Respiratory muscle blood flows during physiological and chemical hyperpnea in the rat.

Whether the diaphragm retains a vasodilator reserve at maximal exercise is controversial. To address this issue, we measured respiratory and hindlimb muscle blood flows and vascular conductances using radiolabeled microspheres in rats running at their maximal attainable treadmill speed (96 +/- 5 m/min; range 71-116 m/min) and at rest while breathing either room air or 10% O(2)-8% CO(2) (balance N(2)). All hindlimb and respiratory muscle blood flows measured increased during exercise (P < 0.001), whereas increases in blood flow while breathing 10% O(2)-8% CO(2) were restricted to the diaphragm only. During exercise, muscle blood flow increased up to 18-fold above rest values, with the greatest mass specific flows (in ml. min(-1). 100 g(-1)) found in the vastus intermedius (680 +/- 44), red vastus lateralis (536 +/- 18), red gastrocnemius (565 +/- 47), and red tibialis anterior (602 +/- 44). During exercise, blood flow was higher (P < 0.05) in the costal diaphragm (395 +/- 31 ml. min(-1). 100 g(-1)) than in the crural diaphragm (286 +/- 17 ml. min(-1). 100 g(-1)). During hypoxia+hypercapnia, blood flows in both the costal and crural diaphragms (550 +/- 70 and 423 +/- 53 ml. min(-1). 100 g(-1), respectively) were elevated (P < 0.05) above those found during maximal exercise. These data demonstrate that there is a substantial functional vasodilator reserve in the rat diaphragm at maximal exercise and that hypoxia + hypercapnia-induced hyperpnea is necessary to elevate diaphragm blood flow to a level commensurate with its high oxidative capacity.

Skeletal muscle microcirculatory structure and hemodynamics in diabetes.

Within skeletal muscle, insulin-dependent (Type 1) diabetes produces straighter, narrower capillaries. To test the hypothesis that these microvascular alterations would be associated with impaired capillary hemodynamics, intravital microscopy techniques were used to study the in vivo spinotrapezius muscle microcirculation of age-matched control (C) and streptozotocin (STZ) induced diabetic (D) rats. D rats exhibited a marked reduction in body weight (C, 266 +/- 5 g; D, 150 +/- 6 g; P < 0.001). At resting sarcomere lengths (i.e. approximately 2.7 microm), the additional capillary length arising from tortuosity and branching was less in D muscle (C, 10.5 +/- 0.8%; D, 5.3 +/- 1.0%, P < 0.01). Capillary diameter was reduced in D muscle (C, 5.4 +/- 0.1 microm; D, 4.6 +/- 0.1 microm; P < 0.001), and was positively correlated (r = 0.71) with the decreased proportion of capillaries sustaining flow (C, 85 +/- 5%; D, 53 +/- 3%; P < 0.001). Within those 'flowing' capillaries, red blood cell (RBC) velocity and flux were reduced 29 and 43%, respectively in D muscle (both P < 0.05). This reduced calculated O2 delivery by 57% per unit tissue width and 41% per unit muscle mass. Capillary 'tube' hematocrit was unchanged from control values (C, 0.22 +/- 0.02; D, 0.22 +/- 0.02). We conclude that, in the diabetic state, microvascular remodeling is associated with a reduced proportion of 'flowing' capillaries and a reduction in RBC velocity and flux in these vessels such that skeletal muscle O2 delivery is markedly reduced.

Effects of emphysema on diaphragm blood flow during exercise.

Chronic hyperinflation of the lung in emphysema displaces the diaphragm caudally, thereby placing it in a mechanically disadvantageous position and contributing to the increased work of breathing. We tested the hypothesis that total and regional diaphragm blood flows are increased in emphysema, presumably reflecting an increased diaphragm energetic demand. Male Syrian Golden hamsters were randomly divided into emphysema (E; intratracheal elastase 25 units/100 g body wt) and control (C; saline) groups, and experiments were performed 16-20 wk later. The regional distribution of blood flow within the diaphragm was determined by using radiolabeled microspheres in hamsters at rest and during treadmill exercise (walking at 20 feet/min, 20% grade). Consistent with pronounced emphysema, lung volume per unit body weight was greater in E hamsters (C, 59.3 +/- 1.8; E, 84.5 +/- 5.0 ml/kg; P < 0.001) and arterial PO2 was lower both at rest (C, 74 +/- 3; E, 59 +/- 2 Torr; P < 0.001) and during exercise (C, 93 +/- 3; E, 69 +/- 4 Torr; P < 0.001). At rest, total diaphragm blood flow was not different between C and E hamsters (C, 47 +/- 4; E, 38 +/- 4 ml . min-1 . 100 g-1; P = 0.18). In both C and E hamsters, blood flow at rest was lower in the ventral costal region of the diaphragm than in the dorsal and medial costal regions and the crural diaphragm. During exercise in both C and E hamsters, blood flows increased more in the dorsal and medial costal regions and in the crural diaphragm than in the ventral costal region. Total diaphragm blood flow was greater in E hamsters during exercise (C, 58 +/- 7; E, 90 +/- 14 ml . min-1 . 100 g-1; P = 0.03), as a consequence of significantly higher blood flows in the medial and ventral costal regions and crural diaphragm. In addition, exercise-induced increases in intercostal (P < 0.005) and abdominal (P < 0.05) muscle blood flows were greater in E hamsters. The finding that diaphragm blood flow was greater in E hamsters during exercise supports the contention that emphysema increases the energetic requirements of the diaphragm.

Diaphragm structure and function in health and disease.

The diaphragm is the primary muscle of inspiration, and as such uncompromised function is essential to support the ventilatory and gas exchange demands associated with physical activity. The normal healthy diaphragm may fatigue during intense exercise, and diaphragm function is compromised with aging and obesity. However, more insidiously, respiratory diseases such as emphysema mechanically disadvantage the diaphragm, sometimes leading to muscle failure and death. Based on metabolic considerations, recent evidence suggests that specific regions of the diaphragm may be or may become more susceptible to failure than others. This paper reviews the regional differences in mechanical and metabolic activity within the diaphragm and how such heterogeneities might influence diaphragm function in health and disease. Our objective is to address five principal areas: 1) Regional diaphragm structure and mechanics (GAF). 2) Regional differences in blood flow within the diaphragm (WLS). 3) Structural and functional interrelationships within the diaphragm microcirculation (DCP). 4) Nitric oxide and its vasoactive and contractile influences within the diaphragm (MBR). 5) Metabolic and contractile protein plasticity in the diaphragm (SKP). These topics have been incorporated into three discrete sections: Functional Anatomy and Morphology, Physiology, and Plasticity in Health and Disease. Where pertinent, limitations in our understanding of diaphragm function are addressed along with potential avenues for future research.

Immunity to hepatitis B, poliomyelitis and measles in fully vaccinated aboriginal and Torres Strait Island children.

OBJECTIVE: To determine the immunity to hepatitis B, poliomyelitis and measles in fully vaccinated Aboriginal and Torres Strait Island children in north Queensland. METHODOLOGY: A cross-sectional survey of immunity in a sample of children; 101 fully vaccinated Aboriginal and Torres Strait Island children, with a median age of 24.5 months, from 10 communities in North Queensland participated in this study. The main outcome measures were the prevalence of adequate antibody levels against hepatitis B, poliomyelitis and measles. RESULTS: Only 54% (95% CI 44-63%) of the children had adequate immunity (> or = 10 m iu/mL) to hepatitis B, and one child had been infected despite vaccination. Although all the children (95% CI 96-100%) had adequate immunity (i.e. neutralizing antibodies at a dilution of > or = 1:8) to poliovirus 2, only 93% (95% CI 86-96%) and 60% (95% CI 50-69%) had adequate immunity to polioviruses 1 and 3, respectively. Nearly all (96%; 95% CI 90-98%) of the children had adequate immunity (i.e. detectable IgG antibody) to measles. CONCLUSIONS: Although a relatively low proportion of the children had adequate antibody levels against hepatitis B the clinical significance of this observation is uncertain. Further studies are needed to determine whether fully vaccinated Torres Strait Island children have been adequately protected and whether they require a booster dose of hepatitis B vaccine. A substantial proportion of fully vaccinated Aboriginal and Torres Strait Island children are inadequately protected against poliomyelitis, and therefore any such child with acute flaccid paralysis should be investigated fully for poliomyelitis. Vaccinated Aboriginal and Torres Strait Island children are well protected against measles, as are other Australian children.

Costal diaphragm blood flow heterogeneity at rest and during exercise.

To gain insight into diaphragm functional heterogeneity, blood flow (expressed as ml.min-1 x 100 g-1) was measured using radiolabeled microspheres in the ventral, medial, and dorsal regions of the costal diaphragm and in the crural diaphragm of sedentary control (S) and exercise trained (ET) female Wistar-Kyoto rats at rest and during treadmill exercise. ET animals had performed moderate intensity exercise training on a motorized treadmill (22 m/min, 10% grade, 60 min/d) for 12 months, while S were cage-confined. The efficacy of exercise training was demonstrated by a 12% increase (P < 0.05) in ventricular weight-to-body weight ratio and increases (P < 0.05) in citrate synthase activity in hindlimb skeletal muscles of ET. At rest, blood flow in the ventral costal diaphragm (16 +/- 1) averaged approximately 61% of that in the medial (26 +/- 3) and dorsal (25 +/- 2) costal regions (P = 0.035), and crural diaphragm flow was 23 +/- 3. During treadmill exercise (5 min at 22 m/min, 10% incline), blood flow increased an average of 5-fold (P < 0.001) throughout the diaphragm, but the heterogeneous flow pattern persisted; i.e., blood flow remained lower (P = 0.003) in the ventral region (77 +/- 7) than either the medial (135 +/- 15) or dorsal (127 +/- 11) costal regions. Flow in the crural diaphragm during exercise was intermediate (105 +/- 9). Exercise training did not alter either the magnitude of blood flows or the flow distribution pattern within the diaphragm. Citrate synthase activity was two-fold that of the plantaris muscle and was uniform across the ventral, medial, and dorsal costal and the crural diaphragm of a second group of age-matched rats (P = 0.57). These data demonstrate that, although oxidative capacity is uniform throughout the diaphragm, there is a significant regional heterogeneity of blood flow within the rat diaphragm both at rest and during locomotory exercise. The greater flow in the medial and dorsal regions of the costal diaphragm suggests that these regions sustain a greater portion of the inspiratory work load at rest and during exercise compared to the ventral region.

Vascular adaptations in rat hindlimb skeletal muscle after voluntary running-wheel exercise.

To test the hypothesis that voluntary running-wheel exercise would elicit vascular adaptations in rat skeletal muscle, male Sprague-Dawley rats (202 +/- 5 g) were cage confined (C, n = 11) or housed in cages with free access to running wheels (R, n = 13) for 12 wk. Vascular transport capacity was determined in maximally vasodilated (papaverine) hindquarters of C and R rats with measurements of total and regional (radiolabeled microspheres) flow capacity and capillary filtration coefficient. R rats voluntarily ran 29 +/- 4 km/wk over the 12-wk period; however, performance of individual rats varied greatly (range 4-74 km/wk). Citrate synthase activity was increased in the medial head (81%, P < 0.001) and the red long head (88%, P < 0.001) of the triceps brachii muscle in R rats but not in the white long head (25%, P = 0.06). Capillary filtration coefficient was 27% greater in R compared with C rats (0.040 +/- 0.003 vs. 0.031 +/- 0.002 ml.min-1.100 g-1.mmHg-1, respectively, P < 0.001) suggesting that there was an increase in microvascular surface area available for fluid exchange. Total hindquarters flow was increased in R rats (P < 0.05) at all perfusion pressures examined, indicative of an increased flow capacity. Regional flows revealed that skin flow was unchanged in R rats and that the increase in total flow was due to increased skeletal muscle flow capacity. These results indicate that voluntary running-wheel exercise elicits adaptive increases in skeletal muscle vascular transport capacity and oxidative capacity comparable to those seen in treadmill-trained rats and support the use of voluntary running-wheel exercise as a less stressful training modality in exercise studies using rats.

Exercise training attenuates the reduction in myocardial GLUT-4 in diabetic rats.

The purpose of this study was to determine the interactive effects of 10-12 wk of streptozotocin-induced diabetes (65 mg/kg) and moderate-intensity exercise training on total myocardial GLUT-4 and GLUT-1 proteins. Sprague-Dawley rats (n = 52) were randomly divided into sedentary control (SC), exercise-trained control (ETC), sedentary diabetic (SD), and exercise-trained control (ETD) groups. Diabetes (SD), and exercise-trained diabetic (ETD) groups. Diabetes resulted in a 70% reduction in myocardial GLUT-4 (28.3+/- 3.1 and 94.6 +/- 3.4% for SD and SC, respectively; P < 0.0001) and an 18.5% decrease in GLUT-1 (62.5 +/- 4.7 and 76.8 +/- 4.5% for SD and SC, respectively; P = 0.06). Exercise training increased citrate synthase activity in the medial and long heads of the triceps brachii in both groups (P < 0.001). Fasting blood glucose improved with training in diabetic animals (348 +/- 27 and 569 +/- 28 mg/dl for ETD and SD, respectively; P < 0.05). The diabetes-induced reduction in GLUT-4 was attenuated with exercise training (46.8 +/- 9.3% for ETD; P < 0.02 compared with SD). In contrast, training resulted in a further 25% decrease compared with SD in GLUT-1 in ETD (46.8 +/- 9.3%; P < 0.03 compared with SD). Exercise training had no effect on either GLUT-4 (87.2 +/- 4.0%) or GLUT-1 (75.4 +/- 5.1%) in ETC. GLUT-4 inversely correlated (r = -0.81; P < or = 0.001) with fasting blood glucose. In conclusion, diabetes resulted in a 70% reduction in myocardial GLUT-4 and an 18% decrease in GLUT-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Microcirculatory structure-function relationships in skeletal muscle of diabetic rats.

The effects of streptozotocin-induced diabetes on microcirculatory structure-function relationships in skeletal muscle were studied in control (C) and diabetic (D; 65 mg/kg streptozotocin ip) rats 6-8 wk after injection. Capillary exchange capacity was determined from measurements of capillary filtration coefficient (CFC) and permeability-surface area product (PS) for 51Cr-labeled EDTA in maximally vasodilated (papaverine), isolated hindquarters of C (n = 9) and D (n = 12) rats. Capillary numerical density, length, surface area, capillary geometry, and muscle fiber cross-sectional area were determined using morphometric methods in perfusion-fixed plantaris muscles from a second series of C (n = 5) and D (n = 6) rats. Hindquarters of D rats (61 +/- 3 g) weighed less than C rats (90 +/- 3 g) because of marked muscle atrophy. Minimal total vascular resistance was lower in D rats (P < or = 0.05), indicating an increased flow capacity. CFC was not different in C and D rats (0.0282 +/- 0.0020 vs. 0.0330 +/- 0.0025 ml.min-1.mmHg-1 x 100 g-1, respectively). The relationship between PS and flow was depressed in D rats (P < or = 0.05) compared with C rats, which indicated a reduced capillary diffusing capacity. Plantaris muscle weight was 41% less in D rats (174 +/- 9 vs. 293 +/- 11 mg; P < or = 0.001). Morphometric analysis revealed that muscle fiber cross-sectional area was reduced 39% in D rats, which, despite a lower capillary-to-fiber ratio (1.59 +/- 0.04 vs. 2.12 +/- 0.13; P < or = 0.001), resulted in a 27% increase in capillary density in D rats. Capillary diameter was less in D rats (3.58 +/- 0.12 vs. 4.51 +/- 0.23 microns; P < or = 0.005). Total capillary surface area was reduced 42% in D rats; however, capillary surface area per muscle fiber volume was unchanged in D rats (231 +/- 34 vs. 237 +/- 16 cm-1). These data indicate that there is remodeling of the capillary bed in skeletal muscle of D rats, resulting in a reduction in total microvascular surface area. The reduction in capillary surface area is proportional to the degree of muscle atrophy in D rats such that functional microvascular surface area per tissue mass (e.g., CFC) is unchanged. The lower diffusing capacity (PS) in D rats suggests that either small solute permeability is reduced and/or there is greater perfusion heterogeneity in D rat skeletal muscle.

Influence of endurance exercise training on distribution of vascular adaptations in rat skeletal muscle.

We hypothesized that an exercise training program consisting of treadmill running at 32 m/min up a 15% incline, 90 min/day, 5 days/wk for 12-14 wk, would elicit vascular adaptation in skeletal muscle of all fiber types in rats. This hypothesis was based on previous reports that this intensity and duration of training caused increases in oxidative capacity in rat skeletal muscle of all fiber types. Skeletal muscle vascular transport capacity was examined with measurements of total and regional (radiolabeled microspheres) flow capacity, capillary filtration coefficient (CFC), and permeability-surface area product (PS) for 51Cr-EDTA in maximally vasodilated (papaverine) hindquarters of control (C; n = 25) and exercise-trained (ET; n = 26) rats. CFC was increased in ET (0.038 +/- 0.001 vs. 0.030 +/- 0.001 ml.min-1 x mmHg-1 x 100 g-1; P < or = 0.001). PS was greater in ET than C (7.80 +/- 0.33 vs. 6.39 +/- 0.37 ml.min-1 x 100 g-1; P < or = 0.01). Citrate synthase activity was increased in the soleus (25%; P < or = 0.05), the medial head (35%; P < or = 0.05), and the red portion of the long head (45%; P < or = 0.005) but not in the white portion of the long head of triceps brachii (P = 0.14) of ET rats. Pressure-flow relationships indicate that total flow was greater (P < or = 0.05) in ET hindquarters at all perfusion pressures. Regional flow data revealed that increases in flow capacity were not evident in muscles composed of all fiber types as predicted.(ABSTRACT TRUNCATED AT 250 WORDS)

Skeletal muscle vascular transport capacity in diabetic rats.

This study aimed to determine the effect of long-term (17-20 weeks) streptozocin (STZ)-induced diabetes on skeletal muscle vascular transport capacity. Vascular transport capacity was determined from measurements of pressure-flow relationships, capillary filtration coefficient, and permeability-surface area product (PS) for 51Cr-EDTA in isolated perfused hindquarters of control (n = 7) and diabetic (n = 6; 65 mg/kg STZ intraperitoneally) rats. Hindquarters were perfused with Tyrode's solution containing albumin (5 g/dl) and horse serum (10% vol/vol) and were maximally vasodilated with papaverine (30 mM). Hindquarters of diabetic rats weighed 42% less than control rats (86 +/- 3 vs. 147 +/- 4 g; P < or = 0.001) because of profound muscle atrophy. Total hindquarters flow (ml.min-1 x 100 g-1) was greater in diabetic rats (P < 0.001) at perfusion pressures between 23 and 75 mmHg, indicative of an increased flow capacity relative to control rats. However, absolute flows (ml/min) were not different between control and diabetic rats. Neither capillary filtration coefficient (control = 0.0243 +/- 0.0010 and diabetic = 0.0297 +/- 0.0024 ml.min-1 x mmHg-1 x 100 g-1) nor isogravimetric PS (control = 3.91 +/- 0.31 and diabetic = 4.39 +/- 0.46 ml.min-1 x 100 g-1) were different in control and diabetic rats. However, absolute values for capillary filtration coefficient (ml.min-1 x mmHg-1) and PS (ml/min) were less in diabetic rats. These results indicate that muscle atrophy in rats with STZ-induced diabetes is accompanied by a proportional reduction in absolute exchange capacity for water (capillary filtration coefficient) and small solutes PS, such that microvascular exchange capacity per tissue mass is maintained at control levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Dependencies of respiratory system resistance and elastance on amplitude and frequency in the normal range of breathing.

We calculated respiratory system resistance (Rrs) and elastance (Ers) from pressure and flow at the mouth in six seated subjects relaxed at FRC (cheeks tightly compressed) during sinusoidal volume forcing (250, 500, and 750 ml) at 0.2, 0.4, and 0.6 Hz. Dependencies of Rrs and Ers on frequency and tidal volume were generally the same in each subject; Rrs tended to decrease with frequency and tidal volume, whereas Ers tended to increase with frequency and decrease with tidal volume. Multiple linear regression of combined data indicated that the frequency and tidal volume effects on Rrs and Ers were significant (p less than 0.05), and that the effects on Rrs decreased at higher flows. Average Rrs was highest (4.43 cm H2O/L/s +/- 0.21 SE) at 0.2 Hz-250 ml, and lowest (3.07 cm H2O/L/s +/- 0.37) at 0.6 Hz-750 ml. Average Ers was highest (12.1 cm H2O/L +/- 1.1) at 0.6 Hz-250 ml, and lowest (7.1 cm H2O/L +/- 0.6) at 0.2 Hz-750 ml. We conclude that frequency and tidal volume dependencies in Rrs and Ers in the normal range of breathing should be considered when interpreting measurements of respiratory system impedance or developing models to describe the mechanical behavior of the respiratory system.

Vascular flow capacity of hindlimb skeletal muscles in spontaneously hypertensive rats.

Total and regional skeletal muscle flows (radiolabeled microspheres) were determined in isolated maximally vasodilated hindquarters of spontaneously hypertensive rats (SHR) and age-matched (11-12 mo) normotensive Wistar-Kyoto rats (WKY) to assess the vascular flow capacity of the skeletal muscle vascular beds. Vascular flow capacity was estimated by measuring total hindquarters and regional muscle blood flows (under conditions of maximal vasodilation with papaverine or papaverine plus isoproterenol) over a wide range of perfusion pressures in WKY and SHR. Capillary exchange capacity was estimated by determining the capillary filtration coefficient. Isogravimetric capillary pressures and segmental vascular resistances were determined in each hindquarter. Isogravimetric flows and capillary pressures were not different between WKY and SHR. However, total and precapillary vascular resistances were significantly elevated in SHR, and postcapillary resistances were not different compared with WKY. Maximal capillary filtration coefficient values for the SHR group averaged 20% lower than WKY values, suggesting that hypertension was associated with a reduction in the microvascular surface area available for fluid exchange and, therefore, the capillary exchange capacity. Over the perfusion pressures studied, total hindquarters flows averaged 60% lower in SHR than in WKY. Flows to individual skeletal muscles averaged 76% lower in SHR than in WKY regardless of the muscle fiber type. Thus, modifications exist in the hindlimb skeletal muscle vasculature of SHR that reduces the capillary exchange capacity and limit the capacity of deliver flow at a given perfusion pressure gradient.

Microvascular injury after ischemia and reperfusion in skeletal muscle of exercise-trained rats.

Ischemia and reperfusion in skeletal muscle is associated with increases in total vascular resistance (Rt) and the microvascular permeability to plasma proteins. To determine whether exercise training can attenuate ischemia and reperfusion-induced microvascular injury in skeletal muscle, intact (with skin) and skinned, maximally vasodilated (papaverine), isolated hindquarters of control (C) and exercise-trained (ET) rats were subjected to ischemia (intact 120 min; skinned 60 min) followed by 60 min of reperfusion. ET rats ran on a motorized treadmill at 32 m/min (8% grade), 2 h/day for 12 wk, whereas the C rats were cage confined. Before ischemia, ET hindquarters had higher isogravimetric flow, lower Rt, and similar solvent drag reflection coefficients (sigma f) compared with C. During reperfusion in intact hindquarters, flow was higher (P less than 0.05) and Rt tended to be lower (15 +/- 2 vs. 25 +/- 5 mmHg.ml-1.min.100 g; P less than 0.1) in ET compared with C; however, in skinned hindquarters flow and Rt (14 +/- 2 vs. 13 +/- 2 mmHg.ml-1.min.100 g) were not different between C and ET. During reperfusion, sigma f was reduced (P less than 0.05) in both intact (C 0.68 +/- 0.03; ET 0.68 +/- 0.02) and skinned (C 0.66 +/- 0.03; ET 0.68 +/- 0.03) hindquarters, indicative of an increased microvascular permeability to plasma proteins. These results indicate that exercise training did not attenuate the microvascular injury (increased Rt and decreased sigma f) associated with ischemia and reperfusion in rat skeletal muscle.

Skeletal muscle oxidative capacity, antioxidant enzymes, and exercise training.

The purposes of this study were to determine whether exercise training induces increases in skeletal muscle antioxidant enzymes and to further characterize the relationship between oxidative capacity and antioxidant enzyme levels in skeletal muscle. Male Sprague-Dawley rats were exercise trained (ET) on a treadmill 2 h/day at 32 m/min (8% incline) 5 days/wk or were cage confined (sedentary control, S) for 12 wk. In both S and ET rats, catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPX) activities were directly correlated with the percentages of oxidative fibers in the six skeletal muscle samples studied. Muscles of ET rats had increased oxidative capacity and increased GPX activity compared with the same muscles of S rats. However, SOD activities were not different between ET and S rats, but CAT activities were lower in skeletal muscles of ET rats than in S rats. Exposure to 60 min of ischemia and 60 min of reperfusion (I/R) resulted in decreased GPX and increased CAT activities but had little or no effect on SOD activities in muscles from both S and ET rats. The I/R-induced increase in CAT activity was greater in muscles of ET than in muscles of S rats. Xanthine oxidase (XO), xanthine dehydrogenase (XD), and XO + XD activities after I/R were not related to muscle oxidative capacity and were similar in muscles of ET and S rats. It is concluded that although antioxidant enzyme activities are related to skeletal muscle oxidative capacity, the effects of exercise training on antioxidant enzymes in skeletal muscle cannot be predicted by measured changes in oxidative capacity.

Effects of treadmill elevation on heart rate, blood lactate concentration and packed cell volume during graded submaximal exercise in ponies.

Six ponies performed a standardised exercise test on a motorised treadmill at each of three randomly assigned treadmill elevations (1, 4, or 7 degrees). The exercise test consisted of four, 4 min increments of increasing treadmill speed from 1.0 to 3.4 m/sec. Heart rate, blood lactate concentration, and packed cell volume (PCV) were determined, during the last min of each exercise level, and at 4 and 12 mins post exercise. Regardless of treadmill elevation, no differences were observed in pre-exercise heart rate (49 +/- 2) beats/min), lactate (1.2 +/- 0.1 mM), and PCV (0.32 +/- 0.01 litres. During exercise, heart rate and PCV were highly correlated to treadmill speed and elevation. Peak exercise heart rates (determined at 3.4 m/sec) were 159 +/- 10, 182 +/- 5, and 216 +/- 6 beats/min at 1, 4, and 7 degrees, respectively, while peak PCVs were 0.37 +/- 0.01, 0.40 +/- 0.01 and 0.42 +/- 0.02 lit/litre at 1, 4, and 7 degrees, respectively. Blood lactate did not change significantly from pre-exercise levels during the exercise test at a treadmill elevation equal to 1 degree, but increased markedly at 4 and 7 degrees. Peak lactates were 1.9 +/- 0.7, 5.3 +/- 1.0, and 18.1 +/- 1.5 mM at 1, 4, and 7 degrees, respectively. There was a highly significant correlation between heart rate and lactate at all treadmill speeds and elevations. Therefore, during graded, submaximal exercise increasing treadmill elevation up to 7 degrees results in increases in heart rate, blood lactate concentration and PCV comparable to those seen with increasing treadmill speed alone.

Ischemia-reperfusion injury in isolated rat hindquarters.

The purpose of this study was to determine the suitability of the maximally vasodilated (papaverine) isolated rat hindquarters preparation to study the effects of ischemia and reperfusion on the microvasculature of skeletal muscle. The osmotic reflection coefficient for plasma proteins (sigma) and total vascular resistance (RT, mmHg.ml-1.min.100 g-1) were determined before ischemic periods of 30, 60, 120, 180, and 240 min in intact (with skin) and 30, 60, and 120 min in skinned hindquarters and again after 60 min of reperfusion. In both intact and skinned hindquarters, reductions in sigma and increases in RT were observed during reperfusion and were correlated with the ischemic period duration. After 120 min of ischemia in intact and skinned hindquarters, sigma was reduced from preischemia values of 0.92 +/- 0.02 and 0.89 +/- 0.02 to 0.61 +/- 0.03 and 0.57 +/- 0.03, respectively, whereas RT was increased from preischemia levels of 8.9 +/- 0.3 and 8.1 +/- 0.1 to 28.4 +/- 2.9 and 74.2 +/- 16.8, respectively. The increases in RT were associated with proportional increases in skeletal muscle vascular resistance. Thus, in isolated rat hindquarters, increasing the duration of ischemia results in progressive increases in the permeability to plasma proteins (decreased sigma) and RT, which are associated primarily with skeletal muscle.

Regional muscle blood flow capacity and exercise hyperemia in high-intensity trained rats.

The purpose of this study was to determine the effects of high-intensity treadmill exercise training on 1) the regional distribution of muscle blood flow within and among muscles in rats during high-intensity treadmill exercise (phase I) and 2) on the total and regional hindlimb skeletal muscle blood flow capacities as measured in isolated perfused rat hindquarters during maximal papaverine vasodilation (phase II). Two groups of male Sprague-Dawley rats were trained 5 days/wk for 6 wk with a program consisting of 6 bouts/day of 2.5-min runs at 60 m/min up a 15% grade with 4.5-min rest periods between bouts. After training, blood flows were measured with the radiolabeled microsphere technique (phase I) in pair-weighted sedentary control and exercise-trained rats while they ran at 60 m/min (0% grade). In phase II of the study, regional vascular flow capacities were determined at three perfusion pressures (30, 40, and 50 mmHg) in isolated perfused hindquarters of control and trained rats maximally vasodilated with papaverine. The results indicate that this exercise training program produces increases in the vascular flow capacity of fast-twitch glycolytic muscle tissue of rats. However, these changes were not apparent in the magnitude or distribution of muscle blood flow in conscious rats running at 60 m/min, since blood flows within and among muscles during exercise were the same in trained and control rats.

High-intensity exercise training increases vascular transport capacity of rat hindquarters.

The purpose of this study was to determine whether high-intensity exercise training increases the vascular flow capacity and capillary exchange capacity in isolated rat hindquarters. One group of 20 male Sprague-Dawley rats underwent six bouts of alternating running (2.5 min) and recovery (4.5 min), 5 days/wk at 60 m/min on a 15% grade for 6-10 wk (high-intensity exercise training), while a second group of 20 rats was cage confined (sedentary controls). Experiments were conducted in isolated, maximally dilated (papaverine) hindquarters perfused with an artificial plasma consisting of a Tyrode's solution containing 5 g/100 ml albumin. Vascular flow capacity was evaluated by measuring perfusate flow rate at four different perfusion pressures. Capillary exchange capacity was evaluated by measuring the capillary filtration coefficient. The efficacy of training was demonstrated by significant increases in succinate dehydrogenase activity in the white vastus lateralis and vastus intermedius muscles. Total hindquarter flow capacity was elevated 50-100% in the trained rats. This increased flow capacity was associated with an increase in the capillary filtration coefficient in the maximally vasodilated hindquarters, thus suggesting that the capillary exchange capacity was increased with high-speed exercise training. These results suggest that the vascular transport capacity in rat hindquarter muscles is significantly increased by high-intensity exercise training.