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~+1 \'- Eur J Appli Phvs ol (143E) := !9b-_00 N OTILF Thfs materialI may b, protected by copyright law (Title 17 U.S. CodeL 7The effects of passive inhalation of cigarette smoke on performance/ .~ .~ Robert G. McMurray, Lindsay L. Hicks, and Dixie L. Thompson Human, Performance Laboratory. Universitv of North Carolina. Chapel Hill„North Carolina 27514 USA Summary. The purpose of this investigation was to evaluate the effect of passive smoke inhalation on submaximal and maximal exercise pertor- mance. Eight female subjects ran on a motor driven treadmill' for 20 min at 70`'.b Vo,T„ fol~ lowed by an incremental change in grade until maximal work capacity was obtained.~Each sub- jacr completed the exercise trial with and' without the presence of residual cigarette smoke. Com- pared to the smokeless trials, the passive inhala- tion of smoke significantly reduced maximal ox • ygen uptake by 0:25 1'- min't and time to exhaus- tion by 2.1' mi.n., The presence of sidestream smoke also elevated maximal R value (1.01 vs 0.93), maximal bloo6 lactate (6.8 vs 5.5 mlvi), and ratings of perceived exertiom (17.4 vs 16.5 units).. Passive inhalation of smoke during subrnaximal exercise significantly elevated the CO2 output (1.68 vs 1.58 [ - min-t), R values (0.91 vs 0.86), heart rate (178 vs 172 bts - min'') and rating of perceived exertion (13.8 vs 11.8' units): These find- ings suggest that passive inhalation of sidestream smoke adversely affects exercise performance. Key words: Residual cigarette smoke - Maximal oxwygen uptake - Lactate - Rating of perceived exertion - Carboxvhemoelobim Introduction RecentlN, studies have been conducted whichh show that non-smokers who inhale the smoke of nearby smokers are exposed to smoke consti- tuents at levels as high as smokers who are inhal- Ojjprrnr requests ro: R. G. McMurray at the above address €uronean ~Joumai oI Applied Physiclogy L s~~.+ce~.ve„>.q iaes exercise ing. Russell (7973)' and Olshansky (1982) deter- mined that during, rest, passive inhalation of to- bacco smoke increased expired' carbon dioxide and blood carboxvhemoglobin levels in both smokers and non-smokers. White (1978) noted that the presence of smoke in the air caused in- creased resting ventilation„oxygen uptake, earbon dioxide prod'uction, heart rate and binod pres- sure. All of these investigations deterr;atned that passive inhalation of cigarette smoke for an ex- tend'ed period of time causes harmful health re- lated problems in non-smokers (Bonham an& Wil- son 1981; Hirayama 1981): With these effects ex- istinsi at rest, one must question what physiolo;i- cal effects passive inhalatiom of cigarette smoke would have on an exercising individual. There- fore, this investigation was designed to evaluate the effect of the passive inhalation of residual, or sidestream, ciQarette smoke on submaximal and maximal exercise. Methods Eieht moderately active. normal women taking part in an aero- bics class were the subjects. They averaged 21.8_2.4 years of a¢e, 162.5 t 5.1 cm in height, weighted t8,7'±2.3 kg, and'had a 1`o,_,_ of 157 I•min' (44.2 ml•kg-'•min-'). Four were smokers (> 1 pack/week) and four were non-smokers. After obtaining written voluntary consent, each subject was screened by a medical history, resting 12-lead electrocardio- gram, and a maximal oxygen uptake test Vo M). The results of the Vo.^_ test were used to interpolate a workload result- ing in 70'Jo Vo.ry to be used for further testing.. Each subject complbted to exercise trials using the same protocol': a control, in which,the subject breathed no cigarette smoke and an experimental trial in which the subject breathed' air mixed with cigarette smoke. The order of the trials was counter-balanced and the subjects received no information concerning whether the session was a control!or experimental! JCOPYRl,',HT ~ 5 SPRiMt,,ER VERLII Zqe NEM YWr2K NY

R. G tvtc\lurrac et al. Exercise a.^.d-t=idual ~moke trial. Room temperature was 2'.5:t0.9°C for all triais. No strenuous physical activity was allowed for 2.3 h preceeding either trial, both took place during the pre-ocuiatoryptiase of the suhiects menstruallcvcles. The subjects reported'to the lab after abstaining from eat~ ing for four hours, and for the smokers, a'ostaining trom smok- ing for the past twelve hours. Heieht and weight were meas- ured. ECG' le.tds were attached. The subject then rested quietly seated on a chair on the treadmill. After 5min of rest the subject becan breathing through a mouthpiece and valve. During the tenth minute of rest, heart rate, minute ventilltion,, oxygen uptake and'carbon dioxide output were measuredi The subject then rested for an additional ~ min during which, in the experimental trial only, smoke was injected into the in- spired air. All measurements were repeated. Once resting measurements were completed, the subject ran for 20 min at approximately 70~•~ of their Vo,_--. Heart rate %%as monitored continuouslc and recorded for the last ten seconds of each minute. Oxygen uptake and CO- output were measured every fifth minute. End-tidal CO'• and O_ were mea- sured for six seconds at'the end of each five minute se=mertt.. During the final minute of the run a~rating of perceived exer- tion tR'PEi1w'as obt. iited (Borg 197'). Then %%athoutstopping.. the treadmil+l rrade %kas increased b~ „e%ery '-min t}iere- after until the subiect indicated that she could no lonser eon- tinue the exercise. During the last minute of each incremental stage and'the 1linal minute of exercise 6'E, V,>., and 1'c-0. were meisured. Pt,CO+ and Pc-O~ were measured for the last six seconds of each stage. Hearn rates %kere monitorrd'and re- cordzd the last ten seconds of'each mint-te. RPE was obtained at' the end of .xercise. Fi%r minutes post exercise a~ venous blood's:arple u;u obtained from an antecubitai vein for ear- box%hemoc?obin and lactate anaksis.. lrts9llrmentcFlbn OK?'gen uptake (t'o;) and carbon dioxide output (Vr-D_) were calculated' based on open circuit spirometry. Minute ventila- tion was obtained from a dry gjs meter, adapted to drive a chart recorder. Fractions of expired 0: and CO: were meas- ured from a nt xing chamber using ox\gen (Applied Elzetro- chemis:rc S-3A) and carbon dioxide i Beckman LB-2) analv- zers. P.,CO•_ and PFTO- were measured' at the l6ell of the mouthpiece using a modified triple Jt~alve and pretiiousliv mentioned gas analyzers adapted to the breathing valNe. Ve- nous blood %%as anal.zed for lactate using the Strom Techni- que (Strom 1919): Carboryhemoglobin levels were obtained by co-oximetry (lnstrumentation Laboratory). Statisticallinter+ pretation of the data was completed using either a one-way or two-«a), analysis ol' %ariance with repeated! measures. A Tukey HSD test %%as applied'aposteriori when necessary to determine the exact' nature of the significance. The 0.05 level of signifi+ cance was used for all computations. During the smoke Lrials a pump apparatus was employed t'hat simultaneously smoked cigarettes. captured' the smoke and' pumped the smoke into the inspired air. The cigarettes were smoked by the machine at a rate of one per four minutes at rest and'two per six minutes during exercise. The pump ap- paratus was positioned out of sight of the subjects. No smo- king occurred before the subject had been on the mouthpiece and noseclips for at least 5 min. The pump was turned on for both,trials so tharthe sound of the motor would be similar for both experiments. Also, the subject was given no information as to which trial involved the smoke until both trials were completed. ;v- Results Maximal oxvoen, uptake during the controll trials was 2.39±0!15 1'-min'' or -t11.1-2'.g ml - k^-' - min'' (Fig. I)', Passive inhalation of smoke significantly reduced, the f-(-)-T to 2.13±0,14 1 • min'' or =6,6~_?.6 ml - kt:-' - min'' (p<0-05). I'U a15o reduced the duration of exercise from 25.75±0:85 min to _3.63± 1-1I6 min (P<0:05). The presence of smoke increased the maximal R value from 0.93 ±0.03 during the controls fo 1'.Oli±0.0y indicatine a greater CO: output at a given Vo,. The rating of perceived exertion at the end of the control trials averaged 16.5±0.6 units and was significantly in- creased to 17:4±0:6 units during the smoke triads (Fig. 2). Maximal hean rate responses were simi- lar for both conditions averacine 19414 sor D I ~ L~ __r*-1 i'I1LI L-1! 1 i - v0 SMpn,E NO S1+CKE Nc SmQwEsMCKE sMC>KE s++CKE FES' SuBMAxiunL reamiMnt Ex-cRUSE ExE4::sE Fig. 1. Mean (ySEb-1') Vo: and Vco; (1-min'') at rest and during exercise with (hash marks) and without (open) smoke in- halation. • significant difference (p<0!05), no smoke %s smoke 20r ~ 116 c ~ w a 12 ~ 8 SUBMAXItvtAL MAXIMAL ti.r EXERCISE EXERCISE ~1 Fig. 2. Rating of perceived exertion during submaximal and maximal exercise with (hash marks),and without (apen) smoke ~1 inhalation (Mean ± SES1)i - significant difference (p <0.05) no ~ smoke vs smoke ZVI ~ ~ ~

198 REST $L'BMIYIMLL MLR1MiL ExERC6E EzERCtSE Fig. 3. Heart rate responses at rest and during exercise with (hash marks) and' without (open) smoke inhalanon, (Meant SE'~4). - significant difference (p<0.05)mo smoke vs smoke bts • mini-' (Fig. 3). Post exercise venous blood lactates averaged 6.8 mh! during the smoke trials, significantly greater than the controls (5.5 mM). As note& in, Tabie 1, sintilarities between controls and smoke trials existed for maximal minute ventilation, PFTCO_, an6 PETO2_ The presence of smoke increased the VE/Vo; ratio at maximal ex- ercise from a mean of 30.5 to 33.5 1 of air per liter, of oxyQeni(P<0.05): Submaximali exercise resulted' in an oxygen uptake of 1.82+0.09 I. min-' (31.3± 1.6 ml - kg''- min-') during the control trials which represented 73t3% Vo.T., (Fig. 1). Inhalation of smoke did not significantly affect the submaximal Vo, (1.85 ± 0.08 1- min-') but increased the rela- tive intensity to 76t3p/o of the smoking, trial R. G McMurray et al.: Exercise and residual smoke Po. . The inhalatiomof smoke significantly ele- vatcd the CO2 output by 1100 ml•min''; P<0.05 (Fig. 1). Consequently, R values were also in- creased with passive smoking (con- trols=0.S6±0.02 vs smoke=0.91 ±0.03). Heart rates during the submaximal exercise control trials averaged 172±3 bts • min-' and were sig- nificantly increased to 1178±4 bts • min-' by breathing the smoke (Fig. 2). RPE was also in, creasedduring the smoke trials from 111.8±0.3 to 13:8+1.01 units (Fig. 2). Ventilation was similar for both, trials as was PETCO2 and PETO._ (Table 1). At rest, inhalation of smoke significantly in- creased the average heart from the normal of 81 ± 3 bts • min -' to 90 ± 4 bts • min'' (Fig. 3). Resting oxygen, uptake was 0.23±0.03 I- min-' for the controls and was unaffected by the smoke (0:22'±0.02 1- min-'). Resting ventilation was not altered by the presence of smoke, nor was CO, outtDut or R value. The presence of smoke raised the carboxyhemoglobin hemoglobin levels of the non-smokers from a pre-level of 1.1% to 2.2% at the end of exercise. Discussion The results of this investigation support the con- tention that involuntary inhalation of residual smoke lowers maximal exercise capacity and al- ters submaximdliexercise response. The reduction in maximal performance is directly attributable to the carbon monoxide from the inhaled' smoke binding with the hemoglobin (COHB) and reduc- ing the oxygen carrying capacity: Rowell (1969) and Lamb (1984) have suggested that a maximal Table 1. Respiratory responses during resting, submaximal and maximal exercise with and without the presence of smoke (Mean = SEht) Rest Submaximal Maximal exercise exercise No Smoke Smoke No Smoke Smoke No Smoke Smoke Ventilation 6.97 6.13 50.04 52.51 72.82 71.51 (1 • min'': BTPS) 0.64 0.52 2.33 3.39 5.52 5.42 VE/ Vo ratio 30.8 2&0 27,5 28.4 30.5 33.5 z 1.1 1.4 2.1 2.2 1.9 2:2 End-tidal CO2 34.9 35:4 33.1 31.8 30.9 33.5 (mm Hg), 0.8 0,'7 1.2 1.5 0.9 1.3 End-tidal02 96.8 97.2 98.7 101.5 104!2 104.7 (inm Hg) 1.9' 1.8 2.5 2.4 3.2 2.8

, R G. Rlctiturray et~al.: Exercise and residual',smok: exertional levels, up to 90~,0 of the oxygen carry• ing capacity may'be needed. If the smoke reduces this capacitv; the muscle cannot attaim the high rate of aerobic metabolism unless cardiac output is further increasedL Since maximal' heart rates were similar during the control and~ smoke trials, the cardiovascular system~ seemed' to be maxi- mally taxed. Therefore, any reduction in the ox- ygen carrying capacity would reduce maximal aerobic performance (VO_=Qx(a-r;)0.):. The greater lactate at a lower Yo, during the smoke trials indicates a greater reliarice on anae- robic metabolism. This alteration is attributable to the increased COHB levels. As a consequence of the anaerobiosis, an increase im CO, output via the bicarbonate buffer system would be expectedl Our results support this response as COZ produc- tiom at a given No- was higher during the smoke trials. Therefore, the combined effect of the re- duced oxygen carrying capacity and the concomi- tant increase in lactate resuited in a reduction in subjective maximal aerobic power and the dura- tion of exercise during the residual smoke trials. Examination of our maximal results suggest that the subjects may not have attained t,ue maxi- mal capacity during the smoke or control' trials. Althoueh maximal heart rate responses were within normal ranse for the subject's respective ages, other indicators, such as R' values over 1.10 or lactates over 8'mM (Lamb 1984) suggest that did not reach maximum. Since the subjects were relatively untrained and since the protocol in- volved approximatelv 20 min of high intensity ex- ercise before the incremental work to maximum, it is likely that they fatigued before attaining max- imal' capacity. Wt did note that the Vo, during the screenins was hieher and R values were above 1.10. Therefore, we believe that the efforts during the control and smoke trials represent the best •suhjective effort they could attain. Passive inhallttion of cigarette smoke signif'!i- cantly, adtered' the submaximal heart rate and R values. Heart rates were increased by approxi- mately 6 bts • min't'in an attempt to improve cel- lular oxygenation, as a result of the elevated COHB. The increased R value during submaxi- mal exercise smoke trials may indicate a shift to- ward greater utilization of glucose or glycogen (as a result of the reduced' oxygen). The shift may not be important during short periods of exercise, but di.triitg prolonged exercise the carbohydrate stores cottlci become depleted resulting in an earlier on- set of fatigue (Karlsson 1979). The possibility also exists that the elevated R was a passive result of C0, produced by the cigarettes.. la9 Passive inhalation of cigarette smoke resulted in a 1% increase in carboxyhemoglobin levels of our non-smokers. Personal communications with the United States Environmental Protection Agency have indicated that the carboxyhemoglo- bin levels ofi the present investisation are repre- sentative of breathing air from a smoke filled room. Also, Russell (1973) noted that spending 78 min in a smoke filled room~ resulted in~ carbox- yhemoglobin levels increasii7g an average of one percent. Therefore, we are conf ident that our re- sults are representative of normal passihe inhala- tion of sidestream, or residual smoke and not the direct inhalation from a ciearette. The subject's awareness of the smoke was re- duced by injecting it into the air line from, a hid- den machine. The subjects never came off the mouthpiece or removed the noseclips; thus pre- ventino smelling the smoke. All of the smokers could tell when they were breathins the smoke but none of the non-smokers knew for certain. In fact, two of the smokers told us tne brand name of the cigarettes! Therefore, it seems that the smok- ers were more sensitive to the presence of the smoke, in agreement with Mak_ud and F9aron (1950), Although the number of subjects in the study were relatively small, the results imply that, pas- sive inhalation of cigarette smoke has a signifi- cant detrimental effect on exercise performance, specifically,, by reducing maximal aerobic power and endurance capacity and increasing the need for anaerobiosis. The results suggest people pani- cipating in activities that demand high, intensity for a prolonged period should avoid smoke filled areas. References Bonham GS. Wilson R (1981) Childrens health in families with cigarette smokers. Am J Public Health 51:290-293 Borg GA (1973) Perceived exeniom a note om history and methods. Med Sci Sports 5:90-93 Hirayama T(1981) Nonsmoking wives of heavy smokers have a higher risk of lung cancer: A study from Japan. Br Med'J 282:183-185 Karisson J(1979) Localized muscular fatigue: role of muscle metabolism and substrate depletion. Exercise Sport Sci Rev 1_1-42 Lamb DR (1984) ,Physiology of exercise: responses & adapta• tions. MacMillan Publishing Company, Ntw York Maksud M, Baron A (1980) Physiological responses to eser- cise in chronic cigarette and marajuana users. Eur J Appl Physiol 43: 127- l34'.

2D!? Olkhansky ST (1952) Is smokervnonsmoker segregation, effec- tive in reducing passive inhalation among smokers° Am J' Public He3tth 7^_:737-739' Rowell L'B (1969) Circulation. Nted Sdi Sports 1:15-22 Russell MAH (,1973)1 Absorption by non-smokers of carbon monoxide from room air polluted by tobaeco smoke. Lan- cet li:576-579 R. G McMurray et al.: Exercisrand residual smoke Strom G(1949)',The influence ofi anoxia on lactate uulization iniman after prolonged muscular work. Acta Physiol Scand 17:440-451 White JR (,1978) Effects of residual smoke on nonsmokers, Cn: Landry F, Orban W (eds) Exercise physiology, vol 4 Sym, posium Specialists, Miami, pp 529-533 Accepted February 23, 1985