O2 Difference Research Articles

Human Muscle Power Generating Capability During Cycling at Different Pedalling Rates

The effect of different pedalling rates (40, 60, 80, 100 and 120 rev min-1) on power generating capability, oxygen uptake (O2) and blood lactate concentration [La]b during incremental tests was studied in seven subjects. No significant differences in O2,max were found (mean +/- S.D., 5.31 +/- 0.13 l min-1). The final external power output delivered to the ergometer during incremental tests (PI,max) was not significantly different when cycling at 60, 80 or 100 rev min-1 (366 +/- 5 W). A significant decrease in PI,max of 60 W was observed at 40 and 120 rev min-1 compared with 60 and 100 rev min-1, respectively (P < 0.01). At 120 rev min-1 there was also a pronounced upward shift of the O2-power output (O2-P) relationship. At 50 W O2 between 80 and 100 rev min-1 amounted to +0.43 l min-1 but to +0.87 l min-1 between 100 and 120 rev min-1. The power output corresponding to 2 and 4 mmol l-1 blood lactate concentration (P[La]2 and P[La]4 ) was also significantly lower (> 50 W) at 120 rev min-1 (P < 0.01) while pedalling at 40, 60, 80 and 100 rev min-1 showed no significant difference. The maximal peak power output (PM, max) during 10 s sprints increased with pedalling rate up to 100 rev min-1. Our study indicates that with increasing pedalling rate the reserves in power generating capability increase, as illustrated by the PI,max/PM,max ratio (54.8, 44.8, 38.1, 34.6, 29.2%), the P[La]4/PM,max ratio (50.4, 38.9, 31.0, 27.7, 22.9%) and the P[La]2/PM,max ratio (42.8, 33.5, 25.6, 23.1, 15.6%) increases. Taking into consideration the O2,max, the PI,max and the reserve in power generating capability we concluded that choosing a high pedalling rate when performing high intensity cycling exercise may be beneficial since it provides greater reserve in power generating capability and this may be advantageous to the muscle in terms of resisting fatigue. However, beyond 100 rev min-1 there is a decrease in external power that can be delivered for an given O2 with an associated earlier onset of metabolic acidosis and clearly this will be disadvantageous for sustained high intensity exercise.

Limiting factors for maximum oxygen uptake and determinants of endurance performance.

In the exercising human, maximal oxygen uptake (VO2max) is limited by the ability of the cardiorespiratory system to deliver oxygen to the exercising muscles. This is shown by three major lines of evidence: 1) when oxygen delivery is altered (by blood doping, hypoxia, or beta-blockade), VO2max changes accordingly; 2) the increase in VO2max with training results primarily from an increase in maximal cardiac output (not an increase in the a-v O2 difference); and 3) when a small muscle mass is overperfused during exercise, it has an extremely high capacity for consuming oxygen. Thus, O2 delivery, not skeletal muscle O2 extraction, is viewed as the primary limiting factor for VO2max in exercising humans. Metabolic adaptations in skeletal muscle are, however, critical for improving submaximal endurance performance. Endurance training causes an increase in mitochondrial enzyme activities, which improves performance by enhancing fat oxidation and decreasing lactic acid accumulation at a given VO2. VO2max is an important variable that sets the upper limit for endurance performance (an athlete cannot operate above 100% VO2max, for extended periods). Running economy and fractional utilization of VO2max also affect endurance performance. The speed at lactate threshold (LT) integrates all three of these variables and is the best physiological predictor of distance running performance.

Effect of nitric oxide upon gas transfer and structural integrity of a polypropylene membrane oxygenator.

Gaseous nitric oxide (NO) may act as a membrane passivator during cardiopulmonary bypass by inhibition of platelet and leukocyte adhesion, activation, and aggregation. However, NO and its by-product nitrogen dioxide (NO2) are potently reactive and may be capable of degradation of membrane oxygenator constituents in an oxygen-rich environment. To test these concepts, nine polypropylene hollow fiber membrane oxygenators received 224 +/- 10 ppm NO and 6.7 +/- 1.7 ppm NO2 in 73% oxygen (O2), and six oxygenators received 73% O2, while being perfused with heparinized thrombocytopenic bovine blood for 6 hours. Oxygenators were used for measurement of O2 and carbon dioxide (CO2) transfer rates, structural integrity by pulsing with 22 psi water at 0.5 Hz for 6 hours, and scanning electron microscopic (SEM) examination of structural integrity. Transfer rates between groups at 0, 1, 3, and 6 hours revealed no differences in O2 or CO2. No oxygenator failed hydraulic tests of structural integrity or exhibited "wet-out" during bypass. No evidence of material degradation was shown in the SEM appearance of oxygenators. There were no differences in hematologic values. These data support the safety of gaseous NO in polypropylene membrane oxygenators for limited-term cardiopulmonary bypass.

Exercise and Physical Activity for Older Adults

SUMMARYBy the year 2030, the number of individuals 65 yr and over will reach 70 million in the United States alone; persons 85 yr and older will be the fastest growing segment of the population. As more individuals live longer, it is imperative to determine the extent and mechanisms by which exercise and physical activity can improve health, functional capacity, quality of life, and independence in this population. Aging is a complex process involving many variables (eg, genetics, lifestyle factors, chronic diseases) that interact with one another, greatly influencing the manner in which we age. Participation in regular physical activity (both aerobic and strength exercises) elicits a number of favorable responses that contribute to healthy aging. Much has been learned recently regarding the adaptability of various biological systems, as well as the ways that regular exercise can influence them.Participation in a regular exercise program is an effective intervention/modality to reduce/prevent a number of functional declines associated with aging. Further, the trainability of older individuals (including octo-and nonagenarians) is evidenced by their ability to adapt and respond to both endurance and strength training. Endurance training can help maintain and improve various aspects of cardiovascular function (as measured by maximal Vo2, cardiac output, and arteriovenous O2 difference), as well as enhance submaximal performance. Importantly, reductions in risk factors associated with disease states (heart disease, diabetes, etc) improve health status and contribute to an increase in life expectancy. Strength training helps offset the loss in muscle mass and strength typically associated with normal aging. Additional benefits from regular exercise include improved bone health and, thus, reduction in risk for osteoporosis; improved postural stability, thereby reducing the risk of falling and associated injuries and fractures; and increased flexibility and range of motion. While not as abundant, the evidence also suggests that involvement in regular exercise can also provide a number of psychological benefits related to preserved cognitive function, alleviation of depression symptoms and behavior, and an improved concept of personal control and self-efficacy.It is important to note that while participation in physical activity may not always elicit increases in the traditional markers of physiological performance and fitness (eg, Vo2max, mitochondrial oxidative capacity, body composition) in older adults, it does improve health (reduction in disease risk factors) and functional capacity. Thus, the benefits associated with regular exercise and physical activity contribute to a more healthy, independent lifestyle, greatly improving the functional capacity and quality of life in this population.

Effects of temperature and physical activity on blood flow shunts and intracardiac mixing in the toad Bufo marinus.

Blood flow in systemic (.Qsys) and pulmocutaneous (.Qpul) arteries was measured as a function of body temperature (10 degrees, 20 degrees, and 30 degrees C) at rest and following enforced physical activity in conscious, adult cane toads (Bufo marinus). Arterial and mixed venous hemoglobin concentration (CHb) and total oxygen content (Co2, tot) were measured in a separate group under identical conditions. Heart rate (fH) and total flow (.Qtot) increased significantly (P<0.001) with elevated temperature and with activity, whereas stroke volume (VS) increased (P<0.001) only with activity. .Qtot ranged about 10-fold, from 10 degrees C (rest) to 30 degrees C (activity); increases in both fH and VS contributed to the increase in .Qtot. The overall distribution of blood to the pulmocutaneous circuit (net L-R shunt) increased with both temperature and activity and was significantly correlated with .Qtot. These data indicate that blood flow distribution in toads is a direct function of cardiac output, and this is linked to relative changes in resistance in the major outflow vessels. Arterial O2 saturation (Sa) was high (mean=93%) in all conditions except activity at 30 degrees C, when it decreased to 74% and contributed to a decrease in the arteriovenous O2 difference. Venous O2 saturation (Sv) was high at rest (76%) and dropped significantly during activity to about 30% at all temperatures. Intracardiac arterial-venous mixing (systemic mixing index) showed the strongest correlation with variation in fH with minimal mixing (17%) occurring at about 50 beats min-1. The most mixing occurred at the lowest fH (13 beats min-1) and at the highest fH (103 beats min-1). The results indicate that the heart of a 0.25-kg toad becomes more efficient from an oxygen transport perspective from low fH to 50 beats min-1 and then less efficient at higher fH, contributing to an uncoupling of blood flow and metabolic rates at these high rates.

MECHANICAL CONSTRAINT OF EXERCISE HYPERVENTILATION AND ITS CONSEQUENCES

327 During heavy exercise in healthy untrained subjects hyperventilation occurs. This response: a) compensates for a widened alveolar to arterial O2 difference (A-aDO2) and arterial PO2 is maintained near resting levels; and b) partially compensates a developing lactacidosis. In many highly trained male and female subjects during heavy exercise: a) alveolar hyperventilation is minimal at a fixed heavy workload; and b) PaCO2 does not fall over time at a fixed heavy workload despite increasing lactacidosis and hypoxemia. We investigated two potential mechanical causes of this ventilatory constraint. 1. Inspiratory muscle unloading. We used a proportional assist ventilator to reduce the inspiratory pressure required at max exercise. This had no effect on V̇E. 2. Expiratory flow limitation. We used HE:O2 breathing to increase the area of the max flow:volume envelope and to eliminate flow limitation during exercise. End expiratory lung volume was reduced and VT and V̇E increased and PaCO2 decreased during max exercise. The ventilatory response to added chemical stimuli was also enhanced. The increased hyperventilatory response relieved much-but not all-of the exercise induced arterial hypoxemia experienced during air breathing. We conclude that expiratory flow limitation-or even impending flow limitation-acting via reflex feedback inhibition from narrowed airways will limit the hyperventilation of heavy exercise and contribute to exercise induced arterial hypoxemia. NHLBI

Respiration of Aquatic and Terrestrial Amphibian Embryos

Respiratory constraints on the structure of single eggs and egg masses have affected the mode of amphibian reproduction in water and in air. Aquatic eggs generally require less oxygen, develop faster, and hatch earlier, but these characteristics are related to small ovum size. A comparison of two species of aquatic and terrestrial breeding frogs with similarly sized ova shows no differences in hatching stage, maximum rate of oxygen uptake, oxygen conductance of the egg capsule, or P o2 difference across the capsule. However, the aquatic species develops about 2.4 times faster and tolerates lower environmental P o2, suggesting adaptation for development in ephemeral water. Modelling of diffusive oxygen transport into a single aquatic egg shows that a large amount of jelly (or a boundary layer) around the capsule may not greatly restrict gas exchange, if the inner radius of the capsule is large. However, gelatinous egg masses that contain other embryos that compete for oxygen are therefore limited in size, unless the eggs are ventilated by convection of water among them. Aquatic egg are often suspended in masses above the substrate, promoting oxygen movement into the mass from all directions. Terrestrial egg masses are more diffusion limited, because gravity and surface tension collapse them, preventing convection between the eggs, and restricting the source for oxygen diffusion. Terrestrial embryos are often larger than their aquatic counterparts and have higher demands for oxygen. Terrestrial conditions have selected for adaptations that reduce respiratory competition between embryos, for example, separating of embryos by large volumes of jelly or reducing the number of eggs in a clutch. The size of foam nests is unlimited, because oxygen for each embryo is supplied directly from the foam.

Cerebral oxygen/glucose ratio is low during sensory stimulation and rises above normal during recovery: excess glucose consumption during stimulation is not accounted for by lactate efflux from or accumulation in brain tissue.

Functional activation stimulates CMRglc more than CMRO2 and raises lactate levels in brain. This has been interpreted as evidence that brain work is supported mainly by energy derived from anaerobic glycolysis. To determine if lactate production accounts for the "excess" glucose consumption, cerebral arteriovenous differences were measured in conscious rats before, during, and 15 minutes after sensory stimulation; the brains were rapidly frozen in situ immediately after completion of blood sampling and assayed for metabolite levels. The molar O2/glucose uptake ratio fell from 6.1+/-1.1 (mean+/-SD) before stimulation to 5.0+/-1.1 during activation (P<0.01); lactate efflux from brain to blood was detectable at rest but not during stimulation. By 15 minutes after activation, O2 and lactate arteriovenous differences normalized, whereas that for glucose fell, causing the O2/glucose ratio to rise above preactivation levels to 7.7+/-2.6 (P<0.01). Brain glucose levels remained stable through all stages of activity. Brain lactate levels nearly doubled during stimulation but normalized within 15 minutes of recovery. Brain glycogen content fell during activation and declined further during recovery. These results indicate that brain glucose metabolism is not in a steady state during and shortly after activation. Furthermore, efflux from and increased content of lactate in the brain tissue accounted for less than 54% of the "excess" glucose used during stimulation, indicating that a shift to anaerobic glycolysis does not fully explain the disproportionately greater increases in CMRglc above that of CMRO2 in functionally activated brain. These results also suggest that the apparent dissociation between glucose utilization and O2 consumption during functional activation reflects only a temporal displacement; during activation, glycolysis increases more than oxidative metabolism, leading to accumulation of products in intermediary metabolic pools that are subsequently consumed and oxidized during recovery.

Nitric oxide participates in early events associated with NNMU-induced acute lung injury in rats.

In this study, the biochemical mechanisms by which N-nitroso-N-methylurethane (NNMU) induces acute lung injury are examined. Polymorphonuclear neutrophil infiltration into the lungs first appears in the bronchoalveolar lavage (BAL) fluid 24 h after NNMU injection (10.58 +/- 3.00% of total cells; P < 0.05 vs. control animals). However, NNMU-induced elevation of the alveolar-arterial O2 difference requires 72 h to develop. Daily intraperitoneal injections of the inducible nitric oxide (. NO) synthase (iNOS)-selective inhibitor aminoguanidine (AG) initiated 24 h after NNMU administration improve the survival of NNMU-treated animals. However, AG administration initiated 48 or 72 h after NNMU injection does not significantly improve the survival of NNMU-treated animals. These results suggest that. NO participates in events that occur early in NNMU-induced acute lung injury. BAL cells isolated from rats 24 and 48 h after NNMU injection produce elevated. NO and express iNOS during a 24-h ex vivo culture. AG attenuates. NO production but does not affect iNOS expression, whereas actinomycin D prevents iNOS expression and attenuates. NO production by BAL cells during this ex vivo culture. These results suggest that NNMU-derived BAL cells can stimulate iNOS expression and. NO production during culture. In 48-h NNMU-exposed rats, iNOS expression is elevated in homogenates of whole lavaged lungs but not in BAL cells derived from the same lung. These findings suggest that the pathogenic mechanism by which NNMU induces acute lung injury involves BAL cell stimulation of iNOS expression and. NO production in lung tissue.

Hemodynamic characteristics during treadmill and bicycle exercise in chronic heart failure: mechanism for different responses of peak oxygen uptake.

The exercise capacity of patients with chronic heart failure (CHF) is greater when assessed by the treadmill rather than the bicycle ergometer, but the mechanism of this difference has not been clarified. The present study aimed to determine the difference between the hemodynamics of these exercise modes and the mechanism underlying the different peak oxygen uptake (VO2). Patients (n = 18) underwent a bicycle test and treadmill test using individual ramp protocols. Respiratory gas analysis and hemodynamic measurements with an opti-catheter were performed during both exercise tests. The peak VO2 was significantly larger in the treadmill test than the bicycle test (1410+/-292 vs. 1630+/-331 ml/min, p<0.001). Both the peak cardiac output (Q; 10.2+/-2.2 vs. 10.9+/-2.1 L/min, p<0.001) and the peak arteriovenous oxygen difference (a-v 02 diff; 13.9+/-1.5 vs. 15.0+/-1.2 vol%, p<0.001) were also significantly higher in the treadmill test. The relative contribution of Q and a-v O2 diff to the increased peak VO2 was equivalent, which suggests that both Q and a-v O2 diff. Contribute equally to the different peak VO2 responses in CHF.

Pulmonary gas exchange during exercise in pigs

Increased ventilation-perfusion (VA/Q) inequality is observed in approximately 50% of humans during heavy exercise and contributes to the widening of the alveolar-arterial O2 difference (A-aDO2). Despite extensive investigation, the cause remains unknown. As a first step to more direct examination of this problem, we developed an animal model. Eight Yucatan miniswine were studied at rest and during treadmill exercise at approximately 30, 50, and 85% of maximal O2 consumption (VO2 max). Multiple inert-gas, blood-gas, and metabolic data were obtained. The A-aDO2 increased from 0 +/- 3 (SE) Torr at rest to 14 +/- 2 Torr during the heaviest exercise level, but arterial PO2 (PaO2) remained at resting levels during exercise. There was normal VA/Q inequality [log SD of the perfusion distribution (log) = 0.42 +/- 0.04] at rest, and moderate increases (log = 0.68 +/- 0.04, P < 0.0001) were observed with exercise. This result was reproducible on a separate day. The VA/Q inequality changes are similar to those reported in highly trained humans. However, in swine, unlike in humans, there was no inert gas evidence for pulmonary end-capillary diffusion limitation during heavy exercise; there was no systematic difference in the measured PaO2 and the PaO2 as predicted from the inert gases. These data suggest that the pig animal model is well suited for studying the mechanism of exercise-induced VA/Q inequality.

Time course of superoxide generation in reperfusion after arterial ischaemia and venous congestion

In order to identify differences in superoxide (O2-) production after reperfusion following arterial ischaemia and venous congestion, we directly quantified O2- in the venous effluent from reperfused hindlimbs in the rabbit. Using a total of 20 rabbit hindlimbs, we made hindlimb-reperfusion models by section of both soft tissue and bony structures exclusive of femoral vessels around the thighs and clamping of the artery alone (group A: n = 10) or vein alone (group V: n = 10) by microvascular clamp. A pilot study revealed that the critical time for venous congestion was 2 h. Accordingly, clamping was performed at 25 degrees C (normothermia) for 2 h. Sham operations were performed in the control (n = 7). Venous effluent blood samples from the femoral vein proximal to the clamping point were collected before reperfusion, and from 5 to 60 min after reperfusion at 5 min intervals. Effluent blood samples were used to quantify O2- using a chemiluminescence method using a derivative of luciferin. The time course of O2- production after reperfusion in group A and group V showed significant differences (P < 0.05), compared with the controls. There was no significant difference in the time course of O2- production in group A and that in group V. In the early reperfusion phase, no difference in O2- production was observed after arterial ischaemia or venous congestion. In future studies, we will test the contributions of free radicals by setting longer ischaemic times, longer reperfusion times, and studying secondary ischaemia.

Factors Affecting the Respiratory Ratio during Cardiopulmonary By-Pass

Despite the wide use of hypothermic cardiopulmonary bypass (CPB) during open heart surgery there is little information about the patient metabolism. In particular no complete studies addressed the assessment of the respiratory ratio (RR) during CPB at different core temperatures. Therefore a clinical study was performed in order to evaluate the oxygen consumption (VO2) and carbon dioxide production (VCO2) in adult patients with valvular or coronary heart disease undergoing CPB. Twenty-five patients (16 male, 9 female) aged between 26 and 76 (54.2+/-12.4 mean +/- SD) were the subjects of this study. Measurements (102) were taken at various perfusion flow rates (from 1.6 to 2.9 L/min(-1) x m(-2)) and temperatures (from 24 to 37 degrees C). Arterial and mixed venous gas analyses were performed and O2 and CO2 concentrations were calculated, including the carbamate contribute. We calculated VO2, VCO2 and then RR from artero-venous differences in O2 and CO2 contents. Both VO2 and VCO2 showed a positive linear correlation with temperature (r = 0.82 and r = 0.59 respectively) and with blood flow rate (r = 0.61 and r = 0.29 respectively). The mean RR was 0.78+/-0.28 and more than 84% of RR values fell in the range 0.5-1.2. No significant correlation between RR and temperature and blood flow rate was observed. VCO2 and RR showed a positive linear correlation with the gas to blood flow rate ratio (r = 0.37 and r = 0.49 respectively).

Effect of prolonged, heavy exercise on pulmonary gas exchange in athletes.

During maximal exercise, ventilation-perfusion inequality increases, especially in athletes. The mechanism remains speculative. We hypothesized that, if interstitial pulmonary edema is involved, prolonged exercise would result in increasing ventilation-perfusion inequality over time by exposing the pulmonary vascular bed to high pressures for a long duration. The response to short-term exercise was first characterized in six male athletes [maximal O2 uptake (V(O2)max) = 63 ml x kg-1 x min-1] by using 5 min of cycling exercise at 30, 65, and 90% V(O2) max. Multiple inert-gas, blood-gas, hemodynamic, metabolic rate, and ventilatory data were obtained. Resting log SD of the perfusion distribution (log SDQ) was normal [0.50 +/- 0.03 (SE)] and increased with exercise (log SDQ = 0.65 +/- 0.04, P < 0.005), alveolar-arterial O2 difference increased (to 24 +/- 3 Torr), and end-capillary pulmonary diffusion limitation occurred at 90% V(O2)max. The subjects recovered for 30 min, then, after resting measurements were taken, exercised for 60 min at approximately 65% V(O2)max. O2 uptake, ventilation, cardiac output, and alveolar-arterial O2 difference were unchanged after the first 5 min of this test, but log SDQ increased from 0.59 +/- 0.03 at 5 min to 0. 66 +/- 0.05 at 60 min (P < 0.05), without pulmonary diffusion limitation. Log SDQ was negatively related to total lung capacity normalized for body surface area (r = -0.97, P < 0.005 at 60 min). These data are compatible with interstitial edema as a mechanism and suggest that lung size is an important determinant of the efficiency of gas exchange during exercise.

Effects of prior exercise on exercise-induced arterial hypoxemia in young women.

Twenty-eight healthy women (ages 27.2 +/- 6.4 yr) with widely varying fitness levels [maximal O2 consumption (VO2 max), 31-70 ml . kg-1 . min-1] first completed a progressive incremental treadmill test to VO2 max (total duration, 13.3 +/- 1.4 min; 97 +/- 37 s at maximal workload), rested for 20 min, and then completed a constant-load treadmill test at maximal workload (total duration, 143 +/- 31 s). At the termination of the progressive test, 6 subjects had maintained arterial PO2 (PaO2) near resting levels, whereas 22 subjects showed a >10 Torr decrease in PaO2 [78.0 +/- 7.2 Torr, arterial O2 saturation (SaO2), 91.6 +/- 2.4%], and alveolar-arterial O2 difference (A-aDO2, 39.2 +/- 7.4 Torr). During the subsequent constant-load test, all subjects, regardless of their degree of exercise-induced arterial hypoxemia (EIAH) during the progressive test, showed a nearly identical effect of a narrowed A-aDO2 (-4.8 +/- 3.8 Torr) and an increase in PaO2 (+5.9 +/- 4.3 Torr) and SaO2 (+1.6 +/- 1.7%) compared with at the end point of the progressive test. Therefore, EIAH during maximal exercise was lessened, not enhanced, by prior exercise, consistent with the hypothesis that EIAH is not caused by a mechanism which persists after the initial exercise period and is aggravated by subsequent exercise, as might be expected of exercise-induced structural alterations at the alveolar-capillary interface. Rather, these findings in habitually active young women point to a functionally based mechanism for EIAH that is present only during the exercise period.

ACSM Position Stand: Exercise and Physical Activity for Older Adults

ACSM Position Stand on Exercise and Physical Activity for Older Adults. Med. Sci. Sports. Exerc., Vol. 30. No. 6, pp. 992-1008, 1998. By the year 2030, the number of individuals 65 yr and over will reach 70 million in the United States alone; persons 85 yr and older will be the fastest growing segment of the population. As more individuals live longer, it is imperative to determine the extent and mechanisms by which exercise and physical activity can improve health, functional capacity, quality of life, and independence in this population. Aging is a complex process involving many variables (e.g., genetics, lifestyle factors, chronic diseases) that interact with one another, greatly influencing the manner in which we age. Participation in regular physical activity (both aerobic and strength exercises) elicits a number of favorable responses that contribute to healthy aging. Much has been learned recently regarding the adaptability of various biological systems, as well as the ways that regular exercise can influence them. Participation in a regular exercise program is an effective intervention/modality to reduce/prevent a number of functional declines associated with aging. Further, the trainability of older individuals (including octo- and nonagenarians) is evidenced by their ability to adapt and respond to both endurance and strength training. Endurance training can help maintain and improve various aspects of cardiovascular function (as measured by maximal V˙O2, cardiac output, and arteriovenous O2 difference), as well as enhance submaximal performance. Importantly, reductions in risk factors associated with disease states (heart disease, diabetes, etc.) improve health status and contribute to an increase in life expectancy. Strength training helps offset the loss in muscle mass and strength typically associated with normal aging. Additional benefits from regular exercise include improved bone health and, thus, reduction in risk for osteoporosis; improved postural stability, thereby reducing the risk of falling and associated injuries and fractures; and increased flexibility and range of motion. While not as abundant, the evidence also suggests that involvement in regular exercise can also provide a number of psychological benefits related to preserved cognitive function, alleviation of depression symptoms and behavior, and an improved concept of personal control and self-efficacy. It is important to note that while participation in physical activity may not always elicit increases in the traditional markers of physiological performance and fitness (e.g., V˙O2max, mitochondrial oxidative capacity, body composition) in older adults, it does improve health (reduction in disease risk factors) and functional capacity. Thus, the benefits associated with regular exercise and physical activity contribute to a more healthy, independent lifestyle, greatly improving the functional capacity and quality of life in this population.

Cardiovascular response to submaximal stationary cycling during hemodialysis

Exercise intolerance is a problem in renal failure. Stationary cycle training during hemodialysis treatment is recommended as safe, effective, and practical, but requires compensations for both exercise and acute changes in uremia. Eight patients pedalled for 5 minutes, at 60% of VO2peak, at 0, 1, 2, and 3 hours of a hemodialysis treatment. Fluid removed, blood pressure, cardiac output, heart rate, O2 uptake, hematocrit, and arterial O2 content were measured. Mean arterial blood pressure, systemic vascular resistance, stroke volume, (a-v)O2 difference, and mixed-venous O2 content were calculated. Fluid removed was 1,356 mL/hr (P < 0.002 for each hour), but with no significant cardiovascular effects during the first 2 hours. At 3 hours, decreasing cardiac output, stroke volume, and mean arterial pressure all reached significance at rest (P < 0.05), and five of eight patients could not exercise. We conclude that the cardiovascular exercise response is superimposed on hemodynamic effects of dialysis and is adequately stable during the first 2 hours of treatment. After 2 hours, cardiovascular decompensation may preclude exercise. (Am J Kidney Dis 1998 Apr;31(4):631-7)

Improved Oxygen Utilization During Mild Exercise in Heart Failure

In heart failure with low cardiac output, exercise tolerance is reduced despite modulated regional blood distribution and oxygen extraction. However, low cardiac output does not necessarily lead to reduced exercise tolerance especially during mild exercise. In the present study, in order to understand the mechanisms regulating exercise tolerance in heart failure, we measured oxygen consumption (VO2) and cardiac output (CO) during both mild and intense exercise. Patients with heart failure were divided into 2 groups; group L (n = 8) consists of patients with low anaerobic threshold (AT) < 13 ml/min per kg and group H (n = 7) consisting of patients with AT > 13 ml/min per kg. At rest, VO2 was similar between groups L and H, whereas CO was lower in group L than in group H (3.5 + 0.3 vs 4.8 + 1.4 ml/min, p < 0.01). Increase in VO2 during warm-up exercise was not significant between the 2 groups (7.4 +/- 0.5 (group L) vs 6.2 +/- 0.3 ml/min per kg (group H), ns), but increase in CO was lower in group L than in group H (2.5 +/- 0.6 vs 3.4 +/- 0.4 ml/min, p < 0.01). After warm-up to the AT point, however, the increase in not only VO2 but also CO was markedly reduced in group L than in group H (VO2: 0.5 +/- 0.4 vs 3.7 +/- 0.8 ml/min per kg, p < 0.01, CO: 0.2 +/- 0.3 vs 1.1 +/- 0.3 L/min, p < 0.01). Based on these measurements, we calculated the arteriovenous oxygen difference (c(A-V)O2 difference) during exercise in individual patients using Fick's equation. The c(A-V)O2 difference was markedly increased in severe heart failure during the warm-up stage, but between the end of warm-up and the AT point, it remained at the same level as that of group H. These results suggest the presence of a unique mechanism regulating the c(A-V)O2 difference in severe heart failure patients, activation of which may, at least during mild exercise, contribute to efficient oxygen delivery to the peripheral tissues thus compensating for the jeopardized exercise tolerance in those patients.

Strength Training in Female Distance Runners

This study determined the effects of a 10-week strength training program on running economy in 12 female distance runners who were randomly assigned to either an endurance and strength training program (ES) or endurance training only (E). Training for both groups consisted of steady-state endurance running 4 to 5 days a week, 20 to 30 miles each week. The ES undertook additional weight training 3 days a week. Subjects were tested pre and post for O2, max, treadmill running economy, body composition, and strength. A repeated-measures ANOVA was used to determine significant differences between and within groups. The endurance and strength training program resulted in significant increases in strength (p < 0.05) for the ES in both upper (24.4%) and lower body (33.8%) lifts. There were no differences in treadmill O2, max and body composition in either group. Running economy improved significantly in the ES group, but no significant changes were observed in the E group. The findings suggest that strength training, when added to an endurance training program, improves running economy and has little or no impact on O2, max or body composition in trained female distance runners.

The effects of Astragalus membranaceus on oxygen consumption in the intestine.

To investigate the effects of Astragalus membranaceus (AM) on intestinal oxygen consumption both in vivo and in vitro. The oxygen consumption of the intestine was measured using an arteriovenous (A-V) O2 difference analyzer after treatment with AM in the intestinal lumen of ten healthy, anesthetized mongrel dogs. The effects of AM on the oxygen consumption of the intestinal mucosa in vitro were observed using constant volume manometers. The oxygen consumption of the intestine in vivo increased significantly (P < 0.05 or P < 0.01) after treatment with AM compared to the saline control. The oxygen consumption significantly increased after treatment with the 30% AM dilution and the 50% AM dilution compared to that of the 10% AM dilution (P < 0.05). There was no significant difference between the 30% AM dilution and the 50% AM dilution (P > 0.05). The effects of AM on oxygen consumption of the intestinal mucosa in vivo were similar to those in vivo. After treatment with the 5% AM dilution and the 1% AM dilution, the intestinal oxygen consumption increased compared to the control (Krebs Ringer phosphate buffer (KRPB)) (P < 0.05 and P < 0.01, respectively). There was no significant difference between treatment with the 10% AM dilution and the KRPB control (P > 0.05). AM improved the function of intestinal oxidative metabolism.