PubMed Health⌕ Search

Biomedical subjects

D Criswell

Publications and source records attributed to D Criswell.

At least 19 recordsLinked to original sources

Exercise and beta-adrenergic regulation of rat cardiac myosin isoforms.

BACKGROUND: The purpose of this experiment was to examine the effects of both exercise and beta-adrenergic receptor blockade on the expression of native cardiac myosin isoforms. Specifically, this experiment tested two hypotheses: 1) treatment of sedentary rats with the beta blocker, propranolol, will promote increased ventricular V3 (slow) native myosin content with a concomitant reduction of V1 (fast) myosin isoforms; and 2) endurance exercise training will result in an increased sympathetic drive and therefore will retard the propranolol-induced shift in cardiac myosin isoform expression. METHODS: Adult, male Sprauge-Dawley rats (120 days old) were randomly divided into 4 groups: 1) exercise-sham (ES); 2) exercise-propranolol (EP); 3) sedentary-sham (SS); and 4) sedentary-propranolol (SP). Propranolol (30 mg drug/kg body wt) and sham (saline) injections (i.p.) were administered 30 minutes prior to daily exercise. Both ES and EP groups completed six weeks (5 day/wk) of treadmill running at approximately 65-70% VO2max. RESULTS: Data analysis revealed that exercise training did not alter (p > 0.05) ventricular myosin isoforms in the sham injected animals. In contrast, propranolol treatment resulted in a significant (p < 0.05) increase in the slow (V3) myosin isoform and a concomitant decrease in the V1 isoform in both sedentary and exercise trained animals. CONCLUSIONS: The observed increase in V3 myosin isoform in propranolol treated rats supports the notion that beta-adrenergic stimulation is an important regulator of cardiac myosin isoform expression. However, our hypothesis that exercise training would retard the propranolol-induced shift in cardiac myosin was not supported.

Adrenergic beta-Antagonists↗

Effects of clenbuterol on contractile and biochemical properties of skeletal muscle.

We investigated the effects of clenbuterol on the muscle mass, contractile properties, myosin phenotype, and bioenergetic enzyme activity in the gastrocnemius (GS)-plantaris (PL)-soleus (SO) muscle complex. Rats were sham-injected or treated with clenbuterol (2 mg.kg-1, subcutaneously) for 14 d. Clenbuterol increased (P < 0.05) body weight and muscle complex weight. Also, clenbuterol treatment resulted in an increase in total muscle force production and maximal shortening velocity (P < 0.05). No difference (P > 0.05) in relative force production (force.g-1 muscle) existed between experimental groups. However, muscle fatigue increased with clenbuterol treatment. Myosin heavy chain (MHC) composition was not altered in the GS or PL muscles, but shifted toward the fast Type II MHC in the SO. Myosin light chain (MLC) composition was not altered in any of the muscles. Clenbuterol caused a decrease in oxidative and glycolytic enzyme activity in the GS and PL, but not the SO. These data suggest that the clenbuterol-induced increase in muscle mass and maximal force generation is due to hypertrophy of both fast and slow fibers. Furthermore, these findings support the notion that beta-agonists may be beneficial in combating conditions that result in muscle wasting and dysfunction.

Adrenergic beta-Agonists↗

Adaptive strategies of respiratory muscles in response to endurance exercise.

The purpose of this review is to discuss the adaptive strategies of mammalian respiratory muscles in response to whole-body endurance exercise training. It is now clear that endurance training results in small (i.e., 20-30%) but significant increases in mitochondrial enzyme activity and the activities of key antioxidant enzymes (i.e., superoxide dismutase and glutathione peroxidase) within the rodent diaphragm. Interestingly, the magnitude of this training-induced increase in costal diaphragmatic oxidative and antioxidant enzyme activity is relatively independent of the exercise duration and intensity. Although the crural diaphragm of rodents is also capable of increasing its oxidative and antioxidant capacity in response to endurance training, high-to moderate-intensity exercise of long duration is required to promote these changes. Endurance training also increases the oxidative capacity of other key rodent inspiratory muscles, such as the parasternal intercostals and external intercostals. Furthermore, endurance training results in small (approximately 10%) increased in the oxidative capacity of key abdominal (expiratory) muscles. Whether the improvement in oxidative capacity of respiratory muscles is of significant magnitude to result in improvement in respiratory muscle performance remains an unanswered question.

Adaptation, Physiological↗

Age-related increases in diaphragmatic maximal shortening velocity.

Recent evidence demonstrates that aging results in an increase in fast (type IIB) myosin heavy chain (MHC) in the rat diaphragm. It is unknown whether this age-related change in fast MHC influences the diaphragmatic maximal shortening velocity (Vmax). Therefore, we tested the hypothesis that aging is associated with an increase in the diaphragmatic Vmax and that the increase in the Vmax is highly correlated with the percentage of type IIb MHC. In vitro contractile properties were measured with costal diaphragm strips obtained from young (4 mo old; n = 8) and (old 24 mo old; n = 8) male Fischer-344 rats. Diaphragmatic maximal tetanic specific force production was 14.5% lower in the old compared with the young animals (23.0 +/- 0.4 vs. 19.7 +/- 0.8 N/cm2; P < 0.05). In contrast, the diaphragmatic Vmax was significantly higher in the old compared with the young animals (5.5 +/- 0.1 vs. 4.4 +/- 0.3 lengths/s; P < 0.05). Although the percent type IIb MHC was significantly higher (approximately +14%; P < 0.05) in the old compared with the young animals, the correlation between Vmax and percent type IIb MHC was relatively low (r = 0.50; P > 0.05). These data support the hypothesis that an age-related increase in diaphragmatic Vmax occurs; however, factors in addition to type IIb MHC are involved in regulating diaphragmatic Vmax. Interestingly, although aging resulted in a decrease in diaphragmatic maximal specific force production, power output at all muscle loads was maintained in the old animals due to the increase in diaphragmatic shortening velocity.

Aging↗

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.

Adaptation, Physiological↗

Regional training-induced alterations in diaphragmatic oxidative and antioxidant enzymes.

We examined the relationship between the intensity and duration of exercise training and the up-regulation of diaphragmatic oxidative and antioxidant enzyme activities. Nine groups of rats exercised for 10 weeks (4 days/week). Groups of animals exercised at three intensities (low, moderate, and high); at each exercise intensity, a group of animals ran at one of three exercise durations (30, 60, and 90 min/day). Sedentary animals served as controls. Muscle oxidative capacity was assessed by citrate synthase (CS) activity while antioxidant capacity was evaluated by total superoxide dismutase (SOD) and total glutathione peroxidase (GPX) activities. All intensities and durations of exercise training promoted significant (P < 0.05) increases in costal diaphragmatic CS, SOD, and GPX activities. Increases in costal CS, SOD, and GPX activity were independent of the exercise intensity and duration. High and moderate intensity exercise of 90 min duration significantly elevated (P < 0.05) crural diaphragm CS activity. Further, high and moderate intensity exercise of durations > or = 60 min promoted significant (P < 0.05) increases in crural diaphragm SOD activities. Exercise did not influence (P > 0.05) crural diaphragm GPX activity. We conclude that the training threshold for up-regulation of oxidative and antioxidant enzyme activities differs between the costal and crural diaphragm.

Animals↗

Influence of exercise and fiber type on antioxidant enzyme activity in rat skeletal muscle.

These experiments examined the influence of exercise intensity and duration on antioxidant enzyme activity in locomotor muscles differing in fiber type composition. Nine groups of female Sprague-Dawley rats (age 120 days) exercised 4 days/wk on a motor-driven treadmill for 10 wk. The impact of three levels of exercise intensity (low, moderate, and high: approximately 55, approximately 65, and approximately 75% of maximal oxygen consumption, respectively) and exercise duration (30, 60, and 90 min/day) was assessed. Sedentary animals served as controls. Oxidative capacity in the soleus and white and red gastrocnemius was assessed by measurement of citrate synthase (CS) activity, and antioxidant capacity was evaluated by assay of total superoxide dismutase, catalase, and total glutathione peroxidase (GPX) activities. In all muscles, CS activity increased as a function of exercise duration. Furthermore, in the soleus and white gastrocnemius, the magnitude of the training-induced increase in CS activity was directly related to exercise intensity. In contrast, the peak increase in CS activity in the red gastrocnemius was relatively independent of exercise intensity. Catalase activity was not increased (P > 0.05) in any muscle with training. Training-induced changes in superoxide dismutase and GPX activities were muscle specific; specifically, exercise training significantly (P < 0.05) increased superoxide dismutase activity in the soleus as a function of exercise duration up to 60 min/day. Conversely, training-induced significant (P < 0.05) increases in GPX activity occurred in red gastrocnemius only; the magnitude of the GPX increase was directly related to exercise duration but relatively independent of intensity. These data demonstrate that exercise training-induced changes in muscle antioxidant enzymes are muscle specific.

Animals↗

Metabolic characteristics of primary inspiratory and expiratory muscles in the dog.

These experiments examined the metabolic properties of the canine respiratory muscles. Because the costal diaphragm (COD), crural diaphragm (CRD), parasternal intercostals (PI), triangularis sterni (TS), and transversus abdominis (TA) are active during quite breathing in the dog, we hypothesized that these muscles would have different metabolic profiles (i.e., higher oxidative and antioxidant enzyme activities) compared with ventilatory muscles recruited only at increased ventilatory requirements [e.g., scalene (SC) and external oblique (EO)] and locomotor muscles [e.g., deltoid (DEL)]. To test this hypothesis, muscle samples were removed from six healthy adult dogs and analyzed to determine the activities of citrate synthase (CS), phosphofructokinase (PFK), 3-hydroxyacyl-CoA dehydrogenase (HADH), and superoxide dismutase (SOD). The activities of these enzymes were interpreted as relative measures of metabolic capacities, and enzyme activity ratios were considered as representing relationships between different metabolic pathways. Analysis revealed that CS and HADH activities were significantly higher (P < 0.05) in the PI, COD, CRD, and TS compared with those in all other muscles. Muscles with the lowest CS, HADH, and SOD activities (i.e., SC, TA, EO, DEL) generally had the highest PFK activities, Furthermore, the PFK/CS ratio was significantly lower in the PI, COD, CRD, and TS compared with that in all other muscles studied. These data support the notion that the canine PI, COD, CRD, and TS are metabolically different from other key ventilatory muscles.

3-Hydroxyacyl CoA Dehydrogenases↗

Biochemical verification of quantitative histochemical analysis of succinate dehydrogenase activity in skeletal muscle fibres.

The purpose of this investigation was to examine critically the validity of a computerized quantitative microphotometric histochemical technique for the determination of succinate dehydrogenase (SDH) activity in skeletal muscle fibres. Sections from the anterior costal diaphragm were removed from Fischer-344 rats (n = 12) and assayed histochemically to determine SDH activity. The SDH activity in individual muscle fibres was computed using a computerized microphotometric histochemical technique which involves measurement of the optical density of deposited diformazan derived from nitroblue tetrazolium within the fibres. To validate the histochemical technique, whole muscle SDH activities were calculated from the histochemical procedure and were compared to SDH activities determined from whole muscle homogenates via a standard quantitative biochemical assay. The mean within-day variability of the computerized microphotometric histochemical technique of determining SDH activity was 6% (range = 0.5-10.9%) for an area containing approximately 50 fibres and 6.1% (range = 1.05-14.9%) for an individual muscle fibre. Similarly, the mean between-day variability of the microphotometric histochemical technique of determining SDH activity was 5.9% (range = 2.6-13.9%) for an area containing approximately 50 fibres and 6.6% (range = 2.2-13.9%) for an individual muscle fibre. The inter-class correlation coefficient between biochemically determined SDH activity and histochemically determined SDH activity was r = 0.83 (p < 0.05). Collectively, these data demonstrate that the quantitative histochemical technique of Blanco et al. (1988) is both valid and reliable in the determination of SDH activity in skeletal muscle fibres.

Animals↗

Rigorous exercise training increases superoxide dismutase activity in ventricular myocardium.

Controversy exists as to the effect of endurance training on myocardial antioxidant enzyme activity. These experiments sought to clarify this issue by examining antioxidant enzyme activities in the rat ventricular myocardium in response to different intensities and durations of exercise training. Female Fischer-344 rats (120 days old) were assigned to either a sedentary control group or one of nine exercise training groups. Animals were exercised on a motorized treadmill for 10 wk; combinations of three durations (30, 60, and 90 min/day), and three levels of exercise intensity (low, moderate, and high) were studied. Exercise training did not alter (P > 0.05) citrate synthase, catalase, or glutathione peroxidase activities in the right or left ventricle. In contrast, high-intensity exercise (all durations) and moderate-intensity exercise (90 min/day) resulted in a significant increase (P < 0.05; +28-30%) in right ventricular superoxide dismutase (SOD) activity. Similarly, high-intensity exercise training (all durations) resulted in a significant elevation (P < 0.05; +14-26%) of left ventricular SOD activity. Furthermore, low- and moderate-intensity exercise training of long duration (i.e., 60-90 min/day) resulted in significant increases (P < 0.05; +10-23%) in left ventricular SOD activity. These data support the hypothesis that high-intensity exercise (> or = 30 min/day) or moderate-intensity exercise of long duration (> or = 60 min/day) is effective in upregulating SOD activity in the ventricular myocardium.

Animals↗

Exercise and glucocorticoid-induced diaphragmatic myopathy.

We tested the hypothesis that a chronically active muscle, such as the rat diaphragm, would be more resistant to glucocorticoid-induced myopathy than a less active locomotor skeletal muscle (plantaris). Furthermore, we sought to determine whether endurance exercise could antagonize the glucocorticoid-induced atrophy in the diaphragm. Rats were assigned to one of seven experimental groups (n = 10 per group) and injected daily over a 10-day period with either a sham solution or prednisolone acetate: group 1: control; sedentary and sham injected; group 2: control; exercise trained and sham injected; group 3; sedentary; prednisolone (0.5 mg.kg-1 x day-1); group 4: sedentary; prednisolone (1.0 mg.kg-1 x day-1); group 5: sedentary; prednisolone (2.0 mg.kg-1 x day-1); group 6: sedentary; prednisolone (5.0 mg.kg-1 x day-1); group 7: exercise trained; prednisolone (5.0 mg.kg-1 x day-1). Slope differences in the dose-response curves suggest that prednisolone-induced muscle atrophy in the plantaris was more severe than that in the diaphragm. Furthermore, high doses of prednisolone resulted in a differential effect on muscle bioenergetic enzyme activities in the plantaris and diaphragm. Prednisolone treatment (> or = 2 mg.kg-1 x day-1) resulted in a significant reduction in phosphofructokinase activity (expressed as microM substrate.min-1 x mg protein-1) and an increase in 3-hydroxyacyl-CoA dehydrogenase activity in the plantaris muscle. In contrast, prednisolone treatment did not influence phosphofructokinase activity (P > 0.05) in the diaphragm but decreased (P < 0.05) relative citrate synthase activity. Finally, 90 min daily of endurance exercise did not antagonize prednisolone-induced myopathy in either the diaphragm or the plantaris.

Adrenal Glands↗

High intensity training-induced changes in skeletal muscle antioxidant enzyme activity.

These experiments tested the hypothesis that high intensity (interval) training is superior to moderate intensity (continuous) exercise training in the upregulation of antioxidant enzyme activity in skeletal muscle. To test this postulate, we examined changes in oxidative and antioxidant enzyme activities in rat skeletal muscle following 12 wk of either interval (6 x approximately 5-min intervals at approximately 80-95% VO2max) or continuous (45 min at approximately 70% VO2max) exercise training. Both continuous and interval training resulted in significantly elevated (P < 0.05) succinate dehydrogenase (SDH) and 3-hydroxyacyl-CoA-dehydrogenase (HADH) activities in the gastrocnemius (G) and soleus (S) muscles compared with controls. SDH and HADH activities in the G and S muscles did not differ between the two exercise groups. Glutathione peroxidase (GPX) activity exceeded controls (P < 0.05) in only the interval trained S muscle. Soleus superoxide dismutase (SOD) activity was higher (P < 0.05) in both exercise groups compared with controls. No differences in SOD activity existed between interval and continuous trained animals. We conclude that when matched for oxygen cost, interval and continuous exercise training result in similar increases in SOD activity. However, high intensity interval exercise is superior to moderate intensity continuous exercise in the promotion of GPX activity in the S.

3-Hydroxyacyl CoA Dehydrogenases↗

Fluid replacement beverages and maintenance of plasma volume during exercise: role of aldosterone and vasopressin.

Previous experiments have demonstrated that consumption of a glucose polymer-electrolyte (GP-E) beverage is superior to water in minimizing exercise-induced decreases in plasma volume (PV). We tested the hypothesis that elevated plasma concentrations of vasopressin and/or aldosterone above that seen with water ingestion may explain this observation. Six trained cyclists performed 115 min of constant-load exercise (approximately 65% of maximal oxygen consumption) on a cycle ergometer on two occasions with 7 days separating experiments. Ambient conditions were maintained relatively constant for both exercise tests (29-30 degrees C; 58-66% relative humidity). During each experiment, subjects consumed 400 ml of one of the following beverages 20 min prior to exercise and 275 ml immediately prior to and every 15 min during exercise: (1) distilled water or (2) GP-E drink contents = 7% carbohydrate (glucose polymers and fructose; 9 mmol.l-1 sodium; 5 mmol.l-1 potassium; osmolality 250 mosmol.l-1). No significant difference (P > 0.05) existed in mean skin temperature, rectal temperature, oxygen consumption, carbon dioxide production or the respiratory exchange ratio between treatments. Further, no significant differences existed in plasma osmolality and plasma concentrations of sodium, potassium, chloride or magnesium between treatments. Plasma volume was better maintained (P < 0.05) in the GP-E trial at 90 and 120 min of exercise when compared to the water treatment. No differences existed in plasma levels of vasopressin or aldosterone between treatments at any measurement period. Further, the correlation coefficients between plasma concentrations of vasopressin and aldosterone and change in PV during exercise were 0.42 (P < 0.05) and 0.16 (P > 0.05), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Exercise-induced hypoxemia in athletes: role of inadequate hyperventilation.

These experiments examined the exercise-induced changes in pulmonary gas exchange in elite endurance athletes and tested the hypothesis that an inadequate hyperventilatory response might explain the large intersubject variability in arterial partial pressure of oxygen (PaO2) during heavy exercise in this population. Twelve highly trained endurance cyclists [maximum oxygen consumption (VO2max) range = 65-77 ml.kg-1.min-1] performed a normoxic graded exercise test on a cycle ergometer to VO2max at sea level. During incremental exercise at VO2max, 5 of the 12 subjects had ideal alveolar to arterial PO2 gradients (PA-aO2) of above 5 kPa (range 5-5.7) and a decline from resting PaO2 (delta PaO2) 2.4 kPa or above (range 2.4-2.7). In contrast, 4 subjects had a maximal exercise PA-aO2 of 4.0-4.3 kPa with delta PaO2 of 0.4-1.3 kPa while the remaining 3 subjects had PA-aO2 of 4.3-5 kPa with delta PaO2 between 1.7 and 2.0 kPa. The correlation between PAO2 and PaO2 at VO2max was 0.17. Further, the correlation between the ratio of ventilation to oxygen consumption vs PaO2 and arterial partial pressure of carbon dioxide vs PaO2 at VO2max was 0.17 and 0.34, respectively. These experiments demonstrate that heavy exercise results in significantly compromised pulmonary gas exchange in approximately 40% of the elite endurance athletes studied. These data do not support the hypothesis that the principal mechanism to explain this gas exchange failure is an inadequate hyperventilatory response.

Adult↗

High intensity exercise training-induced metabolic alterations in respiratory muscles.

Limited information exists concerning the effects of high intensity interval exercise training (HIET) on metabolic alterations in both inspiratory and expiratory muscles. To test the hypothesis that HIET will improve the oxidative capacity of the diaphragm and major expiratory muscles, we examined Krebs cycle and beta oxidation enzyme activities in the diaphragm and three groups of expiratory (abdominal) muscles in rats subjected to 12 weeks (5 days.wk-1) of treadmill exercise. Two groups of female Sprague-Dawley rats (age ca 120 days) were studied: (1) HIET group (n = 10; animals performed 6 x ca 5-min running intervals.day-1 at ca 90-95% VO2max); (2) sedentary control group (n = 7). When compared to controls, HIET resulted in significantly elevated (P less than 0.05) activities of 3-hydroxy-acyl-Co-A dehydrogenase (HADH) and citrate synthase (CS) in the costal diaphragm, rectus abdominus, external obliques, and the plantaris muscles. In contrast, training did not increase (P greater than 0.05) the activities of CS or HADH in the crural diaphragm or the internal obliques/transversus abdominus muscles. By comparison, the training-induced increases in oxidative capacity (e.g., CS activity) in the costal diaphragm, rectus abdominus, and external obliques were relatively small (ca 23, 10, 12%, respectively) when contrasted to the exercise-induced increase in CS activity in the plantaris muscle (ca 47%). We conclude that HIET results in small but significant improvements in the oxidative and beta oxidation capacities of the costal diaphragm and at least two abdominal expiratory muscles.

3-Hydroxyacyl CoA Dehydrogenases↗

Diaphragmatic fiber type specific adaptation to endurance exercise.

Recent evidence suggests that exercise training results in a significant improvement in the oxidative capacity of the mammalian diaphragm; however, limited data exist concerning which diaphragmatic fiber types are metabolically altered due to training. To test the hypothesis that exercise training increases the oxidative capacity of diaphragmatic type I and IIa fibers only, we examined the effects of endurance training on the fiber type specific changes in oxidative capacity, cross-sectional area, and capillarity of the costal diaphragm. Female Fischer-344 rats (age ca 180 days) were divided into either sedentary control group (n = 6) or an exercise training group (n = 6). The trained animals exercised for 10 wks on a motor-driven treadmill (60 min.day-1; 5 days.wk-1) at a work rate equal to ca 55-65% VO2max. Capillaries were identified histologically and fiber types determined using ATPase histochemistry. Fiber cross-sectional area (CSA) and succinate dehydrogenase (SDH) activity in individual fibers were measured using a computerized image analysis system. Compared to control animals, training did not increase the capillary to fiber ratio in any diaphragm fiber type (P greater than 0.05); however, training increased capillary density (capillary No./CSA) in type IIa fibers due to a reduction in cell CSA (P less than 0.05). Further, training resulted in significant (P less than 0.05) increases in total diaphragmatic SDH activity (delta increase = 17.5%) and an increase in SDH activity in both type I (delta increase = 14%) and IIa fibers (delta increase = 17.4%). In contrast, training did not alter (P greater than 0.05) SDH activity in type IIb fibers.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

Exercise training-induced alterations in skeletal muscle oxidative and antioxidant enzyme activity in senescent rats.

Limited data exist concerning exercise training-induced alterations in skeletal muscle oxidative and antioxidant enzyme activity in senescent animals. Therefore, the purpose of this study was twofold: 1) to examine the exercise training-induced changes in oxidative and antioxidant enzyme activity in skeletal muscle of old rats; and 2) to critically analyze the relationship between oxidative and antioxidant enzyme activities in skeletal muscle in both trained and untrained senescent rats. Female Fischer-344 rats (approximately 24-mo-old) were divided into 1) exercised trained (ET; n = 10) and 2) sedentary (S; n = 6) groups. The ET rats performed a 10-week training program of treadmill exercise (approximately 60 min, 5 days/wk). Training significantly (p less than 0.05) improved VO2max (delta 22.8%) in the ET rats above their age-matched controls. Further, the ET group had significantly elevated (p less than 0.05) activities of succinate dehydrogenase (SDH) in the soleus and red gastrocnemius (RG) muscles as well as greater (p less than 0.05) 3-hydroxyacyl-CoA dehydrogenase (HADH) activity in the RG when compared to the S group. However, training did not alter (p greater than 0.05) HADH activity within the white gastrocnemius (WG) or soleus muscles. Activity of the antioxidant enzyme, glutathione peroxidase (GPX) was higher (p less than 0.05) in the soleus and RG in ET rats when compared to the S rats; in contrast, training did not alter (p less than 0.05) GPX activity in the WG. Finally, the correlation coefficients between SDH and GPX activities (combined ET and S groups) for the RG, WG, and soleus muscles were r = .73, .17 and .36, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxyacyl CoA Dehydrogenases↗

Exercise-induced cellular alterations in the diaphragm.

Limited data exist concerning the effects of exercise training on cellular oxidative capacity in the diaphragm of senescent animals. In this study we examined the changes in cellular oxidative capacity, muscle cell cross-sectional area (CSA), and capillarity within the costal diaphragm of senescent animals after a 10-wk endurance-training program. Twelve 24-mo-old female Fischer 344 rats were divided into either a sedentary control group (n = 6) or exercise training group (n = 6). The trained animals exercised on a motor-driven treadmill (60 min/day, 5 days/wk) at a work rate equal to approximately 55-65% VO2max. Capillaries were identified histologically and fiber types determined using adenosinetriphosphatase (ATPase) histochemistry. Succinate dehydrogenase (SDH) activity and CSA in individual fibers were measured using a computerized image analysis system. Exercise training did not increase (P > 0.05) the capillary-to-fiber ratio for any fiber type. However, training significantly decreased CSA (P < 0.05) and increased capillary density (capillary number/CSA) (P < 0.05) in type I, type IIa, and type IIb fibers. Furthermore, exercise training resulted in small but significant increase in SDH activity (P < 0.05) in type I and IIa fibers, whereas training did not alter SDH activity (P > 0.05) in type IIb fibers. These data demonstrate that endurance training in senescent animals results in small relative improvements in both oxidative capacity and capillary density in costal diaphragmatic type I and IIa muscle fibers. The increase in both capillary density and fiber SDH activity was largely due to a reduction in fiber CSA.

Aging↗