Ventilatory and metabolic changes as a result of exercise training in COPD patients

Ventilatory and Metabolic Exercise Antonio and Training Patessio, Claudio Patients training, but not been ance the physiologic can ventilatory requirement have studies COPD improve The CO, in COPD. training healthy We the effective in inducing levels to so in and training patients with effect in patients with training stores” specifically in the training exercise. lactic acid begins threshold) can changes would a high flow and during maneuver”') (in, the identical group, 7.2 mEqfL) low work and work rate less constant work 0.73, p<O.005) and the study decrease are that acidosis during from training work are more had rates effective The COPD less lactate (4.5 after training; less higher the vs the there in the major who findings capacity) leads for lactic work high levels rates lactate activity. low lactate We the I a recent is widely acknowledged better and are able longer after a program that patients with COPD feel to sustain a given level of activity of exercise training. Although it is study There *From the Division Foundation, Reprint Medico (Novara), Medical requests: di Dr. Riabilitazione, Italy of Pulmonary Disease, Clinica del Lavoro Center of Rehabilitation, Veruno, Italy Patessio, Divisione di Pneuinologia, Centro Fondazione Clinica del Lavoro, Veruno 28010 2745 Downloaded From: http://journal.publications.chestnet.org/ on 02/10/2013 previous EFFECTS tilatory though not muscles are of reports Ventilatory in then laboratory. ON VENTILATORY this respiration, and Metabolic in a marked body to the and the increases,” Vo, at maximal reducing the Ventilation- in dead space ventilatory to require- necessary that and to maintain can regardl23; which Changes be these they that to patients: can for identified sustain, a given have discuss (1) and level of one or used the results of CAPACITY possibilities capacity: (1) changing it has been demonstrated effective results muscle of our 2 theoretical and expensive requirement strategies from activity and increase of ventilation examine than which 2 strategies ventilatory of these over a lower frequency, volume to a high performance level volume homeostasis.” framework, the other an leads pH hyper- subjects), muscles. is therefore and exercise the will levels. whole ventilation this reducing of the causes gas the increasing of blood eliciting Within increase respiratory which flow- Dynamic respiratory energetically the to 15% in healthy for the exercising ratio, blood training and that of the of the expiratory muscles ofdynamic hypermnflation, is very to 40% ment.”’#{176}More arterial (2) ability Because tidal airway capacity to hyperinflation, at vital inspiratory the of the inequality volume same higher dynamic (vs 10% available perfusion tidal the The truncation to 35% exercise oxygen capacity. residual consumption often of this experience ventilatory expiratory strategy oxygen lactate in the first group, averaging 71% can achieve physiologic of endurance training engendering than training There was a good correlation the decrease in blood lactate in ventilation. with rate with (expiratory on forced in end functional the longer work significantly Further, tolerance rate test. between exercise a program high engendered group patients responses the (48 vs 55 L/min) (p<O.Ol). in exercise (r high rates VE training and VE decrease was an increase For patient lung impinges a resting increase breathing rate or for a proportionally maximal Increased of the often during the limit inflation recoil exercise recorded at a high rate. the in the system.34 elastic heavy loop passive ventilatory 45 mm/day work be advantageous reduced impairment in the increase ventilation. work and ofthe resistance work rate. Identical tests were performed after program of cycle ergometer training either for at a low to 40% to 20%. derangements an 8-week time in the at which anaerobic physical performance is generally limited low work rates mainly by pathophysiologic progressive and participating COPD whose inappropriately an incremental at a low 5% work of mitochondria, and the glycogen groups 25% by subjects, for aerobic the oxygen uptake in the blood (the by (To,max) frequency. tests normal capacity muscle increase uptake ventilation wave mechanisms In the to in improving physiologic As a result, to accumulate respiratory as 2 square desensitization a role elucidated. increases expected as well as play underlying completely COPD than a work rate not associated with lactic acidosis. Nineteen patients with COPD were selected and performed test such by increasing capillary density, the number the concentration ofthe oxidative enzymes, volume whether exercise lactic acidosis is factors of confidence the been These wished gain tolerance, not oxygen responsible for a rates above the frequency, psychologic and exercise of lactate a physiologic a training to ventilatory specifically do with ability by bicarbonate Further, we sought to determine at a work rate associated with more the of intensity, would the Almost in patients Lower of producing subjects of activity. mechanism for work a program capable known the produced threshold. whether duration by increasing having output. is the likely requirement the to reduce CO, anaerobic determine way nonmetabolic buffering and this lower ventilatory pretraining results training only is to reduce in less negative of exercise VEmax. requirement level that dyspnea endurance system, or by reducing for a given yielded in terms sustain evident have by patho- ventilatory can have perform- mainly be ameliorated they to sustain a of exercise the physical is limited of the that of M.D.; mechanisms Since COPD performance effect physiologic elucidated. with loli, Francesco feel better and are able longer after a program underlying of ventilation M.D.; as a Result Patients* M. D. , F.C.C.P derangements exercise result Carone, Donner, completely of patients level Mauro with COPD level of activity given all M.D.; Ferdinando Changes in COPD to increase the resting lung mechanics, that exercise training and might (2) allow after Exercise strengthening the patient yen- alis the with Training (Patessio et a!) COPD In to sustain normal a higherlevel subjects’ exercise training ofventilation and patients has been shown tory muscles. On the contrary, negative results in patients exercise training having Only Ghristi&’ VEmax after (3.46 On the through been which and Moser’ were able the specific during supposed limited the that by whole The may signs pretraining by exercise test.”' equation, balance expired of carbon dioxide pressure, VD/VT exchange, way it can be is the they cannot onset of output, output. that, PaGO, been is well-correlated does of lactate by bicarbonate responsible above A review for the is the of FEy, decrease = 33% are effect; are of uptake to (2) the because enough abnormalities muscle Vco, is the the latter factor of this Shuey et al’ demonstrated that a mean FEy, of 1 .2 L reached patients higher lactic subjects normal for Sue et al 1 .2 L) and = that is not related by resting the early onset same the Vo, greater than GOPD (mean a mean mEq/L to the in 14 of 22 ability to sustain severity spirometric to the the demonstrated of 4.7 of the measurements. of anaerobic presence lung This metabolism of pulmonary that limit the oxygen supply the reduction in lung volumes. than to induce the a substantial bicarbonate related that that during FEy, is likely fact limited portion acidosis judged likely oxygen and high are fraction so ventilatory to develop of predicted). disease, of maximum acidosis than (mean shown a higher However, able in standard patients these been GOPD maximum recently: lactate (1) by 60% levels. Holle et al”' found a drop in bicarbonate 5 mEq/L in 41% of 68 patients with a metabolic GO, the partial We conducted principles is vascular to the exercising demonstrated training, the anaerobic literature with COPD. Vyas decrease in Ve reveals the in is to in normal lactate level. GO, is the likely requirement quency, logic fall in ventilation nonmetabolic and this ventilatory in decreasing of change difference,”' very duration effect acidosis in GOPD produced of in known in but 10 patients with COPD trained on average for 10 weeks, but no change in Vco, and heart rate. Alpert et aF” and Pierce et al”' showed a decrease in VE and heart rate, but also in the physiologic with COPD of producing subjects (for rate a physio- would in inducing a work MATERIALS clinical history (3) do so in to determine associated with a training not associated effect with lattic to incremental Exercise radial on the with predicted blood catheter. Minute output ventilation were I 101 of the (2) evidence with a reduced lactate >3 mEqfL testing was following: of FEV,/FVC); at by percutaneous Exercise (Vco,) basis COPD; exercise test. testing was preceded artery ergometer. dioxide consistent elevate METHODS selected (FEV,<80% ability AND were CHEST Downloaded From: http://journal.publications.chestnet.org/ on 02/10/2013 capable healthy effective than patients obstruction requirement et a?’ found a significant, (averaging 1.5 IJmin) apply to patients acidosis. Nineteen effects to specifically training is more patients mechanism for work poor TRAINING with GOPD. Further, we wished exercise training at a work rate lactic Lower and training patients whether threshold. ventilatory a study of exercise TO PATIENTS full details of this study see Gasaburi et al#{176}). We specifically wished to determine whether a program of intensity, fre- gas exchange requirement fall in blood pretraining the a lack 0, APPROACH COPD rate of pulmonary not improve been in less buffering a lower or 2 factors: have with that of work was exercise. In 1969, with GOPD with values that metabolism. population expression arterial ventilatory exercise result of the training in patients very small the with levels challenged patient of exercise of inefficiency It has after attain by of roughly GOPD anaerobic on ventilation. performed patients training with A small a duration of4 to 8 weeks, mm/day, 3 to 5 times per rates PHYSIOLOGIC ventilation, is a measure training explained of work rate a physiologic patients is an level heart by Alison for GO,: minute to reduce GO, subjects” exercise fa- and k is a constant. exercise only rates muscle work maximum has improved by an increased training somewhat which efficiency of the lungs as indicated by arterial blood gases30’ or in alveolar-arterial levels their many be attributed ofVo,max; to require achieve is whether respiratory factor ofexercise capacity for a given following mass is the VE reduce a between Thus, observed be intensity or 50% respiratory mentioned. to programs at a minimum rate not was amount in comparison and physi- same work rate was found by decrease was so small it is not might small VE of a true was demonstrated was the the effects relatively VE=KXVC0JPaCO,X(1-VD/VT) . the with REQUIREMENT requiremertt the alveolar Since and specifically of inspiratory in Vo, no influence small heart patient. ventilatory is dictated GO, training that These week, only in 7 of 12 patients. It is very that 6 of the 7 patients who improved VENTILATORY where difference change technique than in rate, to be effective in normal subjects: involving exercise for 30 to 45 attained by the respiratory et al, and Madsen et al’ important question to be answered muscle fatigue is the major limiting of the by The the improved rather decrease patients Ries in VEmax capacity body ofwork Jones and A not in heart in lactate for et al,’#{176} but surprising task, their results only patients whose exercise performance respiratory muscle fatigue can improve: in an individual decrease Mohsenifar effect. but but of an exercise muscle differences. Davis,” an increase electromyographic tigue and muscles. and tolerance to note showed training et al,’ a result of the frequency, very performance, that exercise performance is not muscle training. Pardy et al” found exercise interesting in was respiratory exercise in exercise to the different intensity muscles. Noseda et al,” concluded respiratory change to methodologic to induce respiratory training the improving Sonne increase training VEmax.”'’00 increase the attributed Mittman,” corresponding ologic per- significant hyperpnea can improve However, contradictory in be in part Belman the or endurance. obtained may improve to improve but training breathing and have to and training, hand, resistive strength respira- the L/min). other small ability statistically physical the is more performance fibrosis,” to strengthen muscles observed which exercise. cystic almost all studies have yielded with COPD, both in terms of the of respiratory formance during with the end placement performed on (1) airway and of an of a a cycle uptake (Vo,), and carbon every 30 s. Heart rate was (VE), oxygen measured I 5 I MAY, 1992 I Supplement 2755 HIGH WORK LOW WORK RATE TRAINING GROUP RATE TRAINING GROUP 0 > 0d .> \ 0 Od w 0 .> > C, _ o .> ( _ C, 0 I > \ N C” w > 0 -J 0 > 0 0 Ui .> > I - U FIGURE 1 . Changes in blood lactate, ventilation, 0, uptake, CO, output, ventilatory equivalent for 0,, and heart rate after training at a high work rate (left panel; 11 patients) and low work rate (right panel; 8 patients). Percent change is calculated from the average change in response at the time the pretrain- ing study ended. Vertical (from Casaburi et al,#{176} with measured from measured by sphygmomanometer. the electrocardiogram 1 to 2 mm to measure An incremental was first threshold square wave rate. was work for 8 weeks. groups. Group (8 patients) was work calculated work rate/low There and patients chosen trained work 11 mm Hg), and 4 mm Hg) between blood and pretraining work (p<O.002), (p<0.05). (p<O.OO5). decrease small, The in the although work rate Associated increase RESU LTS in SD), resting wave test between a series carried of 5 days to 1 of 2 ofdaily exercise whereas for a total formula: 45 amount mm 38% work PaGO,, these ± the and by severe impairment blood found (r lactate the and heart high endurance impairment to achieve correlation are time increases less ability as those training in normal subjects, there was p<O.OO5) between the decrease and decrease L). The explanation with COPD failed in to in ventilation is less subjects stems from to hyperventilate the with response. = 0.73, the rate constant significantly that the as likely a physiologic slope of this relationship than that found in normal by 160 (Fig steep a good (2.46 (7.2 in 3). HowL/min/ IJmin/mEq/ fact that in response our patients to metabolic noted PaO,, and physiologic VD/VT did changes, 71% low change. was an in the The GOPD achieve rates were reached much less statistical acidosis. findings experience physiologic high pronounced. significance 2765 Downloaded From: http://journal.publications.chestnet.org/ on 02/10/2013 lactate physiologic for the study are that acidosis during training low major through of this lactic responses training and that of blood lactate eliciting a given reduction likely reflecting ance. Our than group a learning patients ergometer. were Cycling patients exercise from and Metabolic can of engendering than work levels. benefit level in is the blood effect fall in the of exercise, lactate in the decrease ventilatory likely mediated levels. Previous ventilatory in oxygen of perform- and the is less Changes requireuptake, in the efficiency trained performed prone to learning after Exercise Training tests on effects other modes of exercise and the observation B had a smaller response, despite the same Ventilatory with a program training work rates are more effective studies demonstrating reductions ment have shown also substantial a cycle Only major who requirement only in the not there metabolic is a of DISCUSSION The by 15 beats/mm also a significant was decreased endurance high levels 12% reduced decrease averaging and maximal 1), whereas decrease Vco,, as in the on exercise was not significantly lung function (Fig 2). Therefore, and and (p<O.O5); (Fig tolerance with less mEqIL) 1 1 years Hg same was decreased showed test mm by 24% (i<01) rate (49 (41 ±5 Vco, Heart rate same variables high in age at whereas patients ever, of 1), in which blood lactate with resting B X high FEy, (56% ± 14% PaO, (84 ± 9 mm Hg decreased by (Fig elevate correlated at group in VE, as well only by 8%. These improvements were group B than in group A. It is relevant As previously out. ofcycling, allocated rate was AT and training, increased VE rate exercise lactate square changes incremental 1 SEM acidosis as normal subjects usually do; the consequence lesser than expected decrease in ventilation as a result constant work rate test. In group B, the changes blood AT differences ± significant, test. with a of the resting PaGO, the 2 groups. respectively, mI/mm of rest, test, work the of 90% 45 mm following A, lactatethreshold lactate test 90 mm randomly the no significant 81 39 In group rate rate. 56 ± ± work rate preliminary low PaCO2. rate of 10 W/min sessions performed at the 54 ± 8 years; mean 12% of predicted), ± were in the in the After was small seen relationship, ofexercise Only (p<O.O5). were difference ofdaily taken and assessments according were a second consisted The rate mm, a program A (11 patients) work at a work pretraining program a week high 60 out was every Vo,-Vco, determined.’ carried After to the The training the was the pressure were in work rate of 60% of the rate. identical from another at a work maximal tests (AT) test After performed an increase and blood samples pH , PaO,, lactate, with performed anaerobic work blcod test Arterial . Blood lines represent permission). that the practice (Patessio et a!) 0 .9 A considered A 0 . 8 LACTATE THRESHOLD (L/m in) A LA A 0.7 the 0 .6 statistical #{163} 30 40 ‘ of illness, cardiac mine the potential t t 5 . It seems that the criteria 50 ‘ A60 I I0 B 70 , 80 A A 8 PEAK LACTATE (mEg /L) training. acidosis A A A A ‘ A . A A Eh for I I that 40 50 60 70 FEy1 (S Predicted) KM, learning phenomenon. function impairment, ing some resting patients had ranging from severe of these patients 80 are 1977; and 71:145-72 Carter R, Pevler maximal suggested 6 of our Potter WA, expiratory Chest Olafsson 5, ‘ A maximal not M. Load obstructive 9 Spiro the (breathcould Scand 10 A L i 1 Lactate FIGURE 3. Relation between the is i 2 3 Decrease (mEq decrease in blood 4 5 Nery buri et al,#{176} with rate training JO. of physiology: Physiology Br J Dis medicine. J, Fields with Society, Chest S. Predicting chronic obstructive Ventilatory mechanics during exercise J Clin Invest 1971; RE. in patients NB. Flow-volume exercises in J Respir Dis 1971; and with 50:910-19 curves patients and with expiratory chronic airway 77(suppl):23-7 dyspnea, Hahn and . and Ventilatory respiratory HL, Edwards strain RHT, failure. chronic respiratory NB. 1975; W, Oren 25:21-7 An analysis with 30:415-25 JA. Contrast- to exercise pulmonary of in patients A, Davis responses obstructive in chronic 1968; exercise Thorax K, French and ofexercise Pride of submaximal bronchitis. Wasserman cost J AppI Physiol disease. obstructive LE, lactate and the group; r 0.73; p<O.005 permission). (from Casa- RD 1981; MJ, Wasserman Robinson with chronic 10:1-6 ER, muscle function Orenstein DH, Germann I L) KJ, disease. K. Exercise 16 17 Belman MJ, Kjeldgaard in mitral Chest 1983; training pulmonary testing in disease. and Basics of JM. Improvement in ventilatory with running. 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Phys Ther CHEST Downloaded From: http://journal.publications.chestnet.org/ on 02/10/2013 obstructive Horowitz cardipulmonary month supervised in ventilation in response to identical exercise tasks as a of a program of exercise training in patients with COPD. triangles = high work rate training group; open trian- result Closed gl es = low work Handbook Williams Hyatt pulmonary 5G. chronic be 14 decrease Holloszy A AA 0 In: responses, physiological patients -5 WW, 83:446-53 11 chronic Emmanuel flow duringobstructive GE,exercise Moreno in F. emphysema. Distribution J Am Appl Rev and blood 1966; 12 21:1532-44 Lertzman MM, Cherniack RM. Rehabilitation of Physiol patients with pulmonary disease. ofventilation Respir Dis 1976; 114:1145-65 A 0- greater during exercise: protec1975; 354:203-12 adaptability: significance in patients 1990; 97(suppl):59-68 8 Levison H , Cherniack RM satisfac- by Zavala during 13 Belman (L/m,n) the Chest A - is only one of for exercise 1987; 92:253-59 disease. Pride Winder in clinical limitation lung DJ, 7 Younes valve 15r 10 did to deterresponse. acidosis, DC: American ventilation flow pressures is ventilatory patients FW, M, ZinkgrafS, ing cardiovascular E Decrease groups These changes were in tolerance for heavy glycogen Arch muscle performance. disease. obstruction. It may and Bcoth testing exercise pulmonary a not ventilatory patient a criterion lactic effect. increase Washington, 10, chap 19:555-631 sect 1983; of lung not completely 30%), than to mild. were an individual only a range RH, 3 Spiro 5G. Exercises rather measurements maneuvers below effect Our whether Adopting reserve a training spirometric ventilation limited.’ with the muscle. obstructive A, is consistent the greater Fitts metabolism 6 Leaver as group degree of airway obstruction selecting patients suitable physiologic training with a substantial skeletal I FIGURE 2. Relation between the % of predicted FEy, with lactate threshold (top panel) and the arterial lactate level at the highest tolerated work rate (bottom panel). Neither correlation is significant: r = 0.39 and 0.26, respectively. Open triangles = patients in the low work rate training group; closed triangles = patients in the high work rate training group (from Casaburi et al,#{176} with permission). in defining the patients with GOPD do The degree of lung factors such as duration and bronchoreactivity a physiologic training Depletion of muscle and liver tive effect oftraining. Pfluegers 2 Saltin B, Gollnick PD. Skeletal A I 30 tory between of these REFERENCES A &b -I voluntary data A A . 4 but the This during studyexercise suggests couldthat bethe a ability selection to develop criterion. lactic In 1 Baldwin 6 A limited, comparisons function, to achieve the for we found was the associated exercise. A that Omitting not change. 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