Recruitment of lung diffusing capacity with exercise before and after pneumonectomy in dogs

Although the left lung constitutes 42% of the total by weight and volume in dogs, carbon monoxide diffusing capacity (DL) after left pneumonectomy in adults falls less than 30% at rest, indicating a significant increase of DL in the remaining lung. DL normally increases during exercise, presumably by recruitment of alveolar capillaries and surface area as lung volume (Vs) and pulmonary blood flow (Qc) increase. We asked whether the increase of DL in the remaining lung after pneumonectomy in adult dogs could be explained by this kind of passive recruitment by the increased volume and Qc in the remaining lung. We measured the relationship between DL and Qc with a rebreathing technique at increasing treadmill loads in adult foxhounds, before and 6 mo after left pneumonectomy, and the relationship between DL and Vs by the same technique under anesthesia as Vs was expanded. DL was reduced by 29.1% at rest and 26.5% with heavy exercise after left pneumonectomy, indicating either recruitment or new growth in the right lung. With the assumption that the right lung normally receives 58% of the Qc and contains 58% of the DL, DL of the right lung increased with Qc in accordance with the following relationships before and after left pneumonectomy: right lung DL (before pneumonectomy) = 6.44 + 2.40(Qc) (r = 0.963) and right lung DL (after pneumonectomy) = 7.51 + 1.75(Qc) (r = 0.958). Only approximately 7% of the increase in DL from rest to peak exercise could be attributed to the increase in Vs during exercise before pneumonectomy and approximately 15% after pneumonectomy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Attenuation of cardiovascular adaptations to exercise in frail octogenarians.

To determine the mechanisms underlying increased aerobic power in response to exercise training in octogenarians, we studied mildly frail elderly men and women randomly assigned to an exercise group (n = 22) who participated in a training program of 6 mo of physical therapy, strength training, and walking followed by 3 mo of more intense endurance exercise at 78% of peak heart rate or a control sedentary group (n = 24). Peak O2 consumption (V(O2 peak)) increased 14% in the exercise group (P < 0.0001) but decreased slightly in controls. Training induced 14% increase (P = 0.027) in peak exercise cardiac output (Q), determined via acetylene re-breathing, and no change in arteriovenous O2 content difference. The increase in Q was mediated by increases in heart rate (P = 0.009) and probably stroke volume (P = 0.096). Left ventricular stroke work also increased significantly. In the men, the increase in V(O2 peak) was exclusively due to a large increase in peak Q (22%). In the women, the gain in V(O2 peak) was due to small increases in Q and O2 extraction from skeletal muscles. Pulse pressure normalized for stroke volume and arterial elastance during peak effort did not change with training. Controls showed no changes. The results suggest that, although frail octogenarians have a diminished capacity for improvement in aerobic power in response to exercise training, this adaptation is mediated mostly by an increase in Q during peak effort. Furthermore, Q likely plays a greater role in the adaptive increase in V(O2 peak) in old men than old women.     

Hepatic adaptations to iron deficiency and exercise training.

Brooks et al. [Am. J. Physiol. 253 (Endocrinol. Metab. 16): E461-E466, 1987] demonstrated an elevated gluconeogenic rate in resting iron-deficient rats. Because physical exercise also imposes demand on this hepatic function, we hypothesized that exercise training superimposed on iron deficiency would augment the hepatic capacity for amino acid transamination/deamination and pyruvate carboxylation. Sprague-Dawley rats (n = 32) were obtained at weaning (21 days of age) and randomly assigned to iron-sufficient (dietary iron = 60 mg iron/kg diet) or iron-deficient (3 mg iron/kg) dietary groups. Dietary groups were subdivided into sedentary and trained subgroups. Treadmill training was 4 wk in duration, 6 days/wk, 1 h/day, 0% grade. Treadmill speed was initially 26.8 m/min and was decreased to 14.3 m/min over the 4-wk training period. The mild exercise-training regimen did not affect any measured variable in iron-sufficient rats. In contrast, in iron-deficient animals, training increased endurance capacity threefold and reduced blood lactate and the lactate-to-alanine ratio during submaximal exercise by 34 and 27%, respectively. The mitochondrial oxidative capacity of gastrocnemius muscle was increased 46% by training. However, the oxidative capacity of liver was not affected by either iron deficiency or training. Maximal rates of pyruvate carboxylation and glutamine metabolism by isolated liver mitochondria were also evaluated. Iron deficiency and training interacted to increase pyruvate carboxylation by intact mitochondria. Glutamine metabolism was increased roughly threefold by iron deficiency alone, and training amplified this effect to a ninefold increase over iron-sufficient animals.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiopulmonary responses to static exercise

Ventilatory and cardiovascular responses to isometric exercise, with special reference to hand-grip exercise, were reviewed. Blood flow through the forearm (FBF) during muscular contraction is dependent on relative strength to MVC (maximum voluntary contraction), duration of exercise, and hand temperature. FBF could attain steady state during exercise with intensities less than 15% MVC. Heart rate (HR) starts to increase with a latency as short as 0.4 to 0.6 sec in conscious animals and men in response to voluntary as well as electrically induced isometric exercise. This response is vagally transmitted. The sympathetic nerves mediated HR response with a longer delay is also found. Cardiac contractility is augmented via sympathetic beta-receptors during isometric exercise. With aging, HR response tends to be intensified, whereas, stroke volume response tends to be depressed. Thus increased cardiac output is resulted in elevated arterial blood pressure. Total vascular resistance is reported to be unaltered, or to increase, despite of consistent increase in muscle sympathetic activities during the isometric exercise. Ventilation is augmented during exercise, but the pattern of its response is not in full agreement among investigators. The underlying mechanisms to elicit those responses are discussed.     

Maximal lactate steady state in rats submitted to swimming exercise.

The higher concentration during exercise at which lactate entry in blood equals its removal is known as 'maximal lactate steady state' (MLSS) and is considered an important indicator of endurance exercise capacity. The aim of the present study was to determine MLSS in rats during swimming exercise. Adult male Wistar rats, which were adapted to water for 3 weeks, were used. After this, the animals were separated at random into groups and submitted once a week to swimming sessions of 20 min, supporting loads of 5, 6, 7, 8, 9 or 10% of body wt. for 6 consecutive weeks. Blood lactate was determined every 5 min to find the MLSS. Sedentary animals presented MLSS with overloads of 5 and 6% at 5.5 mmol/l blood lactate. There was a significant (P<0.05) increase in blood lactate with the other loads. In another set of experiments, rats of the same strain, sex and age were submitted daily to 60 min of swimming with an 8% body wt. overload, 5 days/week, for 9 weeks. The rats were then submitted to a swimming session of 20 min with an 8% body wt. overload and blood lactate was determined before the beginning of the session and after 10 and 20 min of exercise. Sedentary rats submitted to the same acute exercise protocol were used as a control. Physical training did not alter the MLSS value (P<0.05) but shifted it to a higher exercise intensity (8% body wt. overload). Taken together these results indicate that MLSS measured in rats in the conditions of the present study was reproducible and seemed to be independent of the physical condition of the animals.     

Muscular adaptations to resistance exercise in the elderly

Neuropathic, metabolic, hormonal, nutritional and immunological factors contribute to the development of sarcopenia. This loss of muscle mass associated with ageing, is a main cause of muscle weakness, but the loss of muscle strength typically exceeds that of muscle size, with a resulting decrease in force per unit of muscle cross-sectional area. Recent evidence suggests that, in addition to a reduction in neural drive and in fibre specific tension, changes in muscle architecture contribute significantly to the loss of muscle force through alterations in muscle mechanical properties. Older muscle, however, maintains a high degree of plasticity in response to increased loading since considerable hypertrophy and a reversal of the alterations in muscle architecture associated with ageing are observed with resistive training.     

Cardiopulmonary responses to exercise in obese girls and young women.

A study of exercise performance was carried out in 17 obese girls and young adults. During submaximal steady-state bicycle exercise oxygen intake (Vo2) for a given work output (W) was raised in obese subjects but minute ventilation at a fixed carbon dioxide output, gas exchange, blood gases, and cardiac output at a given VO2 were similar to the values previously found for normals. In obese subjects high levels of VO2 for fixed W were also obtained on the treadmill but when these were standardized for body weight (unlike the bicycle test) it was shown that the obese girls and women exercised within the normal (expected) range of aerobic energy expenditure. During maximal performance the absolute VO2 max was the same in obese and nonobese subjects but for a given body weight, lean body mass, and leg muscle (plus) bone volume, VO2max was reduced by 23.8, 16.3, and 24.5% respectively, in the former group. It was concluded that obesity though having minimal affect on responses to submaximal exercise is nevertheless associated with a marked reduction in physiological performance at or near maximal effort.     

Cardiovascular adaptations to exercise training in the elderly

Maximal O2 uptake (VO2max) and left ventricular function decrease with age. Endurance exercise training of sufficient intensity, frequency, and duration increases VO2max in the elderly. The mechanisms underlying the increased VO2max in the elderly are enhanced O2 extraction of trained muscle during maximal exercise leading to a wider arteriovenous O2 difference, and higher cardiac output in the trained state. However, increased cardiac output during true maximal exercise has not been documented in elderly subjects. Endurance exercise training results in a lower heart rate and rate pressure product during submaximal exercise at a given intensity. However, no improvement in left ventricular function has been reported in the elderly after exercise training. Highly trained master athletes exhibit proportional increases in the left ventricular end-diastolic dimension and wall thickness suggestive of volume-overload hypertrophy compared with age-matched sedentary controls. The magnitude of left ventricular enlargement is similar to that in young athletes. The failure of exercise training to alter the age-related deterioration of left ventricular function in the elderly may reflect an insufficient training stimulus rather than the inability of the heart to adapt to training in elderly subjects.     

Respiratory muscle blood flow in exercising dogs after pneumonectomy.

In three foxhounds after left pneumonectomy, the relationships of ventilatory work and respiratory muscle (RM) blood flow to ventilation (VE) during steady-state exercise were examined. VE was measured using a specially constructed respiratory mask and a pneumotach; work of breathing was measured by the esophageal balloon technique. Blood flow to RM was measured by the radionuclide-labeled microsphere technique. Lung compliance after pneumonectomy was 55% of that before pneumonectomy; compliance of the thorax was unchanged. O2 uptake (VO2) of RM comprised only 5% of total body VO2 at exercise. At rest, inspiratory muscles received 62% and expiratory muscles 38% of the total O2 delivered to the RM (QO2RM). During exercise, inspiratory muscles received 59% and expiratory muscles 41% of total QO2RM. Blood flow per gram of muscle to the costal diaphragm was significantly higher than that to the crural diaphragm. The diaphragm, parasternals, and posterior cricoarytenoids were the most important inspiratory muscles, and internal intercostals and external obliques were the most important expiratory muscles for exercise. Up to a VE of 120 l/min through one lung, QO2RM constituted only a small fraction of total body VO2 during exercise and maximal vasodilation in the diaphragm was never approached.     

Absence of left ventricular and arterial adaptations to exercise in octogenarians.

Recent evidence suggests that octogenarians exhibit attenuated adaptations to training with a small increase in peak O2 consumption (VO2) that is mediated by a modest improvement in cardiac output without an increase in arteriovenous O2 content difference. This study was designed to determine whether diminished increases in peak VO2 and cardiac output in the octogenarians are associated with absence of left ventricular and arterial adaptations to exercise training. We studied 22 octogenarians (81.9 +/- 3.7 yr, mean +/- SD) randomly assigned a group that exercised at an intensity of 82.5 +/- 5% of peak heart rate for 9 mo and 14 (age 83.1 +/- 4.1) assigned to a control group. Peak VO2 increased 12% in the exercise group but decreased slightly (-7%) in the controls. The exercise group demonstrated significant but small decreases in the heart rate (6%, P = 0.002) and the rate-pressure product (9%, P = 0.004) during submaximal exercise at an absolute work rate. Training induced no significant changes in the left ventricular size, geometry (wall thickness-to-radius ratio), mass, and function assessed with two-dimensional echocardiography or in arterial stiffness evaluated with applanation tonometry. Data suggest that the absence of cardiac and arterial adaptations may in part account for the limited gain in aerobic capacity in response to training in the octogenarians.     

Maximal aerobic performance of deer mice in combined cold and exercise challenges

In nature, animals frequently need to deal with several physiological challenges simultaneously. We examined thermoregulatory performance (body temperature stability) and maximal oxygen consumption of deer mice (Peromyscus maniculatus) during intense exercise at room temperature, acute cold exposure, and exercise during cold exposure. Results with exercise and cold exposure alone were consistent with previous studies: there was little difference between maximal metabolism elicited by exercise alone or cold exposure alone in warm-acclimated mice; after cold acclimation (9 weeks at 5 °C), maximal exercise metabolism did not change but maximum thermogenic capacity increased by >60%. Warm acclimated animals did not increase maximal oxygen consumption when exercise was combined with moderate cold (0 °C) and had decreased maximal oxygen consumption when exercise was combined with severe cold (–16 °C). Combined cold and exercise also decreased thermoregulatory performance and exercise endurance time. Cold acclimation improved thermoregulatory performance in combined cold and exercise, and there was also a slight increase in endurance. However, as for warm-acclimated animals, maximal exercise metabolism did not increase at low temperatures. We interpret these results as an indication of competition between thermoregulatory and locomotor effectors (brown adipose tissue and skeletal muscle) under the combined challenges of cold exposure and maximal exercise, with priority given to the locomotor function.Abbreviations BAT brown adipose tissue - T _b body temperature - O ₂ rate of oxygen consumption - O ₂ max maximal O₂ in exercise - O ₂ sum maximal O₂ during cold exposure Communicated by G. Heldmaier     

Neuroplastic adaptations to exercise: neuronal remodeling in cardiorespiratory and locomotor areas.

Neuronal activity has been shown to be attenuated in cardiorespiratory and locomotor centers of the brain in response to a single bout of exercise in trained (TR) vs. untrained (UN) animals, but the mechanisms remain obscure. Based on this finding, dendritic branching patterns of seven brain areas associated with cardiorespiratory and locomotor activity were examined in TR and UN animals. Twenty-eight male Sprague-Dawley rats were kept in individual cages and divided into TR and UN. TR were provided with a running wheel and exercised spontaneously. After 85 or 120 days, exercise training indexes were obtained, including maximal oxygen consumption, percent body fat, resting heart rate, and heart weight-to-body weight ratios. The brain was removed and processed according to a modified Golgi-Cox procedure. Impregnated neurons from seven brain areas were examined in coronal sections: the periaqueductal gray, posterior hypothalamic area, nucleus of the tractus solitarius, rostral ventrolateral medulla, cuneiform nucleus, nucleus cuneatus, and cerebral cortex. Neurons were traced using a camera lucida technique and analyzed using the Sholl analysis of dendritic branching. t-tests were conducted to compare the mean number of intersections per neuron by grouping inner rings and outer rings and also comparing the total number of intersections per animal. There were significant differences between groups in the posterior hypothalamic area, periaqueductal gray, cuneiform nucleus, and nucleus of the tractus solitarius in the inner rings, outer rings, and the total number of intersections per animal. Our results show that dendritic fields of neurons in important cardiorespiratory and locomotor centers of the brain are attenuated in TR animals.     

Postural specificity of cardiovascular adaptations to exercise training

The purposes of this study were to determine 1) whether posture affects the magnitude of cardiovascular adaptations to training and 2) whether cardiovascular adaptations resulting from exercise training in the supine posture transfer (generalize) to exercise in the upright posture and vice versa. Sixteen sedentary men, aged 18-33 yr, were trained using high-intensity interval and prolonged continuous cycling in the supine (STG; supine training group) or upright (UTG; upright training group) posture 4 days/wk, 40 min/day, for 8 wk, while seven male subjects served as nontraining controls. After training, maximal O2 uptake measured during supine and upright cycling, respectively, increased significantly (P less than 0.05) by 22.9 and 16.1% in the STG and by 6.0 and 14.6% in the UTG. No significant cardiovascular adaptations were observed at rest. During submaximal supine cycling at 100 W, significant increases in end-diastolic volume (21%) and stroke volume (22%) (radionuclide ventriculography and CO2 rebreathing) and decreases in heart rate, blood pressure, and systemic vascular resistance occurred in the STG, whereas only a significant decrease in blood pressure occurred in the UTG. During upright cycling at 100 W, a significant decrease in blood pressure occurred in the STG, whereas significant increases in end-diastolic volume (17%) and stroke volume (18%) and decreases in blood pressure and systemic vascular resistance occurred in the UTG. Volume of myocardial contractility, ejection fraction, and systolic blood pressure-to-end-systolic volume ratio did not change significantly after training when measured during supine and upright cycling in either training group. Blood volume increased significantly in the UTG but remained unchanged in the STG.(ABSTRACT TRUNCATED AT 250 WORDS)