, sensitivity was lower for both KCl and NE in vessels from ET animals. Endothelium removal did not influence KCl sensitivity but did abolish the difference in NE sensitivity of vessel segments between ET and SED animals. Maximal vasodilator responses induced by acetylcholine (ACh; NE or prostaglandin F2 alpha preconstriction) were greater in vessel rings from ET rats. However, dilatory responses by sodium nitroprusside (NE or prostaglandin F2 alpha preconstriction) and forskolin (NE preconstriction) were not different between groups, indicating that the augmented ACh-induced dilatory response resulted from an adaptation of the endothelium. Blockade of nitric oxide synthase activity diminished ACh-induced vasodilation by 79 and 100% in SED and ET rats, respectively. These results indicate that training alters vasomotor function in rat abdominal aortas through adaptations of both endothelium and smooth muscle.

Effect of prolonged exercise on muscle citrate concentration before and after endurance training in men.

It has been hypothesized that endurance training reduces carbohydrate utilization during exercise via citrate-mediated inhibition of phosphofructokinase (PFK). To test this hypothesis, vastus lateralis muscle biopsy samples were obtained from eight men before and immediately (approximately 10 s) after 2 h of cycle ergometer exercise at 60% of pretraining peak O2 uptake, both before and after 12 wk of endurance exercise training (3 days/wk running, 3 days/wk interval cycling). Training increased muscle citrate synthase (CS) activity from 3.69 +/- 0.48 (SE) to 5.30 +/- 0.42 mol.h-1.kg protein-1 and decreased the mean respiratory exchange ratio during exercise from 0.92 +/- 0.01 to 0.88 +/- 0.01 (both P < 0.001). Muscle citrate concentration at the end of exercise correlated significantly with CS activity (r = 0.70; P < 0.005) and was slightly but not significantly higher after training (0.80 +/- 0.19 vs. 0.54 +/- 0.19 mmol/kg dry wt; P = 0.16). Muscle glucose 6-phosphate (G-6-P) concentration at the end of exercise, however, was 31% lower in the trained state (1.17 +/- 0.10 vs. 1.66 +/- 0.27 mmol/kg dry wt; P < 0.05), in keeping with a 36% decrease in the amount of muscle glycogen utilized (133 +/- 22 vs. 209 +/- 19 mmol.kg dry wt-1.2 h-1; P < 0.01). The lower G-6-P concentration after training suggests that the training-induced reduction in carbohydrate utilization results from attenuation of flux before the PFK step in glycolysis and is not due to citrate-mediated inhibition of PFK.

Effect of short-term training cessation on performance measures in distance runners.

This study examined if measures associated with distance running performance were affected by short-term (14 d) training cessation in 12 distance runners. VO2max decreased by approximately 3 ml.kg-1.min-1 (mean +/- SE, 61.6 +/- 2.0 vs 58.7 +/- 1.8 ml.kg-1.min-1, p < 0.05) with training cessation. Time to exhaustion (TTE) during the incremental VO2max test decreased by 1.2 min (13.0 +/- 0.5 vs 11.8 +/- 0.5 min, p < 0.001) and maximal heart rate increased (p < 0.001) by 9 beats per minute (BPM). No changes in running economy (75 and 90% VO2max) were evident, although submaximal heart rate increased by 11 BPM (p < 0.001) at both running speeds. Other evidence for detraining were decreases in estimated resting plasma volume (-5.1 +/- 1.9%) and muscle citrate synthase activity (-25.3 +/- 2.6%, p < 0.05). Muscular atrophy (muscle fiber cross-sectional area) was not evident. TTE and submaximal heart rate exhibited relatively large percent changes (-9 and +6%, respectively) compared to VO2max (-4%). These findings indicate that the reduction in VO2max with short-term training cessation is relatively small. TTE and submaximal heart rate may be easily measured, yet more sensitive indicators of decrements in distance running performance.

Plasma glucose kinetics during exercise in subjects with high and low lactate thresholds

The purpose of this study was to test the hypothesis that the rate of plasma glucose oxidation during exercise is inversely related to muscle respiratory capacity. To this end, 14 subjects were studied: in 7 of these subjects, the blood lactate threshold (LT) occurred at a relatively high intensity [i.e., at 65 +/- 2% of peak cycle ergometer oxygen uptake (VO2 peak)], whereas in the other 7 subjects, LT occurred at a relatively low intensity (i.e., at 45 +/- 2% of VO2 peak). VO2peak did not differ between the two groups, but citrate synthase activity in the vastus lateralis muscle was 53% higher (P < 0.05) in the high LT group. A primed continuous infusion of [U-13C]glucose was used to quantify rates of glucose appearance (Ra), disappearance (Rd), and oxidation (R(ox)) during 90 min of exercise at 55% VO2peak. Although both absolute and relative rates of oxygen uptake during exercise were similar in the two groups, mean Ra and Rd were 17% lower (P < 0.001) in the high LT group, and mean R(ox) was 25% lower (21.0 +/- 2.6 vs. 27.9 +/- 2.6 mumol.min-1.kg-1; P < 0.001). The percentage of total energy derived from glucose oxidation was inversely related to muscle citrate synthase activity (r = -0.85; P < 0.01). These data support the concept that skeletal muscle respiratory capacity has a major role in determining the metabolic response to submaximal exercise.

Endurance Exercise Training Causes Adrenal Medullary Hypertrophy in Young and Old Fischer 344 Rats

The purpose of the present investigation was to determine the effects of endurance exercise training on adrenal medullary volume and epinephrine content in young (5 month) and old (23 month) female Fischer 344 rats. Animals from each group underwent 10 weeks of treadmill running (60 minutes per day, 5 days per week). 72 hours following the last training session animals were killed and the adrenal glands removed for subsequent analysis. Plantaris muscle citrate synthase activity increased with training in both young and old animals (39.8% young; 36.4% old). Trained animals had larger adrenal medullary volumes (48% increase in young, and 18% in old) than untrained controls. Trained animals also had higher total adrenal medullary epinephrine content (36% increase in young, and 24% in old). There were no differences in adrenal medullary epinephrine or norepinephrine concentration (micrograms/microliters medulla). It was concluded that the training-induced increase in adrenal epinephrine content is due to an increase in the size of the medulla, and not to a greater medullary epinephrine concentration. Furthermore, similar responses to training occur in both old and young animals.

Myosin heavy chain composition in the rat diaphragm: effect of age and exercise training.

Increases in aerobic capacity in both young and senescent rats consequent to endurance exercise training are now known to occur not only in locomotor skeletal muscle but also in diaphragm. In the current study the effects of aging and exercise training on the myosin heavy chain (MHC) composition were determined in both the costal and crural diaphragm regions of female Fischer 344 rats. Exercise training [treadmill running at 75% maximal oxygen consumption (1 h/day, 5 day/wk, x 10 wk)] resulted in similar increases in plantaris muscle citrate synthase activity in both young (5 mo) and old (23 mo) trained animals (P < 0.05). Computerized densitometric image analysis of fast and slow MHC bands revealed the ratio of fast to slow MHC to be significantly higher (P < 0.005) in the crural compared with costal diaphragm region in both age groups. In addition, a significant age-related increase (P < 0.05) in percentage of slow MHC was observed in both diaphragm regions. However, exercise training failed to change the relative proportion of slow MHC in either the costal or crural region.