-
[show abstract]
[hide abstract]
ABSTRACT: These experiments compared oxidative and glycolytic enzyme activity in the costal and crural diaphragm in seven adult mammals (mouse, rat, rabbit, ferret, sheep, pig, cow) ranging in body mass from approximately 0.03 to 422 kg. Segments of the costal and crural diaphragm from the aforementioned species were homogenized to determine the activities of the glycolytic enzyme, lactate dehydrogenase (LDH), and the Krebs cycle enzyme, citrate synthase (CS). The results indicated that metabolic differences between the costal and crural diaphragm do not exist in all mammalian species. Specifically, CS activity differed (P < 0.05) between the costal and crural diaphragm (costal approximately 36% greater than crural) in only two species (rat and rabbit). Further, the oxidative capacity of the costal and crural diaphragm was significantly correlated with both breathing frequency and resting metabolic rate (r = 0.92 - 0.57; P < 0.05) across the species investigated. In contrast, glycolytic capacity was not significantly correlated (P > 0.05) with either breathing frequency or resting metabolic rate.
Respiration Physiology 08/1997; 109(2):149-54.
-
[show abstract]
[hide abstract]
ABSTRACT: 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.
International Journal of Sports Medicine 02/1995; 16(1):13-8. · 2.43 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: 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.
Respiration Physiology 02/1994; 95(2):227-37.
-
[show abstract]
[hide abstract]
ABSTRACT: 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.
The American journal of physiology 02/1994; 266(2 Pt 2):R375-80.
-
[show abstract]
[hide abstract]
ABSTRACT: This article reviews the principles of pulse oximetry and assesses the accuracy of pulse oximeter measurements obtained during exercise, based on reports of 10 studies that evaluated 24 pulse oximeters. Nine of the studies used cycle exercise, and 1 study utilized treadmill running for mode of activity. Subject populations included patients with cardiovascular or pulmonary disorders, nondisabled individuals, and athletes. Studies were performed under normoxic and hypoxic conditions, and 5 of the 10 studies validated 18 pulse oximeters at arterial oxyhemoglobin saturation (%HbO2) levels of < or = 78%. Sixteen of the 24 pulse oximeters (67%), from 7 of the 10 studies, observed pulse oximeter estimates (%SpO2) during exercise to be accurate, at least when %HbO2 was > or = 85% in nonsmokers. However, the degree of accuracy of the pulse oximeters was variable, even among the same models. Recent studies suggest the current generation of finger-probe-equipped pulse oximeters may be more accurate than ear-probe-equipped models. We recommend that clinicians carefully secure the probe; monitor signal strength; be wary of %SpO2 values of < or = 68% to 78% to avoid undetected severe hypoxemia; and be alert to whether a patient is a smoker, in which case %SpO2 will likely be overestimated. Researchers interested in using pulse oximeter estimates should validate their particular pulse oximeter(s) via arterial blood sampling.
Physical Therapy 01/1994; 74(1):40-9. · 3.11 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: 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.
The American journal of physiology 01/1994; 265(6 Pt 2):H2094-8.
-
[show abstract]
[hide abstract]
ABSTRACT: Arterial oxygenation is well maintained in healthy untrained or moderately trained individuals during exercise. In contrast, approximately 40 to 50% of healthy elite endurance athletes (cyclists and runners) demonstrate a significant reduction in arterial oxygenation during exercise at work rates approaching VO2max. The mechanism(s) to explain this exercise-induced hypoxaemia (EIH) remain controversial. However, hypoventilation and venoarterial shunt do not appear to be involved. By elimination, this suggests that ventilation-perfusion inequality and/or pulmonary diffusion limitations must contribute to EIH in this population. Theoretical and direct experimental evidence exists to support the notion that both ventilation-perfusion inequality and diffusion disequilibrium contribute to EIH; however, the relative contribution of each factor remains to be determined. In athletes who exhibit a profound EIH, the exercise-induced decline in arterial oxygenation results in a limitation of VO2max. Further, athletes who exhibit EIH at sea level suffer more severe gas exchange impairments during short term exposure to altitude than athletes or nonathletes who do not exhibit EIH at sea level. This finding explains much of the observed variance in the decline in VO2max among individuals during short term altitude or hypoxia exposure.
Sports Medicine 08/1993; 16(1):14-22. · 5.16 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: 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.
Journal of Applied Physiology 08/1993; 75(2):763-71. · 3.75 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: 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)
International Journal of Sports Medicine 08/1992; 13(5):412-6. · 2.43 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: We examined the oxidative and antioxidant enzyme activities in respiratory and locomotor muscles in response to endurance training in young and aging rats. Young adult (4-mo-old) and old (24-mo-old) female Fischer 344 rats were divided into four groups: 1) young trained (n = 12), 2) young untrained (n = 12), 3) old trained (n = 10), and 4) old untrained (n = 6). Both young and old endurance-trained animals performed the same training protocol during 10 wk of continuous treadmill exercise (60 min/day, 5 days/wk). Compared with young untrained animals, the young trained group had significantly elevated (P less than 0.05) activities of 3-hydroxyacyl-CoA dehydrogenase (HADH), glutathione peroxidase (GPX), and citrate synthase (CS) in both the costal diaphragm and the plantaris muscle. In contrast, training had no influence (P greater than 0.05) on the activity of lactate dehydrogenase within the costal diaphragm in young animals. In the aging animals, training did not alter (P greater than 0.05) activities of CS, HADH, GPX, or lactate dehydrogenase in the costal diaphragm but significantly (P less than 0.05) increased CS, HADH, and GPX activities in the plantaris muscle. Furthermore, training resulted in higher activities of CS and HADH in the intercostal muscles in the old trained than in the old untrained animals. Finally, activities of CS, HADH, and GPX were significantly (P less than 0.05) lower in the plantaris in the old untrained than in the young untrained animals; however, CS, HADH, and GPX activities were greater (P less than 0.05) in the costal diaphragm in the old sedentary than in the young untrained animals.(ABSTRACT TRUNCATED AT 250 WORDS)
Journal of Applied Physiology 04/1992; 72(3):1068-73. · 3.75 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Eleven highly trained male cyclists [maximal aerobic power (VO2max) = 70.6 +/- 4.2 ml.kg-1.min-1] performed both high intensity constant load (90-95% VO2max) and incremental cycle exercise tests with arterial blood sampling to evaluate the accuracy of pulse oximeter estimates (%SpO2) of arterial oxyhemoglobin fraction of total hemoglobin (%HbO2). Three subjects also performed an incremental exercise test in hypoxic conditions (inspired partial pressure of O2 = 89, 93, or 100 Torr). Arterial %HbO2 was determined via CO-oximetry and ranged from 72 to 99%. Three Ohmeda 3740 pulse oximeters were used to estimate %HbO2, one on each ear lobe and a finger probe. The finger probe tended to provide the best estimate of %HbO2 during exercise: the mean %SpO2 - %HbO2 difference for 232 exercise observations was 0.52 +/- 1.36% (SD). Finger probe %SpO2 and %HbO2 were highly correlated [r = 0.98, standard error of the estimate (SEE) = 1.32%, P less than 0.0001]. The accuracy of pulse oximeters has been questioned during high-intensity exercise. When aerobic power was greater than 81% of VO2max (n = 75), the finger probe's mean error was -0.01 +/- 1.40%. Finger probe %SpO2 and %HbO2 were highly correlated (r = 0.97, SEE = 1.32%, P less than 0.0001). These results indicate that this pulse oximeter is a valid predictor of %HbO2 in elite athletes during cycle exercise.
Journal of Applied Physiology 03/1992; 72(2):455-8. · 3.75 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: 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.
European Journal of Applied Physiology and Occupational Physiology 02/1992; 65(1):37-42.
-
[show abstract]
[hide abstract]
ABSTRACT: Examination of the alveolar-to-arterial O2 tension (A-a PO2 difference) provides a method of examining the efficiency of pulmonary gas exchange during exercise. At present, considerable confusion exists as to the exact pattern of the A-a PO2 difference during incremental exercise. We tested the hypothesis that the A-a PO2 difference during incremental exercise is alinear with respect to metabolic rate. Measurements of the A-a PO2 difference were made on six healthy male subjects during incremental exercise under sea level conditions (PIO2 = 149 torr). An alinear model best described the relationship between the A-a PO2 difference and metabolic rate; only small increases in the A-a PO2 difference occurred at low work rates followed by a rapid increase at higher work rates. The existence of a "A-a PO2 difference threshold" was mathematically confirmed by the use of a computer algorithm to define inflection points. These data provide evidence that the relationship between the A-a PO2 difference and metabolic rate is alinear and that a metabolic threshold exists for a rapid increase in the A-a PO2 difference. We conclude that the efficiency of pulmonary gas exchange during exercise is unaltered from rest during low-to-moderate power outputs, however, high intensity exercise compromises pulmonary gas exchange efficiency as evidenced by a significant widening of the A-a PO2 difference.
International Journal of Sports Medicine 07/1991; 12(3):313-8. · 2.43 Impact Factor
