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PubMed1991

The impact of exercise and diet restriction on daily energy expenditure.

In addition to the direct energy cost of physical activity, exercise may influence resting energy expenditure in 3 ways: (a) a prolonged increase in postexercise metabolic rate from an acute exercise challenge; (b) a chronic increase in resting metabolic rate associated with exercise training; and (c) a possible increase in energy expenditure during nonexercising time. It seems apparent that the greater the exercise perturbation, the greater the magnitude of the increase in postexercise metabolic rate. An exercise prescription for the general population that consists of exercise of low (less than 50% VO2max) or moderate intensity (50 to 75% VO2max) does not appear to produce a prolonged elevation of postexercise metabolic rate that would influence body-weight. Inconsistent results have been found with respect to the effects of exercise training and the trained state on resting metabolic rate. Whereas some investigators have found a higher resting metabolic rate in trained than untrained individuals and in individuals after an exercise training programme, other investigators have found no chronic exercise effect on resting metabolic rate. Differences in experimental design, genetic variation and alterations in energy balance may contribute to the discrepant findings among investigators. A relatively unexplored area concerns the influence of exercise training on energy expenditure during nonexercising time. It is presently unclear whether exercise training increases or decreases the energy expenditure associated with spontaneous or nonpurposeful physical activity which includes fidgeting, muscular activity, etc. The doubly labelled water technique represents a methodological advance in this area and permits the determination of total daily energy expenditure. Concomitant with the determination of the other components of daily energy expenditure (resting metabolic rate and thermic effect of a meal), it will now be possible to examine the adaptive changes in energy expenditure during nonexercising time. A plethora of studies have examined the combined effects of diet and exercise on body composition and resting metabolic rate. The hypothesis is that combining diet and exercise will accelerate fat loss, preserve fat-free weight and prevent or decelerate the decline in resting metabolic rate more effectively than with diet restriction alone. The optimal combination of diet and exercise, however, remains elusive. It appears that the combination of a large quantity of aerobic exercise with a very low calorie diet resulting in substantial loss of bodyweight may actually accelerate the decline in resting metabolic rate. These findings may cause us to re-examine the quantity of exercise and diet needed to achieve optimal fat loss and preservation of resting metabolic rate.

Diet, Reducing↗

PubMed1997

Determinants of oxygen uptake. Implications for exercise testing.

For exercise modalities such as cycling which recruit a substantial muscle mass, muscle oxygen uptake (VO2) is the primary determinant of pulmonary VO2. Indeed, the kinetic complexities of pulmonary VO2 associated with exercise onset and the non-steady state of heavy (> lactate threshold) and severe [> asymptote of power-time relationship for high intensity exercise (W)] exercise reproduce with close temporal and quantitative fidelity those occurring across the exercising muscles. For moderate (< lactate threshold) exercise and also rapidly incremental work tests, pulmonary (and muscle) VO2 increases as a linear function of work rate (approximately equal to 9 to 11 ml O2/W/min) in accordance with theoretical determinations of muscle efficiency (approximately equal to 30%). In contrast, for constant load exercise performed in the heavy and severe domains, a slow component of the VO2 response is manifest and pulmonary and muscle VO2 increase as a function of time as well as work rate beyond the initial transient associated with exercise onset. In these instances, muscle efficiency is reduced as the VO2 cost per unit of work becomes elevated, and in the severe domain, this VO2 slow component drives VO2 to its maximum and fatigue ensues rapidly. At pulmonary maximum oxygen uptake (VO2max) during cycling, the maximal cardiac output places a low limiting ceiling on peak muscle blood flow, O2 delivery and thus muscle VO2. However, when the exercise is designed to recruit a smaller muscle mass (e.g. leg extensors, 2 to 3kg), mass-specific muscle blood flow and VO2 at maximal exercise are 2 to 3 times higher than during conventional cycling. consequently, for any exercise which recruits more than approximately equal to 5 to 6kg of muscle at pulmonary VO2max, there exists a mitochondrial or VO2 reserve capacity within the exercising muscles which cannot be accessed due to oxygen delivery limitations. The implications of these latter findings relate to the design of exercise tests. Specifically, if the purpose of exercise testing is to evaluate the oxidative capacity of a small muscle mass (< 5 to 6kg), the testing procedure should be designed to restrict the exercise to those muscles so that a central (cardiac output, muscle O2 delivery) limitation is not invoked. It must be appreciated that exercise which recruits a greater muscle mass will not stress the maximum mass-specific muscle blood flow and VO2 but rather the integration of central (cardiorespiratory) and peripheral (muscle O2 diffusing capacity) limitations.

Exercise Test↗

PubMed2002

Growth hormone release during acute and chronic aerobic and resistance exercise: recent findings.

Exercise is a potent physiological stimulus for growth hormone (GH) secretion, and both aerobic and resistance exercise result in significant, acute increases in GH secretion. Contrary to previous suggestions that exercise-induced GH release requires that a "threshold" intensity be attained, recent research from our laboratory has shown that regardless of age or gender, there is a linear relationship between the magnitude of the acute increase in GH release and exercise intensity. The magnitude of GH release is greater in young women than in young men and is reduced by 4-7-fold in older individuals compared with younger individuals. Following the increase in GH secretion associated with a bout of aerobic exercise, GH release transiently decreases. As a result, 24-hour integrated GH concentrations are not usually elevated by a single bout of exercise. However, repeated bouts of aerobic exercise within a 24-hour period result in increased 24-hour integrated GH concentrations. Because the GH response to acute resistance exercise is dependent on the work-rest interval and the load and frequency of the resistance exercise used, the ability to equate intensity across different resistance exercise protocols is desirable. This has proved to be a difficult task. Problems with maintaining patent intravenous catheters have resulted in a lack of studies investigating alterations in acute and 24-hour GH pulsatile secretion in response to resistance exercise. However, research using varied resistance protocols and sampling techniques has reported acute increases in GH release similar to those observed with aerobic exercise. In young women, chronic aerobic training at an intensity greater than the lactate threshold resulted in a 2-fold increase in 24-hour GH release. The time line of adaptation and the mechanism(s) by which this training effect occurs are still elusive. Unfortunately, there are few studies investigating the effects of chronic resistance training on 24-hour GH release. The decrease in GH secretion observed in individuals who are older or have obesity is associated with many deleterious health effects, although a cause and effect relationship has not been established. While exercise interventions may not restore GH secretion to levels observed in young, healthy individuals, exercise is a robust stimulus of GH secretion. The combination of exercise and administration of oral GH secretagogues may result in greater GH secretion than exercise alone in individuals who are older or have obesity. Whether such interventions would result in favourable clinical outcomes remains to be established.

Circadian Rhythm↗

PubMed1997

Aerobic exercise capacity remains normal despite impaired endothelial function in the micro- and macrocirculation of physically active IDDM patients.

The aim of the present study was to examine if diabetes in the absence of neuropathy affects the exercising capacity of IDDM patients, and whether regular, intense training has a beneficial effect on endothelial function. Five groups of subjects were studied: 23 healthy control subjects who exercised regularly (age 33 +/- 6 years), 23 nonneuropathic type 1 diabetic patients who exercised regularly (age 33 +/- 6 years, IDDM duration 11 +/- 8 years), 7 neuropathic type 1 diabetic patients who exercised regularly (age 36 +/- 7 years, IDDM duration 22 +/- 8 years), 18 healthy subjects who did not exercise regularly (age 34 +/- 7 years), and 5 nonneuropathic type 1 diabetic patients who did not exercise regularly (age 31 +/- 4 years, IDDM duration 20 +/- 3 years). All groups were matched for age, sex, and body weight. No differences existed in the energy expenditure per week in physical activity among the three exercising groups or between the two nonexercising groups. The maximal oxygen uptake was similar between control and diabetic nonneuropathic exercisers, and among diabetic neuropathic exercisers, control nonexercisers, and diabetic nonexercisers; however, a significant difference existed between the first two and the last three groups (P < 0.0001). A stepwise increase was found in the resting heart rate among the groups, ranging from the lowest in control exercisers to the highest in diabetic nonexercisers, but the maximal heart rate was lower only in diabetic neuropathic exercisers compared with all other groups (P < 0.05). Assessments of endothelial function in both macro- and microcirculation were performed in 12 control exercisers, 10 diabetic nonneuropathic exercisers, 5 diabetic neuropathic exercisers, 17 control nonexercisers, and 4 diabetic nonexercisers. When all diabetic patients were considered as one group and all control subjects as another, the microcirculation endothelial function in the diabetic group was reduced compared with the control subjects (91 +/- 49 vs. 122 +/- 41% flux increase over baseline; P < 0.05). In contrast, no differences existed among the three diabetic groups or between the two control groups. Similarly, in macrocirculation, a reduced response during reactive hyperemia was observed in the diabetic patients compared with control subjects (7.0 +/- 4.5 vs. 11.2 +/- 6.6% diameter increase; P < 0.05), whereas again no difference existed among the three diabetic groups or between the two control groups. These data suggest that diabetes per se does not affect aerobic exercise capacity (VO2max) in physically active individuals, but is reduced in the presence of neuropathy. In addition, regular exercise training involving the lower extremities does not improve the endothelial function in the micro- and macrocirculation of the nonexercised upper extremity in type 1 diabetic patients.

Adult↗

PubMedDate not supplied

A worksite intervention to enhance social cognitive theory constructs to promote exercise adherence.

UNLABELLED: The results suggest social cognitive theory variables associated with the adoption of exercise are changeable in a brief worksite intervention. Self-regulation techniques and outcome-expectancy value improved, but self-efficacy did not improve for the treatment group. One possible explanation is, the intervention did not adequately address the ability to overcome barriers to exercise faced by participants in the intervention. Another explanation may be the effect of experiencing the barriers to exercise faced by subjects during the first 4 weeks of a self-regulated exercise program. Before engaging in exercise, the participants had a perceived level of confidence to overcome barriers to exercise. Once faced with real barriers to exercise, the subjects may have reevaluated their ability to overcome these barriers. It is interesting that the comparison group reported small decreases in all social cognitive theory variables measured in this study. The comparison group received a program of assessment, instruction, and access to facilities that is common to many worksite-based fitness promotion programs. Clearly, this approach did not have a favorable impact on psychosocial variables associated with exercise adherence. These results may be explained by a reevaluation of beliefs and perceived capabilities to exercise, once faced with the real experiences and barriers related to the adoption of an exercise program. The small decreases in social cognitive theory variables in the comparison group may explain high dropout rates in many fitness center programs and warrant further study. IMPLICATIONS: Health promotion specialists at the worksite need intervention programs that are safe, effective, and efficient for their employees. This intervention was based in the classroom, and no exercise was performed during class. This is appealing to employees who do not have access to shower facilities at the worksite. Moreover, in many interventions, subjects exercise during class and have limited time to learn specific skills to help them adopt and maintain exercise outside the structure of the intervention. Having established favorable changes in social cognitive theory constructs attributable to the intervention, a follow-up study should be conducted to determine the extent to which these changes predict adherence to regular exercise. These studies would establish the causal linkages between social cognitive theory constructs and regular exercise. LIMITATIONS: There were specific limitations, and the results should be interpreted cautiously. The sample size was relatively small, although similar to other exercise intervention research reviewed by Dishman. Another limitation of the sample was no random assignment to treatment or comparison group. The results apply only to the subjects who volunteered for this study. The measure of outcome-expectancy value is the most vulnerable of those used to measure outcome expectations and outcome expectancies. It is possible that the results of the study would be substantially altered if a better measure were available. The data were collected through self-administered questionnaires. It was assumed the subjects would provide accurate information, but reliance on self-reported data introduces potential sources of error.

Adult↗

PubMed1999

[Diagnosis of myocardial viability by exercise echocardiography].

This study determined whether the diagnosis of myocardial viability could be established on the basis of the contractile reserve during low level exercise with an ergometer using echocardiography. The study involved 22 patients with transmural old myocardial infarction who underwent exercise echocardiography, followed by coronary intervention after a mean 4 days. Exercise echocardiography was started from 50 W and stepped up by 25 W every 3 min up to a maximum of 150 W. Low level exercise was administered for 1 to 2 min at 50 W. A 16-segment model was used for the left ventricular wall motion, which was evaluated by five-grade scoring, ranging from normokinesis to dyskinesis. If patients showed improvement by one point or more in the score for segments of dyskinesis, akinesis, or severe hypokinesis on the exercise echocardiography, they were considered to have positive viability. The golden standard for the diagnosis of myocardial viability was that wall motion abnormalities before exercise echocardiography should be improved by one point or more after coronary intervention. Before exercise echocardiography, there were 152 segments showing wall motion abnormalities assessed as severe hypokinesis or more. After coronary intervention, improvement of the wall motion by one grade or more was found in 2 of the 18 segments (11%) for dyskinesis, in 38 of the 96 segments (40%) for akinesis, and in 22 of the 38 segments (58%) for severe hypokinesis; improvement for the segments of severe hypokinesis was significantly better than those for dyskinesis and akinesis. Out of 19 segments with akinesis before exercise echocardiography in which wall motion was improved during low level exercise, 16 segments (84%) showed improvement in wall motion after coronary intervention. Out of 77 segments with akinesis before exercise echocardiography in which no change or worsening was seen during low level exercise, 22 segments (29%) showed improved wall motion after coronary intervention. There were 38 segments with severe hypokinesis before exercise echocardiography; out of 12 segments in which wall motion was improved during low level exercise, 7 segments (58%) showed improved wall motion after coronary intervention. Out of 26 segments with severe hypokinesis before exercise echocardiography in which no change or worsening was seen during low level exercise, 11 segments (42%) showed improved wall motion after coronary intervention. Wall motion was improved after coronary intervention in 20 of 25 segments (80%) that showed the biphasic response, in 4 of 7 segments (57%) that showed improvement, in 14 of 43 segments (33%) that showed worsening, in 24 of 77 segments (31%) for no change; the biphasic response showed a significantly higher improvement compared to worsening or no change. If segments in which wall motion was improved during low level exercise are regarded as positive viability segments, occurrences of the sensitivity, specificity and diagnostic accuracy of myocardial viability were 50%, 84%, and 71%, respectively.

Echocardiography↗

PubMed2001

T wave alternans detection during exercise stress test and during dobutamine stress. A comparative study in patients with a recent myocardial infarction.

BACKGROUND: Beat to beat electrical alternans of the T wave (TWA) on the electrocardiogram is a risk marker for the occurrence of life-threatening ventricular tachyarrhythmias. Atrial pacing or exercise are commonly used to increase heart rate to the critical level for TWA detection. However, atrial pacing requires invasive procedures while exercise may cause significant noise on the electrocardiographic recording or may be not performed by a number of patients with cardiac diseases. Dobutamine stress testing is routinely used in post-myocardial infarction patients and may represent an alternative means to detect TWA. However, the comparability of data obtained with exercise and dobutamine needs to be proven. METHODS: We measured TWA during exercise and/or dobutamine stress in 42 patients with a recent myocardial infarction. TWA was detected using a commercially available software while the heart rate was increased to the target range of 105-130 b/min. Each patient performed the two tests in random order with an adequate recovery time in between. RESULTS: The mean level of noise during data acquisition for TWA detection was significantly lower during the dobutamine test than during exercise (1.003 +/- 0.67 vs 1.46 +/- 1.20 microV, p < 0.01). With exercise, 32 (78%) patients had a determinable TWA. Of these, 9 (27%) were TWA positive and 23 TWA negative. In the other patients noise (n = 8) or exercise-induced arrhythmias (n = 1) prevented an appropriate TWA determination. One patient could not exercise. With dobutamine stress, 38 (87%) of the 42 patients studied had a determinable TWA. Arrhythmias prevented TWA determination in the remaining 4 patients. Dobutamine and exercise testing provided comparable proportions of TWA determinability. However, by combining exercise and dobutamine testing, a greater (p = 0.0071) proportion of the patients (41/42, 98% vs 32/42, 76%) had a determinable TWA when compared with exercise alone. A comparative TWA study could be performed in 29 patients who completed both the dobutamine and the exercise stress tests. All 22 patients TWA negative at exercise were so at dobutamine testing also. On the other hand, 5 of the 7 patients TWA positive at exercise were so at dobutamine testing also. Overall, 27 (93%) of the 29 patients in whom internal comparison could be performed showed a concordant result. CONCLUSIONS: Dobutamine testing allows TWA detection with results comparable to those obtained at exercise testing. Combining exercise and dobutamine stress allows TWA determination in most of post-myocardial infarction patients. The present study provides the evidence for a safe and effective TWA determination for risk stratification after myocardial infarction.

Adult↗

PubMedDate not supplied

Effects of intensity and duration of exercise on total leukocyte count in normal subjects.

BACKGROUND: Leucocytes the mobile units of the protective system of the body, may circulate freely in the blood, adhere to the vascular endothelium in sites where blood flow is relatively slow and then once again re-enter the circulation in a process of continuous exchange. This process of continuous exchange of leucocytes is influenced by proper stimulation such as exercise. This study was done to observe the effects of intensity and duration of exercise on total leucocyte count. METHODS: Two groups of normal healthy male adult subjects were exercised on treadmill. Group-I performed exercise by running for a duration of 2-3 minutes, at 7% grade (4 degree inclination) and at constant speed ranging from 7.5 to 9 Km/hour while group-II walked on treadmill for a duration of 7-10 minutes at zero grade and at constant speed ranging from 5 to 6 Km/hour. Blood sample was drawn before exercise, immediately after exercise and after 30 minutes of rest after the exercise. Total leukocyte count was then done by improved Neubauer haemocytometer. RESULTS: The mean of pre-exercise total leucocyte count of Group-I subjects (n = 15) was 9750 +/- 384.47/microliter, while immediately after exercise the mean total leucocyte count increased to 17,856.66 +/- 1213.24/microliter and after 30 minutes rest, it came down to 10,396.67 +/- 648.35/microliter. Whereas, the mean of total leucocyte count of group-II subjects (n = 15) was 10,266.66 +/- 307.60/microliter pre-exercise, 16,336.66 +/- 866.30/microliter immediately post-exercise and 1162.33 +/- 718.85/microliter at 30 minutes post-exercise. The total leucocyte count increased significantly immediately after exercise and it significantly decreased after 30 minutes of rest but was still higher than the pre-exercise count in both the groups CONCLUSION: It is clearly reflected by this study that the magnitude of exercise-induced leucocytosis is higher in exercise of more intensity and less duration.

Adult↗

PubMed2005

[Effect of incremental cycling exercise performed before and 24 hours after blood withdrawal on the concentration of morphologic elements of blood in young health men].

The aim of this study was to evaluate the effect of incremental cycling exercise test performed before and 24 hours after blood donation (withdrawal of 450 ml of blood) on the plasma volume and concentration of morphologic elements of blood. Thirteen subjects (mean +/- SD), age 23 +/- 3 years; body mass 75 +/- 10 kg; BMI 23.4 +/- 2 kg x m(-2); VO2max 2903 +/- 334 ml x min(-1), volunteered for this study. The exercise test started at the power output of 20 W with an increase by 20 W every 3 minutes--until exhaustion. This test was performed once in the control study (7-12 days before blood donation) and repeated 24 hrs after blood donation. The blood samples were taken from the antecubital vein, in a sitting position (1) at rest, (2) at the stage of 100 W power output, (3) at the end of the test (the stage of exhaustion) and (4) at 2 hours after the end of the test. The changes in plasma volume were evaluated according to changes in hemoglobin and hematocrit concentrations. The significance of differences in the studied variables were tested using Wilcoxon test. At the end of the exercise test a significant (p<0.05) decrease in plasma volume was found in both study. It amounted to--11.1 +/- 2.9% in the control study, and to--13.0 +/- 3.9% after blood donation. Within 2 hours after the end of the exercise test plasma volume returned to the pre-exercise value in the control study and exceeded the pre-exercise value by 3.9 +/- 6.7% (p<0.05) in the study performed after blood donation. The MCV, MCH, and MCHC values were not affected by the exercise performed before and after blood donation. In the control study, at the end of the incremental exercise test a significant increase in the leukocyte, lymphocyte and thrombocyte count was found. At 2 hours after exercise thrombocytes count returned to the pre-exercise level, whereas the exercise-induced leucocytosis remained at the end-exercise level. The lymphocyte count decreased to lymphopenic level. During the incremental exercise test performed after blood donation the changes in the concentration of the studied morphologic elements of blood were similar as in the control study. The only difference was noticed in the changes of lymphocyte count which returned to the pre-exercise level within 2 hours after exhaustion. Taking into consideration the changes in plasma volume it was found that during the incremental exercise tests (both in the control study and after blood donation) there was a significant (p<0.05) extra vascular escape of erythrocytes and thrombocytes. This was accompanied by a significant accumulation of neutrophils and lymphocytes in circulating blood. At 2 hours after the end of exercise, neutrophils count increases and lymphocytes migrate into peripheral lymphoid tissues, causing lymphopenia.

Adult↗

PubMed1991

Regulation of muscle sympathetic nerve activity during exercise in humans.

Recent investigations using direct (microneurographic) recordings of MSNA have provided a substantial amount of new information on the regulation of sympathetic nervous system control of nonactive skeletal muscle blood flow during exercise in humans. Some of the new conclusions from these studies discussed in this review include: 1. The direction, pattern and magnitude of the MSNA response to exercise depend on the collective influence of a number of factors, including the mode (isometric or rhythmic), intensity, and duration of the exercise, the size of the contracting muscle mass, and possibly the level of conditioning (physical training) of the exercising muscles. The MSNA response also appears to be tightly coupled with the onset and progression of muscle fatigue, at least during sustained, isometric contractions. 2. Increases in MSNA evoked during exercise with the arms are fairly uniform among different skeletal muscle nerves, and these responses correlate strongly with changes in venous plasma norepinephrine concentrations, limb vascular resistance and arterial blood pressure. Thus, increases in this neural activity during exercise are associated with the expected physiological responses. 3. The MSNA response to the same level of exercise varies markedly among healthy subjects but appears to be consistent over time within a particular subject. 4. The muscle metaboreflex (muscle chemoreflex) is the primary-mechanism by which MSNA is stimulated during small-muscle, isometric exercise in humans. In contrast, central command has a relatively weak influence on MSNA during this type of exercise. 5. Muscle metaboreflex-stimulation of MSNA also occurs during dynamic exercise, but only at or above moderate, submaximal intensities (i.e., not during mild exercise). 6. Muscle metaboreflex-evoked increases in MSNA during exercise are strongly associated with glycogenolysis and the consequent cellular accumulation of hydrogen ions in the contracting muscles. 7. Sympathoinhibitory cardiopulmonary reflexes do not appear to modulate the MSNA responses to isometric exercise in the healthy human. However, arterial baroreflexes exert a potent inhibitory effect on MSNA during this form of exercise. The mechanisms involved in the regulation of MSNA during large-muscle, dynamic leg exercise is an important topic for future investigations, as is the relationship between MSNA and sympathetic outflow to other regional circulations (e.g., heart, viscera, skin) during various forms of exercise.

Environmental Exposure↗

PubMed1997

[Mechanisms facilitating oxygen delivery during exercise in patients with chronic heart failure].

The aim of the study was to estimate the relative importance of the Bohr effect and redistribution of blood from the non-exercising tissues on the arterial-venous oxygen content differences across the exercising extremities and the central circulation in patients with chronic heart failure; the relationship among femoral vein, systemic and pulmonary artery oxygen partial pressure and hemoglobin saturation was determined. It has been reported that the maximal reduction in femoral vein pO2 precedes peak oxygen consumption and lactic acidosis threshold in patients with chronic heart failure and normal subjects during exercise. The increase in oxygen consumption at work rates above lactic acidosis threshold, therefore, must be accounted for by increase in blood flow in the exercising muscles and right-ward shift on the oxyhemoglobin dissociation curve. Since the total cardiac output increase is blunted in patients with chronic heart failure, diversion of blood flow from non-exercising to exercising tissues may account for some of the increase in muscle blood flow. Ten patients with chronic heart failure performed a progressively increasing leg cycle ergometer exercise test up to maximal effort while measuring ventilation and gas concentration for computation of oxygen uptake and carbon dioxide production, breath-by-breath. Blood samples were obtained, simultaneously, from systemic and pulmonary arteries and femoral vein at rest and every minute during exercise to peak oxygen consumption. At comparable levels of exercise, femoral vein pO2, hemoglobin saturation and oxygen content were lower than in the pulmonary artery. PCO2 and lactate concentration increased steeply in femoral vein and pulmonary artery blood above lactic acidosis threshold (due to lactic acid build-up and buffering), but more steeply in femoral vein blood. These increases allowed femoral vein oxyhemoglobin to dissociate without a further decrease in femoral vein pO2 (Bohr effect). The lowest femoral vein pO2 (16.6 +/- 3.9 mmHg) was measured at 66 +/- 22% of peak VO2 and before the lowest oxyhemoglobin saturation was reached. Artero-venous oxygen content difference was higher in the femoral vein than in the pulmonary artery; this difference became progressively smaller as oxygen consumption increased. "Ideal" oxygen consumption for a given cardiac output (oxygen consumption expected if all body tissues had maximized oxygen extraction) was always higher than the measured oxygen consumption; however the difference between the two was lost at peak exercise. This difference positively correlated with peak oxygen consumption and cardiac output increments at submaximal but not at maximal exercise. In conclusion, femoral vein pO2 reached its lowest value at a level of exercise at or below the lactic acidosis threshold. Further extraction of oxygen above the lactic acidosis threshold was accounted for by a right shift of the oxyhemoglobin dissociation curve. The positive correlation between increments of cardiac output vs "ideal" and measured oxygen consumption suggests a redistribution of blood flow from non-exercising to exercising regions of the body. Furthermore the positive correlation between exercise capacity and the difference between "ideal" and measured oxygen consumption suggests that patients with the poorer function have the greater capability to optimize blood flow redistribution during exercise.

Aged↗

PubMed1996

Vasoconstriction in active calf persists after discontinuation of combined exercise with high-intensity elbow flexion.

The present study aimed to determine whether vasoconstriction in active calf occurring during combined exercise diminished or persisted when added low- and high-intensity elbow flexion exercise ceased and single leg exercise continued. Six active women (mean age, 21.2 years) participated in this study. During 10-min plantar flexion exercise at 10% of maximum voluntary contraction (MVC), elbow flexion exercise at 10% MVC was added over the 3rd and 4th min. Calf blood flow did not change significantly upon superimposition and cessation of this elbow flexion exercise. However, when elbow flexion exercise at 50% MVC was added during the 7th and 8th min, calf blood flow above the resting value (2.23 +/- 0.23 mL 100 mL-1 min-1) decreased significantly (P < 0.05) from 6.72 +/- 0.87 (6th min) to 5.14 +/- 1.36 mL 100 mL-1 min-1 after 2 min of combined exercise and was accompanied by a similar change in the non-exercising calf blood flow value. The vascular conductance of the exercising calf decreased significantly (P < 0.01) from 6.48 +/- 1.08 (6th min) to 3.11 +/- 1.27 mL 100 mL-1 min-1 mmHg-1 at the end of the 2nd min of combined plantar flexion exercise with elbow flexion exercise at 50% MVC. After elbow flexion exercise at 50% MVC was discontinued and plantar flexion exercise at 10% MVC alone was performed, the vascular conductance in the exercising calf remained significantly low for the next 2 min. These results indicate that the vasoconstriction induced by adding high-intensity arm exercise is persistent, suggesting a major contribution of metabo-receptor-mediated vasoconstriction rather than central command- and mechano-receptor-mediated vasoconstriction.

Adult↗

PubMed2003

Magnitude- and time-dependence of the effect of treadmill exercise on cell proliferation in the dentate gyrus of rats.

The effect of treadmill exercise on cell proliferation in the dentate gyrus was studied in Sprague-Dawley rats via 5-bromo-2'-deoxyuridine (BrdU)-specific immunohistochemistry. For studying the dependence of this effect on the magnitude of exercise, animals were divided into the control, light-exercise, moderate-exercise, and severe-exercise groups; different exercise regimens were applied to the groups. To study the temporal dependence of this effect, animals were divided into the control, 1-day-exercise, 3-days-exercise, 7-days-exercise, 14-days-exercise, and 28-days-exercise groups; the regimen used on the light-exercise group was applied to each of the exercise group over the respective number of days. Cell proliferation was most prominent in the light-exercise group (p < 0.001) and reached a maximum level after 7 days of exercise (p < 0.001). In this study, it was shown that cell proliferation is modulated by the intensity and duration of treadmill exercise.

Animals↗

PubMed1999

Umbilical artery flow velocity waveforms following maternal exercise.

The effect of acute exercise on pregnant women in the last trimester of pregnancy and the changes in fetal umbilical artery flow velocity waveforms were studied. One hundred and forty-three healthy pregnant women underwent an acute exercise test. The exercise was performed on an upright bicycle ergometer for 5 minutes, followed by 30 minutes of recovery. The baseline control values of umbilical artery velocity waveforms were compared with those after exercise. The mean exercise intensity achieved was 67.4% (55-90%) of submaximal exercise. Maternal heart rate rose significantly from a mean of 89 (68-120) beats per minute at rest to a mean of 144 (116-200) beats per minute after exercise (P<0.001). Maternal blood pressure rose significantly after exercise from a mean systolic of 112 (80-150) mmHg to a mean of 147 (120-200) mmHg (P<0.001), and from a mean diastolic of 67 (40-85) mmHg to a mean of 84 (70-100) mm Hg (P<0.001). The mean fetal umbilical pulsatility index (PI) was shown to decrease significantly following exercise at 2 and 4 minutes of recovery. It is concluded that (1) an acute exercise test of this intensity causes a significant decrease in PI index after 2 and 4 minutes of recovery; (2) an exercise intensity between 55 and 75% causes a decrease in the PI after exercise while exercise of 76-90% of submaximal exercise causes a rebound increase after an initial decrease at 2 minutes; (3) it may be possible to use this pattern of exercise as an exercise test to differentiate between low- and high-risk pregnancies. Studies on high-risk pregnancies are being prepared for publication.

Journal Article↗

PubMedDate not supplied

1979 Memorial Award Paper. Comparison of exercise right ventricular performance in chronic obstructive pulmonary disease and coronary artery disease: noninvasive assessment by quantitative radionuclide angiocardiography.

The right ventricular (RV) response to upright bicycle exercise was assessed in 16 patients with chronic obstructive pulmonary disease (COPD), in 23 patients with coronary artery disease (CAD), and in 19 normal control subjects. Right ventricular (RV) and left ventricular (LV) ejection fractions were determined noninvasively using first-pass quantitative radionuclide angiocardiography, a technique well suited for simultaneous assessment of RV and LV systolic performance. The factors limiting exercise in COPD and CAD are distinctly different, and therefore patients with COPD were studied by means of a single-stage submaximal exercise test, while patients with CAD were studied by means of a graded maximal test. The normal response to exercise, irrespective of exercise protocol, was at least a 5% increase in RV and LV ejection fractions. In 12 of 16 patients with COPD, RV ejection fraction either decreased or remained the same with exercise (abnormal exercise RV reserve). Left ventricular exercise reserve was abnormal only in five patients, probably due to occult CAD. Isolated abnormal exercise RV reserve was present in nine patients. The severity of ventilatory impairment and resting arterial hypoxemia were major determinants of abnormal exercise RV reserve in patients with COPD. In 12 or 23 patients with CAD, RV ejection fraction either decreased or remained the same with exercise (abnormal exercise RV reserve). Left ventricular reserve was abnormal in 18 of 23 patients; RV exercise reserve was abnormal only in CAD patients with concomitant abnormal LV reserve. The presence of proximal right coronary artery stenosis (the major blood supply to the RV) was not a significant determinant of the RV response to exercise in patients with CAD. These data suggest that abnormal exercise RV reserve occurs frequently both in COPD and CAD patients. In COPD the predominant hemodynamic abnormality involves performance of the RV, while in CAD the predominant abnormality involves the LV. The common factor modulating RV exercise performance in both diseases appears to be altered RV afterload.

Angiocardiography↗

PubMed1984

Thermal responses during arm and leg and combined arm-leg exercise in water.

Thermal and metabolic responses were examined during exposures in stirred water at approximately 20, 26, and 33 degrees C while subjects were performing 45 min of either arm (A), leg (L), or combined arm-leg (AL) exercise. Eight males immersed to the neck completed a low exercise intensity for A exercise and both a low and high exercise intensity for L and AL exercise. During low-intensity exercise, final metabolic rate (M) for A, L, and AL exercise was not different (P greater than 0.05) between exercise type for each water temperature (Tw). In contrast final rectal temperatures (Tre) for A and AL exercise were significantly lower than L values for each Tw during low-intensity exercise. These findings were supported by both mean weighted skin temperature (Tsk) and mean weighted heat flow (Hc) values, which were greater during A than L for each Tw. During high-intensity exercise, final Tre values were lower (P less than 0.05) during AL compared with L exercise across all Tw. Final Tsk and Hc values were not different between each type of exercise, although M was significantly lower during L exercise in 20 degrees C water. These data suggest a greater conductive and convective heat loss during exercise utilizing the arms when compared with leg-only exercise.

Adult↗

PubMed2002

Exercise causes a tissue-specific change of NO production in the kidney and lung.

Nitric oxide (NO) is produced in the vascular endothelium and is a potent vasodilator substance that participates in the regulation of local vascular tone. Exercise causes peculiar changes in systemic and regional blood flow, i.e., an increase of systemic blood flow and a redistribution of local tissue blood flow, by which the blood flow is greatly increased in the working muscles, whereas it is decreased in some organs such as the kidney and intestine. Thus we hypothesized that exercise causes a tissue-specific change of NO production in some internal organs. We studied whether exercise affects expression of NO synthase (NOS) mRNA and protein, NOS activity, and tissue level of nitrite/nitrate (stable end products of NO) in the kidneys (in which blood flow during exercise is decreased) and lungs (in which blood flow during exercise is increased with the increase of cardiac output) of rat. Rats ran on a treadmill for 45 min at a speed of 25 m/min. Immediately after this exercise, kidneys and lungs were quickly removed. Control rats remained at rest during this 45-min period. Expression of endothelial NOS (eNOS) mRNA in the kidneys was markedly lower in exercise rats than in control rats, whereas that in the lungs was significantly higher in exercise rats than in control rats. Western blot analysis confirmed down- and upregulation of eNOS protein in the kidney and lung, respectively, after exercise. On the other hand, neither expression of neuronal NOS (nNOS) mRNA and nNOS protein nor inducible NOS (iNOS) mRNA and iNOS protein in the kidneys and lungs differed between exercise and control rats. NOS activity in the kidney was significantly lower in exercise rats than in control rats, whereas that in the lung was significantly higher in exercise rats than in control rats. On the other hand, the iNOS activity in the kidneys and lungs did not differ between exercise rats and control rats. Tissue nitrite/nitrate level in the kidneys was markedly lower in exercise rats, whereas that in the lungs was significantly higher in exercise rats. The present results show that production of NO is markedly and tissue-specifically changed in the kidney and lung by exercise.

Animals↗

PubMedDate not supplied

Diabetes, insulin and exercise.

The metabolic and hormonal adaptations to single exercise sessions and to exercise training in normal man and in patients with insulin-dependent as well as non-insulin-dependent diabetes mellitus are reviewed. In insulin-dependent (type I) diabetes good metabolic control is best obtained by a regular pattern of life which will lead to a fairly constant demand for insulin from day to day. Exercise is by nature a perturbation that makes treatment of diabetes difficult: Muscle contractions per se tend to decrease the plasma glucose concentration whereas the exercise-induced response of the so-called counter-regulatory hormones tend to increase plasma glucose by increasing hepatic glucose production and adipose tissue lipolysis. If the pre-exercise plasma insulin level is high, hypoglycaemia may develop during exercise whereas hyperglycaemia and ketosis may develop if pre-exercise plasma insulin levels are low. Physical activity is often difficult to carry out on a precise schedule and the exercise-induced changes in demand for insulin and calories vary according to the intensity and duration of exercise, time of day, and differ within and between individuals. Thus, physical training can not be recommended as a means of improving metabolic control in insulin-dependent diabetes. However, our present knowledge and technology allows the well-informed and cooperative patient to exercise and even to reach the elite level. To achieve this, pre-exercise metabolic control should be optimal and knowledge of the patient's reaction to exercise is desirable, which necessitates frequent self-monitoring of plasma glucose. It may often be necessary to diminish the insulin dose before exercise, and/or to ingest additional carbohydrate during or after exercise. In non-insulin-dependent (type II) diabetes, exercise is associated with less risk of metabolic derangement, and in genetically disposed individuals physical training may prevent development of overt diabetes possibly by diminishing the strain on the pancreatic beta cell. The latter, however, is only achieved if exercise is not accompanied by increased caloric intake. Whether physical training in diabetes can reduce cardiovascular morbidity and mortality is at present unknown, but training has in diabetic patients been shown to lessen some risk factors for development of arteriosclerosis. However, training of diabetics (especially in the less well-regulated patient) may not lessen coronary risk factors to the same extent as in healthy subjects.

Diabetes Mellitus, Type 1↗