Cardiorespiratory kinetics during exercise of different muscle groups and mass in old and young

The purpose was to compare cardiorespiratory kinetics during exercise of different muscle groups (double-leg cycling vs treadmill walking and single-leg ankle plantar flexion) in old and young subjects. Oxygen uptake (VO2) during exercise transitions was measured breath by breath, and the phase 2 portion of the response was fit by a monoexponential for determination of the time constant (tau) of VO2. Two separate studies were performed: in study 1, 12 old (age 66.7 yr) and 16 young (aged 26.3 yr) subjects were compared during cycling and ankle plantar flexion exercise, and in the study 2, five old (aged 69.6 yr) and five young (24.4 yr) subjects were compared during cycling and treadmill walking. VO2 transients during square-wave cycling exercise were significantly slower in the old compared with the young groups. In contrast, VO2 kinetics did not differ between old and young groups during plantar flexion exercise. Heart rate (HR) kinetics followed the same pattern, with tau HR being significantly slower in the old vs young groups during transitions to cycling but not to plantar flexion. In study 2 tau VO2 and tau HR during on-transients to treadmill square-wave exercise were significantly slower in the old group compared with the young group, but tau VO2 was significantly faster during treadmill exercise than during cycling in the old group. The differences with aging between the modes of exercise may be related to the muscle mass involved and the circulatory demands. On the other hand, slowed VO2 kinetics with age appear to occur in a mode (cycling) in which the muscles are not accustomed to the activity, whereas in a mode of normal activity (walking) and with the muscle groups (plantar flexors) accustomed to the activity, VO2 kinetics are not slowed to the same degree with age.     

Remarks on the structure and course of renal efferent glomerular arterioles

Patients with chronic heart failure have structural and metabolic changes in skeletal muscle, which may be of importance for symptomatology. The origin of these changes are still unknown. The relationship between fiber composition and capillarization in skeletal muscle with exercise capacity and central hemodynamic variables was examined. Biopsies from the lateral vastus muscle were taken in 12 patients with chronic heart failure. Samples from eight normal subjects served as control samples. All patients underwent maximal exercise tests. Central hemodynamic variables were measured during exercise in five patients. The patients had a higher percentage of type II B fibers (P = .03) and fewer capillaries per fiber (P = .02) than the controls subjects. VO2 max correlated with the percentage of type I fibers, whereas the correlation with the type II A fibers was inverse. Cardiac index and pulmonary capillary wedge pressure at submaximal and maximal exercise were related to fiber type composition and relative fiber areas. Skeletal muscle fiber type composition and capillarization was changed in patients with chronic heart failure. These changes might influence exercise capacity. There were relationships between central hemodynamic variables and skeletal muscle changes. What the cause and effects were need further investigation.     

VO2 kinetics in the horse during moderate and heavy exercise

The horse is a superb athlete, achieving a maximal O2 uptake (approximately 160 ml . min-1 . kg-1) approaching twice that of the fittest humans. Although equine O2 uptake (VO2) kinetics are reportedly fast, they have not been precisely characterized, nor has their exercise intensity dependence been elucidated. To address these issues, adult male horses underwent incremental treadmill testing to determine their lactate threshold (Tlac) and peak VO2 (VO2 peak), and kinetic features of their VO2 response to "square-wave" work forcings were resolved using exercise transitions from 3 m/s to a below-Tlac speed of 7 m/s or an above-Tlac speed of 12.3 +/- 0.7 m/s (i.e., between Tlac and VO2 peak) sustained for 6 min. VO2 and CO2 output were measured using an open-flow system: pulmonary artery temperature was monitored, and mixed venous blood was sampled for plasma lactate. VO2 kinetics at work levels below Tlac were well fit by a two-phase exponential model, with a phase 2 time constant (tau1 = 10.0 +/- 0.9 s) that followed a time delay (TD1 = 18.9 +/- 1.9 s). TD1 was similar to that found in humans performing leg cycling exercise, but the time constant was substantially faster. For speeds above Tlac, TD1 was unchanged (20.3 +/- 1.2 s); however, the phase 2 time constant was significantly slower (tau1 = 20.7 +/- 3.4 s, P < 0.05) than for exercise below Tlac. Furthermore, in four of five horses, a secondary, delayed increase in VO2 became evident 135.7 +/- 28.5 s after the exercise transition. This "slow component" accounted for approximately 12% (5.8 +/- 2.7 l/min) of the net increase in exercise VO2. We conclude that, at exercise intensities below and above Tlac, qualitative features of VO2 kinetics in the horse are similar to those in humans. However, at speeds below Tlac the fast component of the response is more rapid than that reported for humans, likely reflecting different energetics of O2 utilization within equine muscle fibers.     

Cardiorespiratory kinetics and femoral artery blood velocity during dynamic knee extension exercise

The kinetics of femoral artery mean blood velocity (MBV; measured by pulsed Doppler) and whole body oxygen uptake (VO2; measured breath by breath) were assessed from the time constant during the on (tau on) and off (tau off) transients to step changes in work rate between complete rest and dynamic knee extension (KE) exercise. Six healthy men performed 5 min of seated KE exercise, with each leg alternately raising and lowering a weight (10% maximum voluntary contraction) over a 2-s duty cycle. Because kinetic analysis of VO2 kinetics during KE exercise is a new approach, the VO2 responses were also evaluated during the on and off transitions to the more familiar upright cycling exercise in which the magnitude of increase in VO2 and cardiac output was similar to that during KE exercise. During KE exercise, VO2 tau on [mean 72.2 +/- 11.2 (SE) s] was slower than VO2 tau off (33.3 +/- 1.8 s; P < 0.01). Cardiac output, measured with impedance cardiography, was not different for tau on (67.1 +/- 20.0 s) compared with that for tau off (52.9 +/- 7.6 s). Likewise, MBV tau on (34.5 +/- 3.9 s) was not different from tau off (35.3 +/- 3.2 s). During cycling, the VO2 tau on (18.0 +/- 2.4 s) and tau off (30.7 +/- 1.2 s) were both faster than KE VO2 tau on (P < 0.01). Even though the MBV kinetics indicated a rapid adaptation of blood flow during KE exercise, there was a slow adaptation of VO2. A transient hyperemia immediately on cessation of KE exercise, indicated by both MBV and calculated systemic vascular conductance responses, suggested that blood flow might have been inadequate and could have contributed to the delayed adaptation of VO2 at the onset of exercise, although other explanations are possible.     

Effect of supplemental oxygen on supramaximal exercise performance and recovery in cystic fibrosis

The effects of supplemental O2 on recovery from supramaximal exercise and subsequent performance remain unknown. If recovery from exercise could be enhanced in individuals with chronic lung disease, subsequent supramaximal exercise performance could also be improved. Recovery from supramaximal exercise and subsequent supramaximal exercise performance were assessed after 10 min of breathing 100% O2 or room air (RA) in 17 cystic fibrosis (CF) patients [25 +/- 10 (SD) yr old, 53% men, forced expired volume in 1 s = 62 +/- 21% predicted] and 17 normal subjects (25 +/- 8 yr old, 59% men, forced expired volume in 1 s = 112 +/- 15% predicted). Supramaximal performance was assessed as the work of sustained bicycling at a load of 130% of the maximum load achieved during a graded maximal exercise. Peak minute ventilation (VE) and heart rate (HR) were lower in CF patients at the end of each supramaximal bout than in controls. In CF patients, single-exponential time decay constants indicated faster recovery of HR (tau HR = 86 +/- 8 and 73 +/- 6 s in RA and O2, respectively, P < 0.01). Similarly, fast and slow time constants of two-exponential equations providing the best fit for ventilatory recovery were improved in CF patients during O2 breathing (tau 1VE = 132.1 +/- 10.5 vs. 82.5 +/- 10.4 s; tau 2VE = 880.3 +/- 300.1 vs. 368.6 +/- 107.1 s, P < 0.01). However, no such improvements occurred in controls. Supramaximal performance after O2 improved in CF patients (109 +/- 6% of the 1st bout after O2 vs. 94 +/- 6% in RA, P < 0.01). O2 supplementation had no effect on subsequent performance in controls (97 +/- 3% in O2 vs. 93 +/- 3% in RA). We conclude that supplemental O2 after a short bout of supramaximal exercise accelerates recovery and preserves subsequent supramaximal performance in patients with CF.     

Increased capillarity in leg muscle of finches living at altitude

An increased ratio of muscle capillary to fiber number (capillary/fiber number) at altitude has been found in only a few investigations. The highly aerobic pectoralis muscle of finches living at 4,000-m altitude (Leucosticte arctoa; A) was recently shown to have a larger capillary/fiber number and greater contribution of tortuosity and branching to total capillary length than sea-level finches (Carpodacus mexicanus; SL) of the same subfamily (O. Mathieu-Costello, P. J. Agey, L. Wu, J. M. Szewczak, and R. E. MacMillen. Respir. Physiol. 111: 189-199, 1998). To evaluate the role of muscle aerobic capacity on this trait, we examined the less-aerobic leg muscle (deep portion of anterior thigh) in the same birds. We found that, similar to pectoralis, the leg muscle in A finches had a greater capillary/fiber number (1.42 +/- 0.06) than that in SL finches (0.77 +/- 0.05; P < 0.01), but capillary tortuosity and branching were not different. As also found in pectoralis, the resulting larger capillary/fiber surface in A finches was proportional to a greater mitochondrial volume per micrometer of fiber length compared with that in SL finches. These observations, in conjunction with a trend to a greater (rather than smaller) fiber cross-sectional area in A than in SL finches (A: 484 +/- 42, SL: 390 +/- 26 micrometer2, both values at 2.5-micrometer sarcomere length; P = 0.093), support the notion that chronic hypoxia is also a condition in which capillary-to-fiber structure is organized to match the size of the muscle capillary-to-fiber interface to fiber mitochondrial volume rather than to minimize intercapillary O2 diffusion distances.     

Muscle oxygenation kinetics measured by near-infrared spectroscopy during recovery from exercise in chronic heart failure

The aim of the present study was to determine the kinetics of recovery of muscle oxygenation (MO) from comparable levels of exercise in chronic heart failure (CHF) patients and normal subjects and to relate MO kinetics to the level of exercise intolerance. The rationale is based on the observation that the O2 debt is increased in patients with heart failure and repayment of the debt is relatively slow. Ten patients with stable CHF (mean age 47 +/- 10 years) and nine healthy control subjects (47 +/- 6 years) were studied. All patients had ischemic cardiomyopathy (ejection fraction 33 +/- 7%). On different days, all subjects performed an upright incremental cycle ergometer exercise test with gas-exchange analysis to determine peak VO2, and a 6-minute constant work-rate (CWR) protocol at 60% of peak VO2. Oxygenation of the vastus lateralis muscle was continuously monitored during exercise and recovery using near-infrared spectroscopy (NIRS). Both MO and VO2 responses to recovery were described by a monoexponential model with a time delay. The time constant and time delay were combined to calculate a mean response time (MRT). Recovery VO2 and MO MRTs for the incremental and constant work rate exercise test were longer in CHF patients than in control subjects (p < 0.05). Both VO2 and MO MRTs were inversely related to peak VO2 (r = -0.73 and -0.52, respectively; p < 0.05 for both). However, both kinetics were not significantly different within each group between the two exercise intensities. In conclusion, the greater the cardiac dysfunction, as assessed by peak VO2, the more the recovery of muscle and total body oxygenation from both maximal and submaximal exercise is delayed.     

Cardiovascular responses to treadmill and cycle ergometer exercise in children and adults

This study was conducted to determine whether submaximal cardiovascular responses at a given rate of work are different in children and adults, and, if different, what mechanisms are involved and whether the differences are exercise-modality dependent. A total of 24 children, 7 to 9 yr old, and 24 adults, 18 to 26 yr old (12 males and 12 females in each group), participated in both submaximal and maximal exercise tests on both the treadmill and cycle ergometer. With the use of regression analysis, it was determined that cardiac output (Q) was significantly lower (P 相似文献   

Oxygen uptake kinetics during low level exercise in patients with heart failure: relation to neurohormones, peak oxygen consumption, and clinical findings

OBJECTIVE: To investigate whether oxygen uptake (VO2) kinetics during low intensity exercise are related to clinical signs, symptoms, and neurohumoral activation independently of peak oxygen consumption in chronic heart failure. DESIGN: Comparison of VO2 kinetics with peak VO2, neurohormones, and clinical signs of chronic heart failure. SETTING: Tertiary care centre. PATIENTS: 48 patients with mild to moderate chronic heart failure. INTERVENTIONS: Treadmill exercise testing with "breath by breath" gas exchange monitoring. Measurement of atrial natriuretic factor (ANF), brain natriuretic peptide (BNP), and noradrenaline. Assessment of clinical findings by questionnaire. MAIN OUTCOME MEASURES: O2 kinetics were defined as O2 deficit (time [rest to steady state] x DeltaVO2 -sigmaVO2 [rest to steady state]; normalised to body weight) and mean response time of oxygen consumption (MRT; O2 deficit/DeltaVO2). RESULTS: VO2 kinetics were weakly to moderately correlated to the peak VO2 (O2 deficit, r = -0.37, p < 0.05; MRT, r = -0.49, p < 0.001). Natriuretic peptides were more closely correlated with MRT (ANF, r = 0.58; BNP, r = 0.53, p < 0.001) than with O2 deficit (ANF, r = 0.48, p = 0.001; BNP, r = 0.37, p < 0.01) or peak VO2 (ANF, r = -0.40; BNP, r = -0.31, p < 0.05). Noradrenaline was correlated with MRT (r = 0. 33, p < 0.05) and O2 deficit (r = 0.39, p < 0.01) but not with peak VO2 (r = -0.20, NS). Symptoms of chronic heart failure were correlated with all indices of oxygen consumption (MRT, r = 0.47, p < 0.01; O2 deficit, r = 0.39, p < 0.01; peak VO2, r = -0.48, p < 0. 01). Multivariate analysis showed that the correlation of VO2 kinetics with neurohormones and symptoms of chronic heart failure was independent of peak VO2 and other variables. CONCLUSIONS: Oxygen kinetics during low intensity exercise may provide additional information over peak VO2 in patients with chronic heart failure, given the better correlation with neurohormones which represent an index of homeostasis of the cardiovascular system.     

Kinetics of oxygen uptake at the onset of exercise in boys and men

The objective of this study was to compare the O2 uptake (VO2) kinetics at the onset of heavy exercise in boys and men. Nine boys, aged 9-12 yr, and 8 men, aged 19-27 yr, performed a continuous incremental cycling task to determine peak VO2 (VO2 peak). On 2 other days, subjects performed each day four cycling tasks at 80 rpm, each consisting of 2 min of unloaded cycling followed twice by cycling at 50% VO2 peak for 3.5 min, once by cycling at 100% VO2 peak for 2 min, and once by cycling at 130% VO2 peak for 75 s. O2 deficit was not significantly different between boys and men (respectively, 50% VO2 peak task: 6.6 +/- 11.1 vs. 5.5 +/- 7.3 ml . min-1 . kg-1; 100% VO2 peak task: 28.5 +/- 8.1 vs. 31.8 +/- 6.3 ml . min-1 . kg-1; and 130% VO2 peak task: 30.1 +/- 5.7 vs. 35.8 +/- 5.3 ml . min-1 . kg-1). To assess the kinetics, phase I was excluded from analysis. Phase II VO2 kinetics could be described in all cases by a monoexponential function. ANOVA revealed no differences in time constants between boys and men (respectively, 50% VO2 peak task: 22. 8 +/- 5.1 vs. 26.4 +/- 4.1 s; 100% VO2 peak task: 28.0 +/- 6.0 vs. 28.1 +/- 4.4 s; and 130% VO2 peak task: 19.8 +/- 4.1 vs. 20.7 +/- 5. 7 s). In conclusion, O2 deficit and fast-component VO2 on-transients are similar in boys and men, even at high exercise intensities, which is in contrast to the findings of other studies employing simpler methods of analysis. The previous interpretation that children rely less on nonoxidative energy pathways at the onset of heavy exercise is not supported by our findings.     

The gas transporting systems: limits and modifications with age and training

The interplay of cardiovascular and cellular oxygen uptake determinants of aerobic performance and the system adaptations to training in different population samples are examined in order to describe the limitation. With VO2max, a central limitation following myocardial infarction and ageing is modified with training. Peripheral adaptations occur and stroke volume may be increased primarily through improved diastolic filling. In submaximal perturbations, control of the increase in O2 uptake at exercise onset (O2 kinetics) is most often under peripheral metabolic control, but in exceptions may also be limited by central factors. In young and old the peripheral machinery is matched to the growth (puberty) and loss (ageing) of muscle mass. Cardiac stroke volume capacity may adjust following the changes in muscle mass. Submaximal endurance is closely influenced by the anaerobic threshold (theta(an)) and peripheral factors of oxidative metabolism. Relative to VO2max, the theta(an) is low in children and high in older adults, perhaps reflecting a slow time course in full development and loss of peripheral adaptations. Remarkable increases in endurance performance are related to relatively small changes in the maximal capacity and the relative intensity of performance.     

A theoretical analysis of factors determining VO2 MAX at sea level and altitude

When maximal VO2 (VO2 MAX) is limited by O2 supply, it is generally thought that cardiac output (QT) is mostly responsible, but other O2 transport conductances [ventilation (VA); [Hb]; pulmonary (DLO2) and muscle (DMO2) diffusion capacities] may also influence VO2 MAX. A numerical analysis interactively linking the lungs, circulation and muscles was designed to compare the influences of each conductance component on VO2 MAX at three altitudes: PB = 760, 464 and 253 Torr. For any given set of conductances the analysis simultaneously solved six equations for alveolar, arterial, and venous PO2 and PcO2. The equations represent pulmonary mass balance, pulmonary diffusion, and muscle diffusion for both gases. At PB = 760, [Hb], DLO2 and DMO2 were as influential as QT in limiting VO2 MAX. With increasing altitude, the influence of QT and [Hb] fell while that of VA, DLO2 and DMO2 progressively increased until at PB = 253, VO2 MAX was independent of QT and [Hb]. Neither the fall in maximal QT nor rise in [Hb] with chronic hypoxia therefore appear to affect VO2 MAX. However, high values of ventilation, DLO2 and DMO2 appear to be advantageous for exercise at altitude.     

Muscle fiber composition and blood ammonia levels after intense exercise in humans

The relationship between fiber type composition and the increase in blood ammonia was examined following a maximal O2 consumption (VO2max) test. Muscle biopsies were taken from the middle portion of the vastus lateralis for determination of fiber type percentages. Two subject groups were selected on the basis of a high (HST) or low (LST) percentage of slow-twitch fibers and compared for blood ammonia and lactate levels after exercise at work loads of approximately 85 and 110% of VO2max. An inverse relationship was found between the percentage of slow-twitch fibers and the increase in blood ammonia. Blood ammonia increased after exercise at both 85 and 110% of VO2max. However, the increase was twofold greater for the LST group following the 110% work effort. The increases in blood ammonia and lactate were positively correlated for both groups following exercise. The results suggest that the proportion of slow-twitch fibers plays an important role in determining the magnitude of the increase in blood ammonia after intense exercise.     

Age alters regional distribution of blood flow during moderate-intensity exercise

During dynamic exercise in warm environments, requisite increases in skin and active muscle blood flows are supported by increasing cardiac output (Qc) and redistributing flow away from splanchnic and renal circulations. To examine the effect of age on these responses, six young (Y; 26 +/- 2 yr) and six older (O; 64 +/- 2 yr) men performed upright cycle exercise at 35 and 60% of peak O2 consumption (VO2peak) in 22 and 36 degrees C environments. To further isolate age, the two age groups were closely matched for VO2peak, weight, surface area, and body composition. Measurements included heart rate, Qc (CO2 rebreathing), skin blood flow (from increases in forearm blood flow (venous occlusion plethysmography), splanchnic blood flow (indocyanine green dilution), renal blood flow (p-amino-hippurate clearance), and plasma norepinephrine concentration. There were no significant age differences in Qc; however, in both environments the O group maintained Qc at a higher stroke volume and lower heart rate. At 60% VO2peak, forearm blood flow was significantly lower in the O subjects in each environment. Splanchnic blood flow fell (by 12-14% in both groups) at the lower intensity, then decreased to a greater extent at 60% VO2peak in Y than in O subjects (e.g., -45 +/- 2 vs. -33 +/- 3% for the hot environment, P < 0.01). Renal blood flow was lower at rest in the O group, remained relatively constant at 35% VO2peak, then decreased by 20-25% in both groups at 60% VO2peak. At 60% VO2peak, 27 and 37% more total blood flow was redistributed away from these two circulations in the Y than in the O group at 22 and 36 degrees, respectively. It was concluded that the greater increase in skin blood flow in Y subjects is partially supported by a greater redistribution of blood flow away from splanchnic and renal vascular beds.     

Role of exercising muscle in slow component of VO2

This paper: 1) Reviews evidence for the location of the slow component of VO2 kinetics either within the exercising limbs or alternatively at some site in the rest of the body, e.g., ventilatory, cardiac or accessory muscles. 2) Presents evidence in support of both the fast and slow components (i.e., < 3 min and > 3 min from exercise onset, respectively) of the exercise VO2 response residing predominantly in the exercising muscle. For a pulmonary VO2 slow component in excess of 600 ml O2.min-1, more than 80% could be attributed to an augmented VO2 across the exercising limbs. 3) Assesses the potential for the lactate ion per se to exert a metabolic stimulatory effect in exercising muscle in the absence of the potentially confounding influences of changes in muscle temperature, H+, blood flow or O2 delivery. Within the surgically isolated, electrically stimulated canine gastrocnemius, square wave infusions that increased arterial blood [lactate] by approximately 10 mM and intramuscular [lactate] to in excess of 9 mM did not increase muscle VO2. In summary, these investigations demonstrate that the exercising muscle is the predominant site of the VO2 slow component. However, despite the close temporal association between changes in blood lactate and VO2 during intense exercise, lactate itself does not mandate an additional VO2 demand in exercising dog muscle.     

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.     

Alanine and glutamine kinetics at rest and during exercise in humans

PURPOSE: The purpose of this study was to quantify both alanine and glutamine kinetics during exercise of moderate intensity to determine the sum total of alanine and glutamine flux. METHODS: Tracer methods were used to quantify alanine and glutamine rates of appearance (Ra) in plasma at rest and during 180 min of approximately 45% VO2max treadmill exercise in six normal volunteers (25 +/- 2 yr, 68 +/- 2.5 kg, VO2max 43 +/- 2.4 mL.min-1.kg-1; means +/- SE). Bolus injections (N = 3) or primed-constant infusions (N = 3) of 2H5-glutamine and 3-13C-alanine were given at rest on 1 d and 10-15 min after the onset of exercise on a separate day less than 2 wk later. Plasma enrichment decay curves and plateau enrichments were used to estimate alanine and glutamine kinetics. RESULTS: Whereas alanine Ra increased significantly from rest to exercise (5.72 +/- 0.31 vs 13.5 +/- 1.9 mumol.min-1.kg-1, respectively; P < 0.01), glutamine Ra was not significantly altered by exercise (6.11 +/- 0.44 and 6.40 +/- 0.69 mumol.min-1.kg-1 at rest and during exercise, respectively). The total of alanine and glutamine flux increased from 17.93 +/- 0.88 to 25.98 +/- 3.04 (P < 0.05). CONCLUSIONS: Since most muscle amino-N is released as alanine and glutamine, these findings provide strong evidence that amino-N delivery from muscle to the liver is increased during exercise. In addition, it appears that alanine, rather than glutamine, is the predominant N carrier involved in the transfer of N from muscle to the liver during moderate intensity exercise.     

Effect of voluntary exercise on maximal oxygen uptake in young female Fischer 344 rats

The effect of voluntary exercise on maximal oxygen uptake (VO2 max) was studied in young female Fischer 344 rats. After 10 weeks of wheel-running training, the absolute VO2 max and VO2 max relative to body mass increased without a decline in body mass. The running speed eliciting VO2 max, heart and soleus muscle mass, and succinate dehydrogenase (SDH) activity in the soleus muscle also increased. These results suggest that voluntary exercise is an effective means of increasing the aerobic exercise capacity of young female Fischer 344 rats.     

Young and old subjects matched for aerobic capacity have similar noradrenergic responses to exercise

Sympathetic nervous system activity as indicated by circulating norepinephrine has been demonstrated to increase with advancing chronological age both at rest and during submaximal exercise. Much of the earlier work investigating this aging phenomenon used a younger group that had a higher peak oxygen consumption (VO2) than did the older group, which made comparisons difficult. In the present study, young [n = 7, 36 +/- 1.0 (SE) yr] and old subjects (n = 8, 61 +/- 1.2 yr) were matched on peak VO2 and then exercised at approximately the same relative submaximal VO2 (75%) and power output on a cycle ergometer for 21 min. Blood samples were collected at rest and in the 7th, 14th, and last minute of a 21-min exercise bout via an indwelling catheter in an antecubital vein. The norepinephrine responses for the young and old groups, respectively, were as follows: rest, 486 +/- 111 vs. 673 +/- 108; 7 min, 1,258 +/- 255 vs. 1,185 +/- 172; 14 min, 1,639 +/- 316 vs. 1,528 +/- 288; and 21 min, 2,038 +/- 488 vs. 1,936 +/- 453 pg/ml. These responses were not significantly different between the groups at any time period. The epinephrine values for the age groups were not statistically different: rest, 115 +/- 60 vs 88 +/- 51; 7 min, 140 +/- 18 vs. 326 +/- 88; 14 min, 216 +/- 33 vs. 366 +/- 104; and 21 min, 324 +/- 100 vs. 447 +/- 113 pg/ml.(ABSTRACT TRUNCATED AT 250 WORDS)     

Structure of skeletal muscle in heart transplant recipients

OBJECTIVES: This study sought to define the ultrastructural characteristics of skeletal muscle in heart transplant recipients (HTRs) in relation to exercise capacity compared with that in age-matched control subjects. BACKGROUND: Muscle structural features seem to play an important role in the limitation of exercise capacity of HTRs long after transplantation. METHODS: The structure of the vastus lateralis muscle was analyzed by ultrastructural morphometry in 16 HTRs and 20 healthy control subjects. Maximal oxygen consumption (peak Vo2) was determined by an incremental exercise test. RESULTS: Peak Vo2 was significantly lower (by 35%) in HTRs. Fiber size, volume density of mitochondria and intramyocellular lipid deposits were not significantly different between HTRs and control subjects. In contrast, the capillary density and the capillary/fiber ratio were both significantly reduced in HTRs (by 24% and 27%, respectively). CONCLUSIONS: A normal volume density of mitochondria and a reduced capillary network are the main characteristics of muscle ultrastructure in HTRs by 10 months after transplantation. The muscle structural abnormalities and reduced exercise capacity might be related to immunosuppressive therapy with cyclosporine and corticosteroids as well as deconditioning.