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The relationship between the hypoxic ventilatory response and arterial desaturation during heavy work Hopkins, Susan Roberta 1988-12-31

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THE  RELATIONSHIP BETWEEN THE HYPOXIC VENTILATORY RESPONSE AND ARTERIAL DESATURATION DURING HEAVY WORK  by  SUSAN  ROBERTA  HOPKINS  B.Med.Sci. Memorial U n i v e r s i t y of Newfoundland, S t . John's, 1978 M.D.  Memorial U n i v e r s i t y of Newfoundland, S t . John's, 1980 A THESIS SUBMITTED IN PARTIAL FULFILLMENT OF THE  REQUIREMENTS FOR THE DEGREE OF MASTERS OF PHYSICAL EDUCATION in  THE  FACULTY OF GRADUATE STUDIES  School of P h y s i c a l Education and Recreation  We accept t h i s t h e s i s as conforming to the required  THE  standards.  UNIVERSITY OF BRITISH COLUMBIA February, 1988  ©  Susan Roberta Hopkins, 1988.  In presenting  this thesis in partial fulfilment of the requirements for an advanced  degree at the University of British Columbia, I agree that the Library shall make it freely available for reference and study. I further agree that permission for extensive copying of this thesis for scholarly purposes department  or  by his  or  her  representatives.  may be granted by the head of my It  is  understood  that  copying or  publication of this thesis for financial gain shall not be allowed without my written permission.  Department The University of British Columbia 1956 Main Mall Vancouver, Canada V6T 1Y3  DE-6(3/81)  ABSTRACT  Arterial intensity  desaturation in f i t athletes,  greater  than  or  equal  t o 90%  during e x e r c i s e at of  VO  max  has  an  been  2 reported remain  by  a number o f  obscure.  respiratory factor this  Inadequate  drive,  i n the  experiment  healthy  yet  the  pulmonary  of  this  ventilatory  s u b j e c t s ( age  etiology  has  been  phenomenon. the  changes  to a  blunted  implicated  I t was  the  yrs.,  as  a  purpose  of  between  to hypoxia  +_ 3.6  these  due  relationship  response  = 23.8  of  ventilation  lung mechanics  to i n v e s t i g a t e  and  male  or  etiology  desaturation  authors  arterial  (HVR).  Twelve  height =  181.6  +_ -1  5.6 cms., W e i g h t = 73.7 + 6.2 k g . , VO max = 63,2 + 2.2 ml .kg . -1 2 .min ) p e r f o r m e d a f i v e m i n u t e e x e r c i s e t e s t on a t r e a d m i l l at 100%  of  max. 2 withdrawn  were every were  VO  15s  Arterial v i a an  throughout  analyzed  analyzer.  w i t h an  Ventilation  samples  indwelling the  f o r pH,  and  VO  , P0 , and 2 2 cannula at rest  arterial  exercise test.  Instrument  PCO  The  blood  Laboratories were  gas  1306  measured  SaO 2 and  samples  blood  by  a  gas  Beckman  2 metabolic  measurement  ventilatory  response  VE  as  SaO  maintain  open  to hypoxia  progressive hypoxia  chamber. to  cart.  circuit  evaluate  2  was  measured  was  On (HVR) induced  a  separate  was  determined  by  adding  changes  gases,  N  a  mixing  oximeter;  were added 2 m e a s u r e d was  ventilation,  and  the  recording  CO  ANOVA f o r r e p e a t e d  i n blood  by  to 2 u s i n g a H e w l e t t - P a c k a r d ear  i s o c a p n i a s m a l l ammounts o f system.  occasion  VO  to  the  used .  to  Simple  2  linear evaluate  regression the  and  multiple  relationship  between  linear the  r e g r e s s i o n was  changes  i n SaO  used and  2  HVR  to  and  the  descriptive  decline test  S u b j e c t s showed  in arterial  saturation  and  < 0.01,and  p < 0.01).  Four  (p  modest  variables.  decreases  i n SaO  to  (94.6  PO  over 2 subjects  +_ 1 . 9 % ) ,  a  the  significant  c o u r s e of  (Mild)  the  exhibited  three  (Moderate)  2 showed  an  intermediate  (Marked)  demonstrated  (SaO  90.0  =  response  91.6 +_ 0.1%) 2 decrease i n arterial  a marked  + 1.2%).  The  (SaO  differences  2 Mild  and  0.01); VE,  VO  by  the  Marked  there  groups  w e r e no  were s i g n i f i c a n t  significant  i n P0  and  2 ( p <  differences  and  five  saturation  SaO  between 2  0.05,  and  between  p  groups  < in  , pH o r PCO . T h e r e was no s i g n i f i c a n t c o r r e l a t i o n b e t w e e n 2 2 the l o w e s t • SaO r e a c h e d a n d HVR, o r any of the descriptive 2 variables. N i n e s u b j e c t s d i d n o t r e a c h m a x i m a l VE ( a s d e t e r m i n e d VO  exhibited maximal  2  max  similar VE,  desaturation.  test)  on  the  ventilation,  but  fell  Oxygen  and  into uptake  exercise  test,  two  the remaining s u b j e c t  the M i l d exceeded  group that  with  subjects exceeded  respect  recorded f o r the  to VO 2  max  determination  group; values. related  the It  for four  remaining was  of  the  subjects  concluded  to blunted hypoxic  that drive.  five  subjects  demonstrated arterial  in  lower  the or  desaturation  Marked similar was  not  T A B L E OF  CONTENTS  Abstract  .. i i  List  of Symbols  List  of Tables  List  of F i g u r e s  v .. v i „.. . v i i  Acknowledgements  .viii  Introduction  1  Methods  5  Results  .9  Discussion  '.  ...17  References  28  Appendix A Review  of l i t e r a t u r e  34  Ventilation  during  Respiratory  drives  Respiratory  factors limiting  Hypoxemia  during  Hemoglobin Arterial B PO  exercise  34 36 performance  exercise  affinity  42  f o r oxygen  desaturation  during  s a t u r a t i o n normogram  39  during  heavy  exercise  exercise  % f o r whole  blood  45 46 51  2 C Subject  physiologic  D Pulmonary  function  E Hypoxic v e n t i l a t o r y F Subject  data  52  tests  .53  response  data  G Equipment  54 55  and s u p p l i e s  61  H Consent form  62 i v  L I S T OF  FEV  forced  expiratory  forced  vital  SYMBOLS  volume  i n one s e c o n d  1 FVC 2,3-DPG + H  capacity  2,3-diphosphoglycerate hydrogen i o n  HVR  hypoxic ventilatory  HCVR  hypercapnic ventilatory  PCO  partial  pressure  response response  of carbon  dioxide  2 pH  negative  PO  partial  2 SaO . 2 VE VO max 2  arterial  logarithm pressure oxygen  of hydrogen  of  oxygen  saturation  expired  minute  ventilation  maximal  oxygen  consumption  ion concentration  LIST Table  I  Table  II  Physiological 15  second  blood  OF  TABLES  characteristics  i n t e r v a l measures  v a l u e s , VO  and  9  for  arterial  ventilation  for  2 Table  III  Table  IV  all  subjects  Anova  results  Differences oxygen  11 ......14  in ventilation  uptake  between  VO max  and  maximal  determina-  2 Table  t i o n and f i v e - m i n u t e e x e r c i s e t e s t HVR a n d s p o r t f o r e a c h s u b j e c t  vi  15 16  L I S T OF Figure Figure  1. 2.  Changes  i n PO  Changes  2 i n SaO  FIGURES over over 2  vii  time time  12 .13  ACKNOWLEDGMENTS The  finished  combined time,  effort  effort  available  at  o f many  and b l o o d , a l l hours  members who r e v i e w e d grateful. advisor all  I extend and f r i e n d  phases This  product  of t h i s thesis  that  people:  this  thesis  my s u b j e c t s  my d a t a  collection  of t h e day.and  and a d v i s e d . special  represents who  gave  donated  assistants,  night,  their  who w e r e  a n d my  committee  To a l l o f y o u I am  sincerely  a p p r e c i a t i o n to Dr.  who f r e e l y  i s the  time  Don M c K e n z i e ,  and energy  my  t o me  during  and  Barbara  project. i s dedicated  H o p k i n s who s e t t h e p r e c i d e n t  t o my p a r e n t s ,  f o rhigher  Bob  education.  INTRODUCTION  In  healthy  system  i s  not  performance research  generally  during  (Dempsey  Wollcock, in  individuals  thought  maximal  et a l . ,  1978; W i l l i a m s  arterial  e x e r c i s i n g at sea level  oxygen  t o be a  aerobic 1984;  tension  suggests  the r e s p i r a t o r y system  work  particularly  outputs.  temperature, produce  During  a rightward  curve,  resulting  of  to  97  (Thompson on  0  i n  shift  of blood  may  the combined  i n the oxygen  i s minimal  effect  of this  at the lung  This  limiting high  increasing  hemoglobin  to  cause  tasks.  of  and  decline  of very  effect  i n s a t u r a t i o n from  The  a  of  capable  94  recent  to  i n 2,3-DPG,  to approximately  1974).  exercise  be c a p a b l e  individuals  i n a decline  and Dempsey,  maximal  to  1984; Young  magnitude  pH a n d a l t e r a t i o n s  98% s a t u r a t e d  content  during  exercise  decreased  factor  However,  et a l . ,  of s u f f i c i e n t  of hemoglobin  performance,  pulmonary  e t a l . , 1986) has demonstrated  desaturation that  limiting  exercise.  Powers  the  combine  to  dissociation a  normal  95%  value  saturated  rightward  where  shift  the  partial  2 pressure oxygen  of oxygen partial  release muscle  pressures  of oxygen, cell  exercise, arterial  are low,  dating  above  at the working  the net effect  the diffusion  (Thompson  desaturation,  described  However,  preserving  mitochondria  Arterial changes  i s high.  has been  from.1919,  that  reported  when  s a t u r a t i o n to 85% immediately  1  than  Harrop  i s  gradient  and Dempsey,  greater  muscle  where  increasing into  the  1974). expected  during observed  very  from  the  intense  a decline i n  f o l l o w i n g heavy  exercise.  in  very  highly  trained i n d i v i d u a l s with  exercising  at  an  (Dempsey e t  a l . ,  exercise 1984;  intensity  Powers et  a high  greater  a l . ,  aerobic  than  1984;  90%  capacity  of  maximal  Williams  et  a l . ,  1986) . Maximal aerobic  oxygen  performance  (DiPrampero, increasing 1954; (Buick  partial  et  et  1978),  considered  factors  such  circulation exert of  pressure  1980)  and  decrease  with  Welsh,  1987  as  the  max  oxygen  i s set  In  by  with  maximal  of  two  oxygen  the  legged  acute  to a e r o b i c  oxygen at  red  factors  cell  hypoxia  transport  diffusion  some c o n s t r a i n t .  VO  limitation  mitochondrial oxygen  number  f o r r e v i e w ) and  main  be  a  hence  max i s o b s e r v e d t o i n c r e a s e with 2 o f o x y g e n ( B a n n i s t e r and Cunningham, and  the  and  VO  others)  to  and  max),  2 by  and  a l . , 1982;  (VO  limited  As  1970;  Buskirk, a l . ,  is  1985).  Kaisjer,  been  consumption  infusion  (Squires anemia  and  (Woodson  performance  system.  Clearly,  utilization, working  has other  peripheral  muscle  can  also  exercise, approximately  transport  with  the  75%  remaining  25%  capacity  and  2 being  equally  peripheral be  seen  delivery  diffusion  limit  although may  be  and  that  arterial  and  decreased  significantly a  accounted  to  effect VO  max 2"  VO can  some a u t h o r s on  the  order  performing  at  maximal  performance  may  be  for  by  perfusion  mitochondrial (Diprampro,  desaturation  2  diffusion max. be  The observed  leading  to  gradient  at  level has  (Squires  and  of  percent.  four  levels  any  significant.  2  1 9 8 5 ) . Thus  of  Buskirk, In  decrement  decreased the  been 1982) the in  can  oxygen  muscle  desaturation  not  i t  at  can which  established, feel  that  i t  elite  athlete  maximal  aerobic  A these  variety  observations  perfusion  latter issues  may  pulmonary (Dempsey 2.  1987).  considered  pulmonary  respiratory  et  Current  may  to account  be  the  ,  ventilation  diffusion  limitation  t h i n k i n g suggests  most  likely.  for  that  T h u s two  the main  :  ventilation  system  proposed  h y p o v e n t i l a t i o n and  explanations be  been  including v e n o a r t e r i a l shunting  Williams,  two  blunted  mechanisms have  inequality ,  ( P o w e r s and  1.  of  i s not  d r i v e or  t o meet t h e  adequate  of  e i t h e r as  a mechanical  high  levels  of  a result  inability  of  of  ventilation  the  required  a l . , 1984).  pulmonary  ventilation  limited  by  shortened  diffusion  distance  pulmonary  blood  red  due  flow  i s adequate  to  cell  localized  (Dempsey  et  but  diffusion  of  transit  time  or  edema a t  very  high  a l . ,  1984;  oxygen  is  increased levels  P o w e r s and  of  Williams,  1987) . It  has  ventilation breathe  been  represent  with  breathing  suggested  the  the  et  ( Martin  low  ventilatory  demonstrated athletes.  in  Therefore  exercise  individuals of  this  hypoxic  is  with  study  a was  ventilatory  to  chemical  is  logical  et  response  examine response  to  arterial may to  the and  by  et  be  the  work  in  1979)  with  exercise  have  that  desaturation more l i k e l y  in  a  been  non-endurance  consider  Thus  relationship  to of  a l . , 1 9 7 9 . ) and  a l . ,  hypoxia.  changes  exercise  stimulus  a decrease  a t h l e t e s compared  desaturation  blunted  the  Martin  (Martin  factor in  that  Both  1978a;  response  i t a  1985).  a l . ,  endurance  hypoventilation intense  et  factors determining  c o n s t r a i n t s imposed  a l . ,  ventilation  the  i n t e g r a t i o n of  mechanical  (Dempsey  hypoxic  that  during  in  the  those purpose  between  arterial  i f  the  oxygen  saturation athletes  in  during  healthy high  endurance  and  non-endurance  i n t e n s i t y e x e r c i s e at sea  4  level.  trained  METHODS  A  non-probability  selected study. and  from  a  total  Criteria  sample of of  16  maximal  for participation  oxygen  healthy  i n d i v i d u a l s who  r e s p i r a t o r y f u n c t i o n , normal  and  12  consumption  (VO  max)  subjects  volunteered  included  arterial  male  normal  was  for  the  cardiovascular  c i r c u l a t i o n to the hand -1 -1 _> 60 ml.kg .min . Of  2 the  sixteen  volunteers,  requirements catheter the  and  was  experiment on  endurance  and  that  Pulmonary  division  to  of  A  the  informed  arterial  consent  British  total  of  and  Columbia  six  elite  a t h l e t e s were r e c r u i t e d . I t  subjects  sports  between  would  predominantly  give  a  range  of  hypoxia.  physical  f o r each  flow  autospirometer  speed  gave  eligibility  of  U n i v e r s i t y of  non-endurance  rate, (Minto  oxygen  was  uptake  until  gases  was  volitional performed  one  to  two  weeks  i n c l u d i n g FVC, carried  Medical was  t r e a d m i l l (Quinton -1 was 3.08 m.sec and  minute  characteristics  subject  function testing  peak  graded  the  the  Data  determined  Maximal  by  meet  insertion  A l l subjects  non-endurance  Descriptive  and  to  Experimentation.  the  responses  failed  subject  approved  six elite  and  ventilatory  Baseline  was  Human  predicted  endurance  one  unsuccessful.  Committee  was  in  three  out  Science  %  Co.  fatigue.  predicted subject  utilizing  a  test.  Analysis  of  by  were testing.  FVC,  model  increased  (Beckman M e t a b o l i c  max  2 to  Ltd.,  24-72 t r e a d m i l l ) was  VO  prior  f o r each  determined  this  and  FEV  using  , 1 an  AS-700). continuous  The  0.22  expired  Measurement  starting -1 m.sec per  respiratory Cart)  and  measurements were 3052A  data  average  acquisition  of  oxygen  tabulated  the four  uptake.  treadmill  system  highest  This  velocity  every  15  .  VO  max 2 consecutive  result  which  seconds  was  by  was 15  a Hewlett Packard  determined second  used  r e p r e s e n t e d 100%  the  measures  to  o f VO  by  of  calculate  a  max. 2  Exercise  Test  Subjects later  having refrained  exercising of  a five  by  were a s k e d  i n the minute  a five  to r e t u r n  from  last  24  hours.  treadmill  minute  eating  again approximately i n the  The  last  two  exercise  hours  protocol -1  one  week  and  from  consisted  warm-up a t 3 . 0 8 - 3 . 5 2 m.sec  run at a speed  that  corresponded  followed  to  100%  of  V0 2  max .  Data C o l l e c t i o n Prior (Arrow,  to the e x e r c i s e #  20  percutaneously with  local  sterile  before  by  Jelco  the r i g h t  radial  anaesthetic  cannula  tube  normal  saline  was  u/1)  had  withdrawn  Each  subject  via  was  and  and  attached. with  the  #22  was  artery  A minimum way  saline  inserted infiltration and  for  using adequate  (Allen's volume  (1.2  s t o p c o c k (PVB) patency to which  was  test) cc) filled  maintained  heparin  sodium  the o n s e t of s a m p l i n g the  saline  arterial  6  after  checked  cannula  was  Hydrochloride)  Cannula  normal At  two  arterial  gauge)  artery,  the u l n a r  inserted.  been added. and  indwelling  (1% Xylocaine  (Cutter)  frequent flushing  (2000 was  in  an  or  circulation  the  extension with  gauge,  technique.  collateral  test,  samples  were  anaerobically  collected  in pre-heparinized  sampling  (15  between  samples,  patent  s)  until  did  the  Arterial the  onset  the  start  not nor  end  of  blood  of  the  of  allow  for  i t required.  the  sampling  session  Each  2  using  ml a  was  test  was  Instrument  and  and  at  analyzed  15  of  and  batch  calibration  prior  to  a n a l y s i s and  analyzed  for  on  one  blood  performed.  of  collection  a  Gas/  two  point  calibration  The  samples  calculated temperature  as  were  previously  temperature  Exercise  measured  pH  PCO  core  at  f o r VO  15  was  ventilation second  max  not and  measured expired  intervals  by  during  gas  the  the  be  Blood  point  sample.  The  ice until  minutes  using  to after  , and PO ; o x y g e n s a t u r a t i o n (SaO ) 2 2 2 automatically. The s a m p l e s w e r e n o t corrected  collection.  pH,  samples.  calibrated  every  prior  intervals  automated  was  after  remained  immediately  21  1306  machine  peformed  cannulas  analysis could  This  automatically  in saline  maintained  Analyzer.  batch  of  heparin  second  w i t h i n .90  Laboratories  frequency  period.  for a total  complete  sample  All  samples were w i t h d r a w n test  The  r e i n f u s i o n of  s a m p l e s were a n a e r o b i c a l l y capped test  syringes.  was  exercise  the  plastic  the  was were was for data  concentration  system  described  determination.  2 The  subjects  responses  returned  were measured  Weil  et  a l . ,  (1970).  from  a  mixing  chamber  Rudolph  valve.  Under  hypoxia  was  mixing  chamber.  Packard  induced  47201A  by  using  third  (volume  continuous the  time  the  hypoxic  =  subjects  13.5  1),  cardiac  a d d i t i o n of s a t u r a t i o n was  oximeter  and  a m o d i f i c a t i o n of  Basically  Oxygen ear  a  and  the  ventilatory  the  method  breathed  room  through  monitoring,  100%  nitrogen  measured amount  of  a  of air  two-way  progressive gas  via a  into  the  Hewlett-  nitrogen  was  increased 80%  at  one m i n u t e  was r e a c h e d .  isocapnia  intervals  End t i d a l  PCO  until  was m e a s u r e d  2 _+ 2 t o r r  was m a i n t a i n e d  an o x y g e n  of  (Beckman LB-2)  by t h e a d d i t i o n  gas d i s t a l t o t h e m i x i n g 2 v i a a l o w r e s i s t a n c e pneumotach  saturation  of very  and  small  a m o u n t s o f 1 0 0 % CO  chamber.  was  a n d a n d t h e d a t a was  measured  recorded  and  accquisition program  until  A  used  to  between  SaO  were  seconds  BMDP P:1R, determine  simple the  v i a an linear  slope  of  IBM  regression, the  linear  above  i n v e n t i l a t i o n c o u l d be e x p l a i n e d 2 i n SaO (R _> 0 . 7 ) o r u n t i l consistant 2  software,  to s t a t i s t i c a l l y  ventilation, P:2R,  a n d V0 Multiple  relationship  over  test time.  P : 2 V , ANOVA f o r r e p e a t e d changes  2 Linear Regression  between  changes  HVR.  i n blood  P:1R, S i m p l e  i n SaO  measures  gas  parameters,  Linear  Regression,  were used  to determine the  and d e s c r i p t i v e 2  including  tested  Analysis  BMDP s t a t i s t i c a l used  data  obtained.  Statistical  and  15  70% of t h e v a r i a t i o n  the b a s i s of changes  values  was  every  and v e n t i l a t i o n . S u b j e c t s were 2 i s o c a p n i a was m a i n t a i n e d w i t h i n t h e r a n g e s p e c i f i e d  until  on  system.  was  relationship  and  tabulated  Ventilation  variables,  RESULTS Baseline  Measures  Mean  values  for are  the  twelve  subjects  results  were w i t h i n n o r m a l  physiologic  reported  i n Table  limits  Means +  Pulmonary  function  S.D. 23.8  HEIGHT ( c m s )  +  3.6  181.6+5.6  WEIGHT ( K g ) max  .  the  CHARACTERISTICS  (yrs)  VO  I  of  for a l l subjects.  TABLE I . PHYSIOLOGICAL  AGE  characteristics  (ml.kg  .min  )  73.7  +  6.2  63.2  +_  2.2  2  The runners  subjects (10  Olympic one  km,  medalist),  team.  respective  three  cyclist  All  sports  at  minutes  of  of  full  and  fifteen  from  testing  twelve  Means  and  from  but  standard  9  (400,  training  one  800  m), field  for  their  Exercise completed  subject  terminated  analysis,  and  the i n v e s t i g a t i o n . -  subjects  data  distance  C a n a d a ' s Pan-Am  were a c t i v e l y  remaining  The  long  collegiate  runners  member o f  of  three  (one  distance  Gases With  t i m e and  seconds.  statistical  purposes.  the  e x e r c i s e . The  the  one  time  Blood  oarsmen  middle  and  the  triathletes,  two  subjects  Changes i n A r t e r i a l Eleven  two  marathon),  competitive  hockey  included  the this  was  unable  test  after  subject  were r e t a i n e d deviations  the  for  full to four  were for the  five  complete minutes excluded  descriptive 15  second  interval  measures  subjects  who  completed  Resting normal  of  values  limits  pH,  PCO  PCO  for a l l subjects.  a significant  (F - 141,  occured;  pH  from  7.21+0.06  a t t h e end o f f i v e  all  subjects  there  was  2 respect  directed  groups.  Mild  little  only  2 2 are reported  r e s t i n g value  minutes  decline  within  from  intense acidosis  Averaged  to over  ( F == 2 6 . 1 , 2 fell  into  p  three  i n PO  subjects  fell  (Moderate) responders,  decline  were  7.43+0.03  i n P0  Subjects  eleven  a n d SaO ; f u r t h e r a n a l y s i s 2 2 characterizing differences between these  three  and Marked  the  i n Table I I .  of  of e x e r c i s e .  p < 0.001).  t o changes  towards  As  intermediate from  ( F =64.8,  in  p < 0.001) m e t a b o l i c  was a s i g n i f i c a n t  < 0 . 0 0 1 ) a n d SaO groups with  a  a n d SaO  , PO , a n d SaO , 2 2 2 As w o u l d be e x p e c t e d  exercise  declined  PO  2 test  the f u l l  f o r pH,  ,  groups  only.  into  Figures Four  group  of  1 and. 2 r e p o r t  data  subjects  the  (Mild)  showed  i n PO  and 0 saturation, with r e s t i n g values of 2 2 PO at 105.8+12.6 t o r r (SaO 98.2+0.6%) d e c l i n i n g to 87.5+5.7 2 2 t o r r (SaO 94.6+. 1.9%) a f t e r t h e f i v e m i n u t e e x e r c i s e t a s k . Three 2 subjects ( M o d e r a t e ) d e m o n s t r a t e d a n i n t e r m e d i a t e d e c l i n e i n PO 2 and SaO , w i t h r e s t i n g P0 1 0 2 . 5 + 3 . 5 (SaO 98.2+0.1%) declining 2 ' 2 2 to 76.5+_2.1 t o r r ( S a O 91.6+ 0 . 1 % ) . The r e m a i n i n g f i v e subjects 2 (Marked) demonstrated a marked decline i n saturation with resting  PO  d e c l i n i n g from  71.4+3.5  2 torr  (SaO  used  to determine  2  90.1+  111.0+8.9  1.2%).  differences  AN0VA  between  torr  98.5+0.4%) 2 • f o r mixed model d e s i g n mild  (SaO  and marked  to was  groups f o r  P0  , SaO , pH, PCO , V0 , a n d VE. The results of these 2 2 . 2 2 s t a t i s t i c a l analyses are presented i n Table I I I . As w o u l d be expected  during  intense  exercise,  10  averaged  over  a l l  TABLE II 15 SECOND INTERVAL MEASURES FOR ARTERIAL BLOOD VALUES,VO , AND VENTILATION FOR ALL SUBJECTS: 2 (Mean + SD.) TIME (rain) pH  R  0:15 0:30 0:45 1:00 1:15 1:30 1:45 2:00 2:15 2:30 2:45 3:00 3:15 3:30 3:45 4:00 4:15 *4:30 *4:45 *5:00  7.43 7.45 7.45 7.43 7.42 7.40 7.37 7.36 7.34 7.33 7.32 7.31 7.29 7.28 7.27 7.25 7.25 7.25 7.23 7.23 7.21 0.03 0.02 0.02 0.02 0.03 0.03 0.03 0.03 0.03 0.03 0.04 0.04 0.04 0.05 0.05 0.05 0.05 0.06 0.05 0.06 0.06  PQ02 (torr) 36.3 35.9 37.8 37.3 38.1 38.4 38.3 38.6 38.5 38.0 38.2 38.0 37.4 37.5 38.4 36.9 37.2 36.9 36.6 36.2 36.4 4.3 3.5 2.7 2.5 2.0 2.7 2.0 2.2 2.2 2.3 2.8 2.1 2.5 2.2 2.6 2.5 2.6 2.6 3.0 2.7 3.3 P02 (torr) Sa02 (%) V02(l/min) YECl/ndn BTR  107 112 102 9.2 14.4 11.5  93 8.9  89 7.5  89 7.8  89 6.8  89 9.0  88 8.6  86 9.3  85 9.2  83 83 9.2 10.1  82 9.0  81 9.6  82 9.9  80 9.6  79 7.5  79 8.5  78 7.5  78 8.6  98.3 98.4 98.0 97.2 96.9 96.8 96.6 96.3 96.0 95.9 95.3 94.9 94.6 94.3 93.7 93.8 93.1 92.8 92.6 92.3 92.0 0.44 0.9 0.9 1.0 0.9 0.9 0.9 1.2 1.2 1.4 1.3 1.5 1.6 1.7 2.1 2.1 2.2 1.9 2.2 2.2 2.5  -  1.53 2.36 3.78 4.13 4.08 4.17 4.27 4.29 4.29 4.31 4.38 4.41 4.31 4.44 4.50 4.57 4.44 4.61 4.56 4.43 0.56 0.51 0.62 0.48 0.43 0.39 0.46 0.48 0.39 0.50 0.45 0.44 0.34 0.49 0.42 0.42 0.51 0.44 0.43 0.51 57.8 78.4 102.1 115.2 120.9 127.5 134.5 139.2 138.2 141.2 143.7 143.9 142.6 145.3 145.7 148.0 145.8 149.8 149.1 148.0 19.5 16.5 20.5 21.3 18.4 17.1 17.6 18.9 18.2 18.6 17.8 16.7 17.6 17.4 17.0 13.0 17.4 15.3 13.6 17.3 * N = 11 subjects  100  subjects, over  there  time.  degree  The  both  significant  t h e Marked  PO  than the  differences i n  interaction,  a l lvariables  which  reflects  the  g r o u p s e x h i b i t e d t h e same c h a n g e o v e r  time  d i f f e r e n c e s f o r PO  for  two m e a s u r e s w e r e s i m i l a r  then 9  g r o u p by t i m e  to which  revealed these  were s i g n i f i c a n t  group  f o r both  demonstrated a  M i l d group.  and  SaO .  2  2  groups u n t i l  steeper  r a t e of  T h e r e w e r e no s i>gn i f i c a n t  z b e t w e e n g r o u p s f o r pH, PCO , VE,  Values  one m i n u t e , decline  in  differences  a n d V0 .  2  2  T A B L E I I I . AN0VA RESULTS VARIABLE PO  9 SaO pH  2  GROUP  TIME F ( p )  9  (<0.001)  2 . 7 (<0.001)  20. 1 (<0.01)  64.8  (<0.001)  9.8 (<0.001)  1 .0 O 0 . 0 5 )  96.0  (<0.001)  2. 1  1 . 1O 0 . 0 5 )  91.4  <1 .0  Fifteen  during values be  second  2  recordings  are presented the  the  obtained seen  ventilation  i n Table  five  minute  during  t h e V0  (<0.001)  that nine during  1 . 1O 0 . 0 5 ) <1 .0 <1 .0  f o r VE a n d V0 II.  Maximal  exercise test  2  <1 .0  (<0.01)  83 . 2 (<0.001)  C h a n g e s i n VE a n d V0  subjects  TIME F ( p )  22.4  VE VO  GROUP x  10.1 (<0.05)  <1 .0  PCO  can  F(p)  2  ventilation are  and  i n Table  subjects  t h e V0 max d e t e r m i n a t i o n  twelve  contrasted  max d e t e r m i n a t i o n  of the twelve  f o r the  achieved  than  during  V0  2  with  III.  It  higher the f i v e  2 minute and  test.  I n two, t h e v e n t i l a t i o n  i n one s u b j e c t  peak v e n t i l a t i o n 14  was s i m l i a r was h i g h e r  on t h e two t e s t s during  the  five  minute five  exercise  minute  test.  exercise  individuals  Four  on t h e 2 t h a n on t h e VO max d e t e r m i n a t i o n . T h e s e 2  test  a l l fell  subjects  info  achieved higher  t h e marked  group  VO  with  respect  to  desaturation. TABLE I V D I F F E R E N C E S I N V E N T I L A T I O N AND MAXIMAL OXYGEN UPTAKE BETWEEN V02 MAX DETERMINATION AND F I V E MINUTE E X E R C I S E TEST GROUP S U B J E C T  OXYGEN CONSUMPTION ( l i t e r s / min) V02MAX  VENTILATION ( l i t e r s / min  %  5 min  100.0 91.3 92.4 93.6  MILD  1 . 2 . 3. 4.  4.78 4.58 4.46 4.99  4 .78 4. 18 4.12 4.67  MOD  5. 6. 7 .  4.51 4.13 5.17  4.30 4.11 5.08  MARKED 8 . 9. 10. 11 . 12 .  4.39 5.45 4 .10 4.58 4.54  92 . 7 4.01 101 . 1 5.51 4.32 , 105.3 4.82 105 . 2 4.60 101.3  95.3 99 . 5 98.3  VEmax  VE  186.4 127.2 166.0 178.2  169.0 140.8 135.8 140.5  90. 111. 81 . 78.  145.1 142.4 148. 2  142.0 132.0* 149.3  97 . 92 . 100.  158. 2 191.8 148.6 162 . 7 143. 2  143.1 182 . 7 151.9 154.9 137.9  90. 95. 102 .  * obtained Hypoxic  ventilatory  The subject  measured  within  classified  as  diminished analysis Moore  hypoxic ventilatory  our  sample  normal  response  of  (N)  (B).  96.  a t 4:15  appeared  distinct  into  t o be two Six  and  subjects  s i x as  these groups  having  and C a m p b e l l , ( 1 9 7 4 ) of the l i n e  i n SaO  was f o u n d 2  15  were a  was b a s e d on  by F l e e t h a m e t a l . , ( 1 9 8 0 ) ;  The mean s l o p e  p e r 1% c h a n g e  f o r each  responders  e t a l . , ( 1 9 8 2 ) ; Rebuck  ventilation  98.  r e s p o n s e and s p o r t  subjects.  Division  of data published  Woodley,(1975).  %  5min  response  i s r e c o r d e d i n T a b l e V. T h e r e  groups  BTPS)  Grindlay-  and Rebuck and  described  by c h a n g e i n -1 t o be 1.08 1 .min .1%  -1 ASaO  ;  2 reflecting  -1 -1 l.min. .1% ASaO 2 the p o s i t i v e l y skewed d i s t r i b u t i o n of v a l u e s . standard  TABLE V  deviation  was  0.97  HVR AND SPORT FOR EACH SUBJECT (n = 12)  SUBJECT 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11 . 12.  SPORT  HVR (A VE/l%ASa02) N or B (l.min. l%ASa02)  F i e l d hockey 400 m, 800 m rowing 800 m marathon marathon triathlon 400 m rowing triathon 10 k cycling  0.43 0.43 0.78 1.12 1 .05 1 .03 0.22 0.22 1.22 0.87 0.43 0.26  B B N N N N B B N N B B  -1 (l.min 1 .02 + 0.15 0.33+0.10 0.67+0.36  MEAN  normal diminished all  Relationship  of HVR to a r t e r i a l  Correlation relationship lowest  was  -1 ' )+ S .D  desaturation performed  to  determine  between... the hypoxic v e n t i l a t o r y response  observed  coefficient  analysis  .l%ASa02  of  and  the the  SaO . This analysis yielded a correlation 2 0.06, which was n o n - s i g n i f i c a n t (F<1.0). A  multiple  regression  between  the  a n a l y s i s revealed  no s i g n i f i c a n t r e l a t i o n s h i p  degree of a r t e r i a l desaturation  and  the  dependant  v a r i a b l e s age, height, weight, V0 max, or t r e a d m i l l speed of each 2 subject.  16  DISCUSSION Arterial subjects  desaturation  tested.  parameters  The  during  occured  t o some e x t e n t  traditional  exercise  has h e l d  view  of changes  that  PO  i n a l l of  the  i n blood  gas  i s relatively  stable  2 and  alterations  during  intense  magnitude  t o cause  observed  i n the l i t e r a t u r e  been  attributed  increasing  community,  not  possibly  during  evidence  demonstrate  0-Barr  Perhaps SaO  2  study, high  any  sixteen metabolic  and  has been  changes  saturated)  have  decreasing  Dempsey,  pH,  19 74)  because  ignored  of d i f f i c u l t y  exercise  or because  less  changes  intense  as e a r l y by  and  as  the  of the  1919  scientific  i n obtaining  arterial  preponderance  exercise,  which  does  i n PCO  o r PO (Bjurstedt 2 2 e t a l . , 1964; S u s k i n d e t a l . , 1950). study  i n v e s t i g a t i n g changes  i n t h e w o r k o f Dempsey e t a l . , endurance  rates  insufficient  The s m a l l  of  reported  generally  during  of  et a l . , 1980).  t h e most c o m p l e t e  i s found  effects  (Thompson  was  maximal  obtained  W i g e r t z , 1971;  and  but  t o 94-98%  combined  (Klein  are  of hemoglobin.  (decline  desaturation  1919),  samples  the  i n 2,3-DPG  Arterial  of  to  temperature  alterations  (Harrop,  desaturation  exercise  (VO  (1984).  and  i n PO In  2 this  athletes, max  capable of s u s t a i n i n g very -1 -1 72+_2 m l . k g .min ) performed a  =  2 progressive saturation pH,  PCO  exercise  was m e a s u r e d  ,and PO 2  cannula.  It  demonstrated to  an  test  PO  2 was  t o maximum  a decrease of l e s s than  treadmill.  by means o f a n e a r o x i m e t e r ,  were measured found  on a  Hemoglobin  and  arterial  by means o f an i n d w e l l i n g  arterial  that  eight  in arterial 75 t o r r .  2 17  of  oxygen The m o s t  the  sixteen  content severe  subjects  o f 21-35 hypoxemia  torr, was  associated  with  little  helium  breathing  unload  the  was  or  no  used  alveolar  to  reduce  r e s p i r a t o r y muscles  hyperventilation.  turbulent  exercise  flow  When  and  ventilation  thus  increased  substantially. The heavy the  mechanisms a c c o u n t i n g  work  have not  possible  arterial  limitation  4.  and  introduction  the  1-1.5% of are  venous  circuation  decline  shunt:  blood  bronchial  of  of  this  the  At  speculation  following  rest  i n the  cardiac  output  shunted  via  blood  therefore  i n oxygen  cause  the  however  during  areas:  as  1.  to  veno-  diffusion  hypoventilation.  (approximately of  considers  desaturation  2 . v e n t i l a t i o n - p e r f u s i o n i n e q u a l i t y . 3.  Veno-arterial  volumes  been e l u c i d a t e d ,  causes  shunt.  for a r t e r i a l  supply do  not  poorly  tension decline  individual  (Bachofen the  et  into  PO  no  blood  small 1973))  veins  the  p a r t i c i p a t e i n gas  in arterial  a l . ,  thebesian  directly  oxygenated  in  healthy  systemic  exchange.  results in a  blood.  and  The small  If shunting  change would  be  were  expected  in  2 oxygen In  tension  fact  this  with i s not  correcting  the  (Dempsey  al.,  1985)  et  and  1985).  at  the  i n t r o d u c t i o n of  the  case,  hypoxemia 1984;  altitude  seen  Gale ( Gale  et et  perfusion  of  the  gravity  the  does  apex.  the  base  maximal  lung of  are  the  during al.,  exercise  1985;  lung  and  then  for  18  due  to  a greater  perfusion  arterial  of  hyperoxia  at  sea  Torre-Bueno  must a c c o u n t  receives  mixture.  Torre-Bueno  1985;  non-uniform:  gas  exist  inequality: Generally  If ventilation exercise  reports  al.,  T h u s some o t h e r . m e c h a n i s m Ventilation-perfusion  during  as  a hyperoxic  this  level et a l . ,  et  al.,  phenomena.  ventilation the  effects  blood  flow  inequality  hypoxemia  and of than  increased  would  also  increase the  as  lung.  both  passed  During  apical  tending At  blood  to  more  low  intensity  ventilation  greater intense  which  changes  levels  are  i n PO  Diffusion arterial  limitation. transit  In  time  circulation  is  equilibration reaching to  well  high  seconds  or  flow.  If  areas  of  lung,  than  0.25  could the  pulmonary  fluid also et  be  i n the explain  during  the  time  required  In  the  mean t r a n s i t  i s also  transit  times et  et  to  etiology  of  may  be  diffusion  exercise  the for  complete  a t h l e t e capable time  may  be  in  to  Diffusion  capillary  lead  fluid  and  an  Thus d i f f u s i o n  in arterial  to  less  distance  i n t r a v a s c u l a r pressures  space.  reduced  underventilated  i f high  leak  of  pulmonary  f u r t h e r reduced  1982).  the  pulmonary  increased  changes  a l . , .the  to  increases  directed  a l . ,  to  in  for  heavy  through  blood  (Dempsey  relates  cell  secondary  interstitial the  exercise  blood  levels,  lung.  changes  account  possible  seconds).  less,  the  seconds  also  0.25  to  result  the  ( Gale  in  exercise.  individual  red  work  blood  the  heavy  of  minor  found  of  increase  overall  areas  only been  i s an  the  different  Another  within  (about  very  0.40  the  there  i n magnitude  maximal  sedentary  v e - n t i l a t e d segment  with  exercise  sufficient  during  for  exercise  within  limitation:  the  poorly  perfusion  of  during  hypoxemia  a  i n e q u a l i t y have  not  seen  2  and  homogenity  ventilation-perfusion 1985)  through  within  increase  limitation  s a t u r a t i o n observed  in may  (Dempsey  a l . , 1982). Hypoventilation:  genesis  of  uncertain.  arterial In  the  That  hypoventilation plays  hypoxemia study  seems of  19  likely,  Dempsey  et  but  a role  to what  a l . ,  in  the  extent  is  (1984),  the  individuals hypoxemia  demonstrating  e x h i b i t e d the Our  individuals  data  the  lowest  indicate  engaged  i n high  greatest  ventilatory that  level  our  degree  of  response  to  subjects  competition.  arterial exercise.  were w e l l - t r a i n e d Their  mean VO  max 2  is  lower  studies  than  (Dempsey  higher  than  and  this  a  was  incurred  during a  a l . ,  recorded test  the  first  relative  at  subjects  a  was  pH  to  The  of  h y p e r v e n t i l a t i o n as  of  elite,  data  is  athletes  our  the  the  who  that  subjects  average  completed subject  but  indicates  end  full  was  of five  unable  to  7.13. i n ten  of  twelve  exercise. This  P0  1986)  perform;  who  observed  seconds  less  gas  desaturation  al.,  a c i d o s i s with  7.. 2 1 + 0 . 0 6 .  i n pH thirty  blood  some  et  using  task  metabolic  obtained  increase  The  exercise  eleven  in  Williams  in studies  Dempsey, 1974).'  f o r the  the  for subjects  1984;  reported  difficult  pH  test  An  reported  a significant  exercise  complete  et  that  (Thompson  minute  that  levels  subjects  corresponded  increased  f o r the  to  first  2 15 not the  seconds.  Changes  correlate with increase  within  the  within  the  working  changes  have  similar  may  working a  of  the  i n pH  phosphate,  i n PCO pH  2 change  reflect  muscle  muscle  been r e p o r t e d intensity  greatest  the  consumption the  which  ( Hultman by  other  (Dempsey  decline  T a b l e I I ) w e r e v a r i a b l e and d i d 2 (R = 0 . 0 5 ) . It is possible that  during  b u f f e r i n g process  c h a n g e s were a t t r i b u t e d to The  (see  hydrolysis has  and  a hydrogen of  ion  creatinine  resulted in  Sahlin,  alkalosis  1980).  Similar  i n v e s t i g a t o r s during  exercise  et  al.,  declines  i n PCO  i n P0  of  occured  1984.) . 2 within  however  the  first  these  45  to  2 60 seconds of e x e r c i s e , which corresponded to the period of g r e a t e s t r i s e i n V0 and VE ( s e e T a b l e I I ) . C h a n g e s w e r e s i m i l a r 2 20  for  a l l subjects  group  showed  showed  a  were  for  first  45  seconds,  then  some l e v e l i n g w h i l e ' s u b j e c t s  greater  true  the  of  rate  the  of  decline  changes  on  (Figure  SaO  i n the  1).  (Figure  those  Mild  Marked  Similar  2),  i n the  group  observations  however  both  the  2 Mild  and  Marked  reflecting  groups  the  hemoglobin  continued  effects  of  minutes  for a l l  (Williams  et  a l . ,  saturation  to  87.0+0.2%  (B i o x  collection et  .  therefore  decreases  as  i n our  of a  Arterial individuals 1984; of  max. 2  that  expected This  r e s u l t of  to  greater and  of  V0  of  VE,  has  pH,  degree  and  2  and  been  in  92.6+0 . 7%  i n  an  ear  method of  data  (Sm y t h e  SaO  work  small  and  desaturation  is  i n temperature  of  in saturation  to  be  outputs  exercising  PCO  subjects  would  compared  to  be the  acidosis.  shown  were 2  21  of  a rise  decrease  1987),  s tudy  d e c l i nes  in  made i n o u r  Assuming  high  f i na 1  2  is relatively  very  Williams, ,  with  the  using  this  differences  the  hypoxemia  desaturation capable  oxygen-  Another  were o b t a i n e d  observed  for  close  subjects  values  subjects.  0.5%.  P o w e r s and V0  the  i n agreement  study.  thus u n r e l i a b i l i t y  likely  c e l c i u s the  order  in trained  measurements were not  is  underestimated  the  on  saturation  .-.  i t  degree  in this  demonstrated  These  account  Temperature  in  1986)  I I ) , and  may  a l . , 1986)  one  ( 9 2 . 0 + 2 .5%)  subjects.  r e s u l t s are  (91.9+_0.6%) i s a l s o  observed  oximeter  Our  acidosis  in  ( 1 9 8 4 ) who s h o w e d s i m i l a r p a t t e r n s of The mean s a t u r a t i o n a t t h e end o f five  subjects,  saturation  untrained  show a d e c l i n e  increasing  d i s s o c i a t i o n curve.  those o f Dempsey e t a l . , d e c l i n e i n PO and SaO .  to  at  more  likely  (Dempsey greater  et  a l . ,  than  s i m i l a r between  in  90%  Mild,  Moderate  and  differences  Marked  in  final  desaturation SaO  canot  be  groups, explained  therefore on  the  the  basis  of  2 differences who  showed  in fitness the  greatest  Generally  onset  for  the  of  differing  decline  our  compensation subjects  or  showed  metabolic  showed  little  a c i d o s i s of  r e s t i n g s a m p l e w h i c h was  exercise  i n the  group  in saturation.  subjects  the  work i n t e n s i t y  a depressed  exercise.  taken  PCO  respiratory  just  In  prior  most  to  (mean = 36.0+_4.4  the  torr).  2 This  i s not  was  s u r p r i s i n g as  straddling  expired  gas  the  the  s a m p l e s were t a k e n  t r e a d m i l l with  in place.  PCO  then  the  as  mouthpiece  increased  to  the  for  subject measuring  a mean v a l u e  of  37-  2 t o r r and d e c l i n e d t o l e s s t h a n 37 t o r r o n l y i n t h e l a s t m i n u t e exercise. The c h a n g e s i n PCO are l e s s than t h a t reported by 2 Dempsey et a l . , (1984), e v e n when h y p e r v e n t i l a t i o n p r i o r t o t h e  38 of  onset the in  of  e x e r c i s e was  relative their  and  lack  exercise.  with  might  of  during  and  (Dempsey  a l . , 1984).  our  subjects  on  the  VO  partial  since max  for  This  nine  of  twelve than  was  the  on  blood  the  gas  five  that  constraint desaturation acidosis  of  increase  does not  subjects  felt  given  replacement  possibility  the  determination  respiratory  l e d t o an  c o r r e c t i o n of This  to a r t e r i a l  this  i n v o l v i n g the  mixtures.  ventilation et  evidence  studies  helium-oxygen  f o r the  al.,(1984)  to m e c h a n i c a l  have c o n t r i b u t e d  compensation  Preliminary  obtained  Dempsey e t  h y p o v e n t i l a t i o n secondary  subjects  the  considered.  of  by  data  room  air  in  the  abnormalities seem l i k e l y  showed minute  in  greater  VE  exercise  2 test.  One  minute  exercise  the  Mild  subject  group  test  exhibited greater than  with  the  VO  respect 22  ventilation  on  max d e t e r m i n a t i o n , b u t 2 to desaturation. The  the  five  fell  into  remaining  subjects the  had  Moderate  possible  that  temperature  s i m i l a r v e n t i l a t i o n i n both s i t u a t i o n s ; group  the other  secondary and  was  modifiers  i n the Marked  of e x e r c i s e  cathecholamine production  1981)  may  VO  determination  max  ,  have c o n t r i b u t e d  of  group.  was  in  It  is  v e n t i l a t i o n such (Wasserman  to the increased  f o r the m a j o r i t y  one  et a l . ,  ventilation in  the s u b j e c t s .  as  the  Certainly  2 it  would  se,  are not It  (Bye  seem t h a t  in this  that  mechanical factors  per  significant.  i s possible  e t a l . , 1983)  compensation  instance  that  may  be  r e s p i r a t o r y muscle  oxygen  responsible  limited respiratory  f o r the  consumption  a c i d o s i s d u r i n g heavy e x e r c i s e . At -1 ventilations greater than 100 l . m i n t h e VO of respiratory 2 . -1 muscle (VO r e s p ) has been e s t i m a t e d t o be 2-8 ml 0 .1 VE~ 2 2 ( M c K e r r o w and O t i s , 1956; B r a d l e y and L e i t h , 1 9 7 8 ) . T h e r e f o r e i n -1 our s u b j e c t s w h o s e mean p e a k v e n t i l a t i o n was 149.8 l . m i n , VO -1 2 resp c o u l d r a n g e f r o m 0.3 t o 1.2 l . m i n , r e p r e s e n t i n g 6 t o 26% of any 140  f o r the metabolic  VO  max. I t h a s b e e n a r g u e d t h a t t h e c r i t i c a l v e n t i l a t i o n w h e r e 2 i n c r e a s e i n VO w o u l d go e n t i r e l y t o r e s p i r a t o r y m u s c l e s is -1 2 l.min (Otis, 1954). Our s u b j e c t s e x c e e d e d t h i s l e v e l of  ventilation,  thus  due  delivery.  to oxygen The  trivial, and  amount o f and  i t may  be  respiratory  a s i m i l a r arguement  1982) .  throughout muscle  optimum  l a c t a t e produced  r e s p i r a t o r y compensation.  distribution  that  could  It i s possible  can  r e s p i r a t o r y muscles be  Assuming  body  water,  r e a c h as  that  by  high  at maximal  23  ventilation is limited  applied  no  i s not  t o CO  excretion 2 l a c t a t e c o n s u m p t i o n and  lactate as  production from -1 10 m m o l . l (Roussos,  exercise,particularly in a  situation could CO  be  where  oxygen  reached  excretion  d e l i v e r y may  where  would  be c o n s t r a i n e d ,  any i n c r e a s e  be b a l a n c e d  a  in ventilation  by an i n c r e a s e  situation  to  in  increase  respiratory  2 muscle it  lactate production  may  be t h a t  exercise  may  the l e v e l represent  leading  i n an i n c r e a s i n g a c i d o s i s . T h u s  of v e n t i l a t i o n an o p t i m u m  reached  during  ventilation,  maximal  balancing  0 2  delivery the  to the working  a c i d o s i s of e x e r c i s e  muscle with  and r e s p i r a t o r y c o m p e n s a t i o n  the increasing metabolic  for  demands o f  the  r e s p i r a t o r y muscles. The mean hypoxic v e n t i l a t o r y response f o r our subjects - 1 - 1 (0.67+0.36 l . m i n .l%ASaO ) i s l e s s than that r e p o r t e d f o r the 2 -1 -1 n o r m a l p o p u l a t i o n (1.09+0.9 7 l . m i n .l%ASaO ; Fleetham et a l . , 2 1980; G r i n d l e y - M o o r e e t a l 1984; Rebuck e t a l . , 1976; Rebuck and Woodley,  1975)  athletic 1982; is  i n d i v i d u a l s (Byrne  Martin not  values  et a l . ,  bell-shaped fell  general  within  population  responses close while  and p o s s i b l y r e f l e c t s  to  -Quinn  the lower  et a l . ,  1 9 7 8 b ) . The c u r v e  but i s p o s i t i v e l y the normal  range  i t was a p p a r e n t  hypoxia.  reported f o r  Mather  of the normal  of values  Six subjects  t o t h e mean r e p o r t e d s i x s u b j e c t s ( B ) showed  1982;  skewed  that  HVR  there  .  population  While  a l l our  expected  f o r the  were  distinct  (N) showed  f o r the normal responses that  et a l . ,  two  HVRs  that  were  population above, were approximately -1 -1 one t h i r d o f t h o s e v a l u e s (N = 1.02+0.15 l . m i n .l%ASa0 vs B = -1 -1 2 0.33+0.10 l . m i n .l%ASa0 ) . T h e r e was no r e l a t i o n s h i p b e t w e e n 2 , s p o r t a n d HVR. T h a t i s , i n o u r s u b j e c t s who w e r e s i m i l a r i n V0 2 max, t h e r e was no d i f f e r e n c e b e t w e e n e n d u r a n c e t r a i n e d (mean HVR -1 -1 = 0.64+0.35 l.min .l%ASa0 ) and n o n - e n d u r a n c e t r a i n e d (mean -1 2 -1 HVR = 0.70+0.37 l . m i n .l%ASaO ) a t h l e t e s . In t h i s a n a l y s i s the 2 24  two  oarsmen were  the  race  considered  distance  complete.  At  specific  i s 2000m a n d t a k e s  the  training  Martin  et  a l . ,  time  for this (1979),  athletes  athletes  a n d non a t h l e t i c  athletes for  at  compared  higher  the d i f f e r e n c e s  work  Martin  ventilation 1978), blunted  blunted  response  1978b;  that  to the i n d i v i d u a l  be a r e d u c t i o n  efficient  pattern  in  contrast in  of  to  endurance  non-endurance  subjects than  VO max 2  was  non-endurance  in fitness  may  exercise  account  Stockley, (Martin that  be  cause that  be e v i d e n t able  i n r e s p i r a t o r y work, This  and  of  et a l . , exercise  1978b;  hypoventilation  of being  of v e n t i l a t i o n .  1978 )  et a l . ,  be e x p e c t e d  would  ventilation  e t a l . , 1979; M a r t i n  might  would  to hypoxia  a t h l e t e s were  HVRs  athletes  have a lower  (Martin  drives  then  to  groups.  athletes  et a l . ,  It  In these  since  6 minutes  is in  blunted  and d i f f e r e n c e s  intensity,  respiratory  advantage would  normals.  between  was p r e d i c t e d  desaturat ion.  found  data  t o a c o n t r o l group  i s r e l a t e d t o HVR  i t  This  i n the endurance  endurance  any g i v e n  1978a;  who  and n o n - a t h l e t e s  Since  event.  athletes  approximately  of t e s t i n g (May) t h e s e  trained  significantly  t o be n o n - e n d u r a n c e  Stockley,  secondary the  to  arterial  some e v i d e n c e  of  i n our s u b j e c t s .  The  to "ignore"  hypoxemia  and p o s s i b l y  a  was n o t o b s e r v e d  more  in  our  subjects; there was no s i g n i f i c a n t r e l a t i o n s h i p b e t w e e n HVR a n d lowest SaO reached. Thus i t seems unlikely that blunted 2 respiratory  drive  plays  a r o l e i n the desaturation  seen  in  these  individuals. The limitation  remaining and t h e r e  possibility  t o be c o n s i d e r e d  i s some i n d i r e c t 25  evidence  is  diffusion  to support  this  as  a  mechanism  subjects.  for  Eight  exercise or  the  subjects  than  on  their  1.1  to  5.0  logical  pooling the  reach  with  respect marked  percent  for by  blood.  exercise  increase.  test  this  to  would  was  much  of  five  exercise  test  d i f f e r e n c e ranged speculative,  i s that to  decreased  than  the  during  from  the  a greater  since  Of  the  This  expected  less  four  minute  due  our  desaturation.  five  Although  be  in  max on t h e f i v e m i n u t e 2 subjects f e l l into the  desaturation  subjects  This  observed  arterial  increase  these  VO  these  s c o r e s f o r VO on t h e . . . 2 VO max d e t e r m i n a t i o n . 2  achieved  of  desaturation  exception  developed  explanation was  one  group  who  higher  output  With  Moderate  scored  arterial  s u b j e c t s -did not  test.  Mild  the  only-  cardiac  peripheral  duration the  of  VO  max 2  determination (13-18 peripheral p o o l i n g of five  minute  VO  test be  minutes). b l o o d due  and  greater  max 2 oxygen  can  transport  (DiPrampero,  output  would  expected  limitation of  considered  be  due  arterial  to  and  result  in a increase  cardiac  therefore  output  i t could also 2 the f i v e s u b j e c t s  subjects Marked  who  any  ranging (90.1%).  transit  be  marked  desaturation (SaO  There  no  time,  the  observed  from M i l d  which  to  cause  changes  If  be  the  i n SaO  observed  cardiac diffusion  were  desaturation. was  in  I f the of  to  limitations  the  increased would  less the  limits  increase  desaturation..  to  developed  was  due  VOmax. 2 t r a n s i t time  factor  in arterial  summary a r t e r i a l  any  red. c e l l  the  75%  have during  Since  increase  shortened  explain  about 1984)  were c o n s i d e r e d  VO  In  be  to  desaturation,  output  venous r e t u r n .  to  shortened,  Thus s u b j e c t s would to t h e r m o r e g u l a t i o n  cause  cardiac  expected  to  changes  in  increase  in  i n four  of  -2  i n a l l of  our  = 94.6%) , Moderate (91.6%) to 2 d i f f e r e n c e s between groups i n VE,  26  VO max, 2 factors  pH  .  and 2 limiting  subjects during degree  ,  t h e VO max 2  test.  transit  time-  that  unlikely  are s i g n i f i c a n t  or exceeded  of d e s a t u r a t i o n suggests  a n d i t seems  ventilation  approached  evidence cell  PCO  There  was  and h y p o x i c diffusion  i s t h e most  phenomena.  27  maximal  that since  ventilation  no r e l a t i o n s h i p ventilatory  limitation likely  mechanical only  two  determined between  response.  the  Indirect  due t o s h o r t e n e d r e d  explanation  for  this  REFERENCES  Anholm J.D., Houston, C.S., Heyers, T.M. 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Young, I.H., W o l l c o c k , A.J. Changes i n a r t e r i a l blood gas tensions during unsteady-state exercise. J ; Appl. Physiol.: R e s p i r a t . E n v i r o n . E x e r c i s e P h y s i o l . 4 4 ( l ) : 9 3 - 9 6 , 1978.  33  APPENDIX A R E V I E W OF L I T E R A T U R E VENTILATION The  DURING  EXERCISE  ventilatory  response  described  i n three phases.  beginning  before  known a r e a o f the  first  steady  initial  phase  metabolite  breath varies response.  almost  In a n i m a l s ,  ion  at  the  chemoreceptor  agents  percent decrease  in ventilatory  when  afferent  are  of  and  issue  is  demonstrated varies  of  exercise transit total  reach  VE  increases  up  to  100%  a  with  of  i s accompanied  the  by  as  metabolic rate initial until  is  generally  some m e d i a t o r  ventilation  seen  The  an  increase  studies  thought  i s the  small  surrounding in  man  have motion  reached. of  with  the  1978).  The  summation  of  (Whipp, the  (phase  the onset  consistant  i s then  rise  I I I ) is  following  to the chemoreceptors  34  motion  e t a l . , 1981),.  t o be  state  a  likely  of h i n d l i m b  (phase  I I response  of  much a s  the  there i s a slow  state  use  to h i n d l i m b  evidence  similar  (Wasserman  i n steady  as  ventilation  i s independant  steady  The  suggesting that  fibers.  ventilation  this  1978).  response  to e x e r c i s e  the d e l a y i n phase this  of  drive  conflicting  in ventilation  Because  this  (Whipp,  blocked  nonmyelinated  that  with  Following II)  fibers  neurogenic  myelinated  and  change  occurs,  could  i n a n i m a l s has . d e m o n s t r a t e d  fifty  this  no  commonly  increase  work  extent that  is  a n d d e c r e a s e i n PCO ; thus i t i s argued t h a t the 2 2 increase i n v e n t i l a t i o n cannot r e f l e c t the a c t i o n , of  blocki.ng  source  I a rapid  of muscular  The  from  exercise  i n P0  hydrogen neural  In  chemoreception.  state  increase  any  to muscular  the  humoral  ventilation minute  and has  continuing  been  ventilation  neurogenic  demonstrated  of  carbon  to  be  dioxide;  stimuli.  linearly CO  and  +  Exercise  related  H  are  to  the  generally  2  considered  to  ventilation  (Favier  et  individuals  who  undergone  c a r o t i d body  ventilation  does not  appear  be  individuals,  be  the  have  however  phase  II ventilation  half  that  arterial  of  pH  develop  al.,  they  normal  chemoreception  1983).  Of  to  exercise  the  an  to  exercise  interest  is  work  resection.  is  also  inability for  suggests  i n VE  these  metabolic the  r e l a t e d to  these during  demonstrate  that  I  approximately  of  the  in  Phase  altered in  increase  that  They  compensation  intimately  stimuli  significantly  demonstrate  evidence is  humoral  controls.  secondary  This  to  during  respiratory  exercise.  ongoing  one  a  lower  subjects  to  acidosis  of  carotid  exercise  body  ventilation  ( W a s s e r m a n et' a l . , 1 9 7 5 ) . This  neurohumoral  accounts by  for  the  suggesting  followed  by  neurogenic  there  slower  component  including  voluntary  proprioceptor  of  exercise  v e n t i l a t o r y responses  that a  theory  is first humoral  are  neurogenic  from  from  the  mechanisms  exercise component,  Included  muscle  control  muscular  component.  and  a f f e r e n t s . Humoral  during  a rapid  imputs  imputs,  ventilatory  in  cerebral spindles  suggested  -the  cortex,  and  joint  include  CO +  flow  to  the  increase  in  lungs,  alterations in intramedullary  pulmonary  blood  flow,  and  and  CSF  [H  oscillations  of  2  ], PCO 2  about  an  unchanged  ventilation slowly  are  developing  catecholamines  mean.  body  Secondary  temperature  modifier which  of  may  factors affecting which  primary provide  35  would  stimuli  appear and  additional  exercise to  be  a  circulating drive  to  hyperventilate The the  (Whipp,  rise  in ventilation  ventilatory  response 1978).  1978).  response  to hypercapnia  responses  (Martin  could  ventilation  for  consistantly  documented  Martin  et a l . ,  between  VO  with  expected  given  level  correlates  as w e l l  et a l . ,  athlete  be  any  exercise  to hypoxia  Thus t h e endurance  these  during  as  1979;  Stockley  a  and t h e v e n t i l a t o r y  has  been 1978a;  has been  to exercise  of  exercise  et a l . ,  relationship  response  blunting  This  i n the l i t e r a t u r e (Martin  1 9 7 9 ) a n d an i n v e r s e  et a l . ,  lower  exercise.  both  ventilatory  a documented  t o have  of  the  with  found  (Morrison  et  2 al.,  1973).  work a  The  of b r e a t h i n g ,  low e x e r c i s e  who  exhibit  respiratory dyspnea to  use o f p r e s s u r e  has d e m o n s t r a t e d  ventilation  exercise  work,  therefore  and  that  facilitate  a  athletic DRIVES  The  ventilatory  The  hypoxic  sensitivity hypoxic  efficien  the physiologic  1962).  Subjects  will  perform  experience  less  dyspnea.  physical t  work,  ventilatory  the  advantage of  entilation  less As  i t reasonable pattern  would  response  ventilatory  r e sponse  is  o f t h e c o r t i c a l and p e r i p h e r a l  stress.  to calculate  performance.  RESPIRATORY hypoxic  v  l i m i t a t i o n to more  curves  ( M i l i c - E m i l i et a l . ,  a decreased  i s a powerful  expect  volume  The  i n v e s t i g a t i o n of  a  measure  regulating  t h e HVR  of  centers  involves  a  the to  circuit  w h e r e PO is  a n d PCO c a n be c o n t r o l l e d. The c o n c e n t r a t i o n o f o x y g e n 2 2 gradually l o w e r e d i n t h i s c i r c u i t by t h e a d d i t i o n o f nitrogen  until al.,  alveolar 1978;  oxygen  Hirshman  tension  i s 1owered  t o 40 t o r r  e t a l . , 1975; S c o g g i n  36  (Collins  e t a l . , 197 8;  et  Schoene  et  a l . ,  about  1982)  80%.  dioxide  Changes  secondary  addition  of  mixture. ear  which  Arterial  supine partial  pressure  (SaO  dioxide oxygen  and  comparison  of oxygen  ventilation  (VE) i s a l i n e a r  hypoxia  32),  as  oxygen  asymptote.  1983).  o f an  carbon  to  by  the  the  gas  by means o f a n  recorded  in  ventilation  nature  the graph  of  i n which  versus  hemoglobin  of  o f SaO  the  the  oxygen  versus minute 2 the s l o p e of t h e  individual's  sensitivity  to  tension  The g r a p h  in  The A v a l u e d e s c r i b e s  Statistical  1971; C o l l i n s  Moore  torr  et a l . ,  values  of  analysis et a l . ,  to 80.  is  t h e shape  a skewed  et a l . ,  Similar  analysis  et  a l . ,  (Bryne-Quinn  et  1975; G r i n d l a y -  distribution  of studies  a  t o h y p o x i a and  (Collins  studies  a mean A v a l u e o f 145 a n d  extrapolated  of the curve, with  to hypoxia  of several  the  response  1978; Hirshman  1974;) i n d i c a t e  A mith  a n d Vo  ventilatory  A value a blunted response  1978).  equal  i s then  minute  function,  A value denoting a brisk  low  al.,  a function  (Tammling,  alveolar  a  i s monitored  or percent s a t u r a t i o n  curve,  of  are prevented  Due t o t h e " S " s h a p e d  dissociation  pressure  of  o f VE v e r s u s PaO i s a curve . 2 i s d e s c r i b e d by t h e h y p e r b o l i c f u n c t i o n VE = Vo + A / ( P A 0 2 where VE i s the observed ventilation (BTPS), PAO i s 2  which  high  of  saturation  quantities  ventilation  made.  varies  i n small  saturation  ) i s 2 hemoglobin  line  partial  hyperventilation,  The m i n u t e  subject  to a hemoglobin  i n the a l v e o l a r to  carbon  oximeter.  corresponds  tov/ard  standard comparing  lower  deviation VE t o . SaO 2.  (Fleetham  et a l . ,  1980;  Campbell  1975;  indicates  a similar  Rebuck  Grindlay-Moore et a l . ,  and Woodley  skewed  1975;  distribution 37  Rebuck  with  1984; Rebuck and et  a l . , 1976)  t h e mean s l o p e e q u a l  to  1.09+0.97 l . m i n  . When t h e h y p o x i c 2 i s m e a s u r e d u n d e r c o n d i t i o n s w h e r e t h e CO 2 to f a l l ( p o i k i l o c a p n i c h y p o x i a ) the observed  response allowed less  than  constant effect  under  .  conditions  (isocapnic of  l%ASaO  where  carbon  hypoxia).  d e c r e a s i n g CO  on  This  dioxide  tension  is  response  is  tension  reflects  ventilation  ventilatory  the  remains inhibitory  (Grindley-Moore et  a l . ,  2 1984). Some the  interesting  ventilatory  response  Elite  mountaineers  have  been  to  found  hypoxia  distance  al.,  1971;  al.,  1982).  value for  of  Some  the that  one  (Schoene  sectional  athletes  responses  of  . the  observed  response  while e l i t e  and  (Bryne-Quinn  et  1979,  et  found  controls  Schoene  to have  exhibited  are  raised  that  show a b l u n t i n g degree  the  to  an  a value  relatives  differences  is  that  who  are  1978).  A  of  because  o f an  illness 38  groups;  and  ability the  the trait.  true.  Elite  i s reflected  in  not  in  engaged  T h i s would  i n t h e c l i m b e r vs i n these  whether  acquired  former  o f HVR  et a l . ,  to a l t i t u d e  as  i s a g e n e t i c or  suggest  (Collins  middle  1982).  response  at a l t i t u d e  succumbing  ventilatory  w h i l e the c o r r e s p o n d i n g value  Normal  represents selection  successful  altitude  M a r t i n et a l . ,  S.D.),  groups.  of  c l i m b e r s were  questions  first  same a c t i v i t i e s  without  et a l . ,  studies  extremes  enhanced  controls  1978;  series,  49.3+7.1.  ventilatory  population is  In  the  regarding  athletic  show a b l u n t e d r e s p o n s e  et a l . ,  intriguing  endurance the  runners  normal  158.9+_29.9 ( m e a n t  109.9+21.0  Cross  with  come t o l i g h t  in different  of a t t a i n i n g  t o have a g r e a t l y  Collins  r u n n e r s was  hypoxic  to h y p o x i a  capable  compared  long  o b s e r v a t i o n s have  suggest  endurance  runner  the  climber  to  climb  runner  who  who high  isable  to  run  f a s t ,because  respiratory that  the  altitude  work  ventilatory  Hypercapnic  ventilatory  by  graph  ventilation,  I t i s interesting  to hypoxia i s  as endurance  blunted  less  to  note  in  high  runners.  response  o f an i n d i v i d u a l  maintaining  concentration  exercise  dyspnea.  response  as w e l l  sensitivity  measured  decreased  and l e s s  residents  The  of  of carbon  a  constant  PO  dioxide  and  i s a linear  function  can  be  increasing  the  circuit.  The  the slope of  which  2 i n the rebreathing  dioxide  o f VE v e r s u s PCO  to carbon  2 varies wide  as a f u n c t i o n range  (Read,  of i n d i v i d u a l  of responses  1966;  Irsigler,  responders  t h e n men.  individual  variability  t o CO  sensitivity  i s seen  2 1976)  with  to hypercapnia.  among n o r m a l  A  individuals  women t e n d i n g t o be  lower  T h e mean s l o p e o f t h e r e s p o n s e line has -1 -1 been r e p o r t e d t o be 2.60 l . m i n .torr i n c r e a s e i n PCO with a -1 -1 . 2 s t a n d a r d d e v i a t i o n o f 1.2 l . m i n .torr ( I r g s i l e r , 1976). Since i s so g r e a t ,  i t may  be more r e a s o n a b l e t o -1 -1 consider CO response i n terms of l o w (<1.5 l.min .torr ), 2 - 1 - 1 -1 -1 medium (1.5-5.0 l.min .torr ) , and h i g h (>5.0 l . m i n .torr ) responders. R E S P I R A T O R Y FACTORS L I M I T I N G It  was n o t u n t i l  considered  to  performance demonstrated exercise There  in  which  are  some  some  offers  three  recently  exert  a decline  PERFORMANCE that  t h e pulmonary  constraint  individuals. in arterial  evidence  possible  on  39  this  by w h i c h  has been exercise  authors  saturation  to encourage  mechanisms  maximal  Several  oxygen  system  with  have intense  line  of thought.  the  respiratory  system  could  limit  maximal  Dempsey,  1 9 8 6 ; Dempsey  1.  mechanics.  lung  exercise  and F r e g o s i , 2.  performance  198 5;  energetics  Dempsey  a n d 3.  ( B y e , 1984; et a l . , 1982):  r e s p i r a t o r y , muscle  fatigue . Lung  mechanics:  exercise, maximal limits  flow of  exceeded on  the  this  1983) to  shortening  flow  volume  loop,  maximal  (Olafson  expected  of  tidal  side  thus  lead  i n d i v i d u a l s performing  volume.loop however,  flow  where  exceeding  may  be  These  moderate  within  the  exercise,  the  approached  limits  the  maximal  muscles  volumes lungs  or  are reached  becomes i n d e p e n d e n t o f  to h y p e r i n f l a t i o n of the  of the i n s p i r a t o r y  well  maximal  loop  1969). flow  falls  in  volume  and H y a t t ,  the expiratory  (Hyatt,  In normal  effort  could  be  resulting  in  and i n c r e a s e d  elastic  work  breathing. Energetics:  limited, increase  such  In  a  situation  as a t maximal  exercise,  i n r e s p i r a t o r y muscle  available  oxygen  where  VO  (VO  2 f o r non-respiratory  ventilation,  t h e p o r t i o n o f VO  possible  reach  oxygen  transport  i ti s possible r e s p ) would  2. muscles.  i s  that  any  decrease  the  At low l e v e l s of  supplying r e s p i r a t o r y muscles i s 2 r e l a t i v e l y low. At l e v e l s of e x e r c i s e , v e n t i l a t i o n g r e a t e r than -1 -1 100 l.min , VO resp may be a s g r e a t a s 2-8 ml 0 .1 VE 2 2 (McKerrow and O t i s , 1956). Some a u t h o r s h a v e a r g u e d t h a t i t i s to  a s t a t e where any i n c r e a s e  i n VO  would  be  2 consumed  entirely  Respiratory be the  defined force  diaphragm,  by t h e r e s p i r a t o r y m u s c l e s muscle  fatigue:  a s t'he f a i l u r e to this  produce occurs  (Otis,  Respiratory  195 4 ) .  muscle  of the r e s p i r a t o r y muscles a  given with  pleural  pressures 40  fatigue to  pressure.  that  a r e 40% of  can  generate For  the  maximum  pressure the  while,  f o r the i n s p i r a t o r y  p l e u r a l pressure  (Bye,  1983).  required  The  unique  muscles,  i s greater  characteristics  with  ability  to maintain  very  this  muscle  relatively  r e s i s t a n t ' to  skeletal  muscle  studies  have  maintained 1984;  that  indefinitely  Martin  ventilatory maximum  (Wasserman  shown  et a l . , muscles  et  high  may  concern  been  150 m i n u t e s  This  reduced  of maximal  heart  rate  and v e n t i l a t o r y  where  this  ventilatory  exhaustion  endurance  breathing  f o r t h e two g r o u p s  of  that  can  hyperventilation program control  when  has  of  the  a fall in and  considerations Reduced  time to  maximal  (Martin  be a l . ,  pressures  et  exercise  a l . ,  1982).  at a s i g n i f i c a n t l y  lower  the c o n t r o l  shown  to  identical  for  strength  may  41  occur  i n MVV 15  involved  and B r a d l e y ,  training  to  be  situation  greater  in  costs  of  energy  investigated (Martin  subjects  (Leith  muscle  been  despite  be s u s t a i n e d  in  Bye e t  with  these  during  shown an i n c r e a s e  compared  subjects  ventilatory  have  race  short-term  than  cannot  w o r k was n o t p e r f o r m e d .  non-athletes  studies  that  occurred  several  i n the strength  mouth  ventilation  rate  than  Training  1985;  et a l . , 1982).  during  time  athletes  MVV  suggests  with  However,  of v e n t i l a t i o n  A decline  renders  compared  1981)  and M a r t i n ,  (Loke  shown  after  Ventilatory  levels  muscle,  capacity,  fatigue  expiratory  pressures  has  of diaphragm  a t t h e end o f a m a r a t h o n and  50 - 7 0 % o f maximum  oxidative  a l . ,  (Bender  transdiaphragmatic  exhaustion  high  1981).  . inspiratory  be o f p r a c t i c a l  than  fatigue results i f  et a l . ,  and t h e p e r c e n t a g e  minutes  of  i n an e n d u r a n c e training  1976). during  1981).  voluntary training  individuals This  suggests  endurance  and that  exercise  training. HYPOXEMIA DURING Hypoxia  and  EXERCISE  altitude  Conventional  wisdom  lungs  i s exposed  travel  to  to  hypoxia  high  altitude.  of  sufficient  magnitude  be  found  sea  level  et  in healthy (Dempsey  a l . ,  1986;  physiologic minute  et  and  to  body  that  under  I t has cause  a l . ,  normal  athlete  seen  circumstances  normal  only  that  desaturation  hemoglobin  Powers et  of  at  altitude.  high  other  main  changes,  and  centres  in turn-acts  to  and  at  Williams  stimulus An  can  levels  a l . , 1984;  i s the  with  hypoxemia  maximal  Hypoxia  chemorespiratory This  with  become a p p a r e n t  1984;  precedes  system.  the  a t h l e t e s e x e r c i s i n g near  alterations  medullary  carotid  held  others).  ventilation  through  has  to  the  increase  in  is  mediated  through  decrease  the  arterial  PCO 2  which  acts  on  ventilation. is  the  be  sum  an  p e r i p h e r a l chemoreceptors Thus the  of  two  of  altitude,  the  changes are In  vasodilator, in  countered which (Sutton  a  and  as Grey,  segment  of  this lung,  the  of  mechanism decreased  effects  of  a v a s o c o n s t r i c t o r of 1982).  The  42  supply.  high  altitude  has  been  shown  normal  protects  against at  to  hypoxia  This  these  high  pulmonary acts  optimises  cerebral  i m p l i c a t i o n s of  to  during  accompanying  the  minute  at  leading  which  the  decrease  however,  cerebral circulation,  a situation by  level,  more g e n e r a l i z e d ,  protective  i n part  acts  the  Hypoxia  vasoconstrictor  sea  hypoventilated  hypertension.  delivery  At  to  observed  stimuli.  pulmonary  responses.  perfusion  ventilation  conflicting  important  regulatory  net  and  as  a  oxygen  effect  is  hypocapnia vasculature changes  are  important  considerations  in  the  pathogenesis  of  altitude  sickness. Altitude  illness  Many  investigators  believe  the  mechanisms  of the d i f f e r e n t  altitude  Generally,  altitude  i s thought  of  water  fluid the  handling.  from  the  this  an  vasodilatory  relative  line to  development this  of  highest  the  disorder shift  of  space.  In  intravascular  vasoconstriction. secondary  to increased  individual  mechanisms  In  to  the  filtration It  who  of can  exhibits  have a g r e a t e r  to increased  offer  some  found  (AMS) i s g r e a t e r i n minute  to extreme  were a b l e  that  illnesses.  I t has been  In climbers  altitude,  to a  in  flow  will  suggests  should  increase  who  leading  thought  of the a l t i t u d e  Sickness  individuals  a  to S t a r l i n g ' s law.  the pathologic  hypoxia  greatest  1979).-  leads  that  from  same.  degree  v a s o d i l a t i o n and described  above  1983).  reasoning.  Mountain the  of  and G r e y ,  This response  blood  according  and h y p e r c a p n i a ,  exageration  (Sutton  by t h e i n c r e a s e  cerebral  appreciated  leads  the  to the i n t e r s t i t i a l  hypoventilation at a l t i t u d e  hypoxia  an  formation  pathologic  t o be  to result  to a l t i t u d e  e f f e c t s of hypoxia  be  illnesses  to the hypoxia-mediated  increased  a n d edema  therefore  of  i s augmented  secondary  brain,  fluid  Exposure  the i n t r a v a s c u l a r space  lung,  pressure  illness  underlying  h a d an e x a g e r a t e d  brisk  protection Several  ventilatory against  studies  the incidence  i n those  the highest response  of  (Anholm  i t was f o u n d  Acute have  eta l . , that  and s l e e p  to hypoxia  the  support  i n d i v i d u a l s who  ventilation  altitude,  to climb  43  that  a  at  the the  (Schoene  et  a l . , 1982).  response  to  suggests  hypoxia  environment and  This  PCO  .  those  optimise  where oxygen  alveolar  that  their  is limited  The  i n d i v i d u a l s with oxygen  and  advantages  uptake  maintain of  this  a  brisk  in  low  are  a  an  arterial threefold:  2 firstly,  a decrease  increase the  i n the  i n a l v e o l a r carbon  alveolar partial  respiratory  alkalosis  dioxide  pressure  facilitates  of  the  allows  a  relative  oxygen. binding  Secondly,  of  oxygen  to  hemoglobin, thus a h i g h e r p r o t i o n of h e m o g l o b i n i s s a t u r a t e d f o r a g i v e n PO . Thirdly, a lower carbon d i o x i d e t e n s i o n minimises 2 the v a s o d i l a t o r y e f f e c t s of hypoxia.  E x e r c i s e i n a hypoxic environment Performance  increases  linearly  with  i n c r e a s i n g PO  and  drops  2  off  sharply  mild  with  hypoxia  decreasing  (inspired  PO  PO  ( s e e W e l s h , 1987 f o r r e v i e w ) . 2 120 t o r r ) t h e c h a n g e s a r e small  In and  2 not  statistically  increasing exercise uptake  significant,  desaturation (Squires  and  i s r e l a t e d to  hemoglobin diffusion  gradient to  oxygen  for  higher  Maximal  oxygen at  peripheral and  the  (DiPrampero,  altitude  limits  altitudes  particularly oxygen  d e l i v e r y , (cardiac output  oxygen,  seen  at  i s found  1982).  curve)  utilize  d-esaturation  hemoglobin  Buskirk,  .dissociation  mitochondria arterial  of  however,  blood  and  with  oxygen oxygen-  flow  and  ability  of  the  1985).  Thus  the  VO  max  by  limiting  2 the  diffusion  hypoxia  on  active  muscle  of  oxygen  oxygen  into  d e l i v e r y are  is affected  by  the  muscle  complex, arterial  cell.  The  however, oxygen  as  effects blood  tension  flow  (Hogan  of to and  Welsh, 1986). D u r i n g s u b m a x i m a l e x e r c i s e , no e f f e c t i s s e e n on VO unless hypoxemia i s severe (Welsh, 1987). During acute 2 44  exposure,  little  exercise,  although  1987).  VE  change  hypoxia  maximal  increased a right  exercise,  temperature  shift  i s seen  output  exercise  An  the  effects  alterations  i n 2,3  i n the hemoglobin-oxygen  (Welsh  little in  the  or  no  pH  is  effect  of  1987).  EXERCISE  and  maximal  beds  increase  OXYGEN DURING combined  and  reflecting  (Welsh,  during  in active  exercise.  ventilation  HEMOGLOBIN A F F I N I T Y FOR  cardiac  f o r subrnaximal e x e r c i s e  subrnaximal  pulmonary  During  on  vasodilation  during  during on  i s seen  i s increased  i s seen  observed  effect  (HbO  of DPG  decreased serve  to  pH,  produce  ) dissociation  curve.  2 Generally, remains  this  highly  facilitates tensions; decreased increase  change  is relatively  saturated  with  i n c r e a s e d oxygen during exercise binding  in 0  in  delivery  the  minor,  oxygen  delivery in the lungs  at the  such  that  (94-98%).  hemoglobin  This  change  to t i s s u e s at low oxygen normoxic condition, the  i s more  tissues.  than  offset  During hypoxic  by  the  exercise,  2 eventually is  the  balanced A  pH  by  point loss  decrease  i s reached i n oxygen  from  7.4  w h e r e any  loading  t o 7.2  at  will  gain  in tissue  delivery  the l u n g s . cause  a decrease  in  SaO  2 a t a PO of 90 torr. o 2 o Similarly, an increase i n t e m p e r a t u r e f r o m 37 C t o 38 C will cause a decrease i n SaO from 97% to 96.4%' ( s e e Appendix B). 2 from  97%  During  to  a p p r o x i m a t e l y 94%  exercise,  additive  the combined  (Thompson  and  that in  the  acts  i n the  following  red c e l l ways:  effects  Dempsey,  2,3-Diphosphoglycerate  1.  saturated  of  temperature  pH  are  1984).  ( 2 , 3 - D P G ) i s an to a l t e r  inorganic  i t s oxygen  carrying  2,3-DPG b i n d s d i r e c t l y  45  and  to  phosphate capacity hemoglobin,  combining in  this  more r e a d i l y  state.  molecule the  2.  i s unable  to  deoxyhemoglobin  When s y n t h e s i s e d to  cross  the  D o n n a n e q u i l i b r i u m and  thus  alter  the  HbO  curve  red  acts  through  tending  i n s i d e the  cell  to  and  red  membrane.  decrease effect  on  to  hold  cell,  i t this  This  alters  intracellular  pH  pH  1972).  (Kloche,  and  2 Short-term in  exhaustive  hemoglobin  pH,  that  can  affinity be  i s required  50%  the  alteration  increase in  i n oxygen  an  increase  and  CI  of  to  have the  that  The  of  the  1974). been  changes  is  not  aside  documentation  new from  as  In  documented in arterial  arterial  (Rowell  of  the  focus  interest on  recently.  The  i n the  of  arterial  (Bjursted  and  gas  part  data  Wigertz, 46  during  result  per  30-  for  exercise  of  of  100  ml  about  small seen  by  2 ml  is  an  changes accounts  leading per  to  ml + , K  which  saturation during  an  100 +  i n NA  ( K l o c h e , 1972)  desaturation  reports  lack  intense  , may  exercise.  EXERCISE  scattered until  accounted  a d d i t i o n , changes  however,  this  a  order  1919),  1974)  Very  and  approximately  be  occurs  (Harrop,  Dempsey,  exercise  of  change  temperature  hemoconcentration  A R T E R I A L DESATURATION DURING HEAVY The  changes;  1.0-1.5 g h e m o g l o b i n content  of  a  a l . , 1980).  mechanism  Dempsey,  ions  contribute  et  carrying capacity  i n oxygen  ( T h o m p s o n and  these  produce  i n 2,3-DPG.  i n s a t u r a t i o n can  concentration.  increase  show t o  independent  changes  produce  (Klein  adaptive  hemoglobin  for  to  i n 2,3-DPG  been  f o r oxygen  variability  Another  has  a t t r i b u t e d to  exercise of  exercise  this et  the  1964;  likely  and  explanation  for  community  during  0-Barr  ignored  Thompson  scientific  obtained 1971;  heavy- w o r k  p h e n o m e n a was  a l . ,  most  during  et  was  subrnaximal a l . ,  1964;  Suskind  et  al.,  hemoglobin factors  1950)  saturation  previously  investigating Dempsey  which  et  that  could  discussed.  changes  a l . ,  did  and  2 his  In  not  be  Perhaps  i n PO  1984.  not  SaO  show  Hemoglobin  oximeter, of  an  the  and  the  indwelling  sixten  content  of  arterial  subjects 21-35  pH,  to  by  the  complete  i s found  study,  was  i n the  study  work  of  sixteen  endurance  rates  (VO  athletes  max  =  7 2+_2  2 exercise  measured  by  test  means o f  on  a  an  ear  PCO  , and PO w e r e m e a s u r e d by means 2 2 cannula. I t was f o u n d t h a t e i g h t of  demonstrated  torr,  most  for  in  2  saturation  arterial  decline  accounted  capable of s u s t a i n i n g very h i g h m e t a b o l i c -1 -1 ml.kg min ) performed a progressive treadmill.  any  a PO  a decrease  of  in arterial  less  than  75  associated  with  little  helium  breathing  torr.  oxygen  The  most  2 severe  hypoxemia  was  hyperventilation.  When  turbulent  thus  flow,  ventilation The heavy to  and  increased  work  have  not  causes  diffusion  limitation.  2.  Venoarterial  et  a l . ,  thebesbian  small 1973)  the  systemic  gas  exchange.  4.  to  reduce exercise  arterial  desaturation  however,  the  the  following  At  of  bronchial  circulation  during  speculation  lines:  1.  inequality.  as  veno3.  hypoventilation.  (approximately  The  for  along  shunt:  and  used  ventilation-perfusion  amounts  veins  alveolar  substantially.  proceeds  shunt.  was  no  r e s p i r a t o r y muscles,  been e l u c i d a t e d ,  arterial  are  the  mechanisms a c c o u n t i n g  possible  there  unload  or  rest  i n the  1-1.5% of blood  and  47  of  are  blood  therefore  introduction  cardiac  that  venous  this  healthy  individual,  output shunted  (Bachofen via  the  supply  directly  do  participate in  poorly  not  oxygenated  into  blood  causes  a  shunting  small were  decline  the  i n oxygen  cause  of  the  tension  decline  in arterial  i n PO  , no  blood.  change  If  would  be  2 expected gas  i n oxygen  mixture.  hyperoxia  tension  with  the  fact,  this  i s not  In  correcting  level  (Dempsey  et  al.,  1985).  Thus  the  a l . ,  i n t r o d u c t i o n of  hypoxia  1984;  the  seen  Gale,et  some o t h e r  case  during  a l . ,  mechanism  a  with  hyperoxic reports  exercise  1985;  of  at  sea  Torre-Bueno  must a c c o u n t  for  et  this  phenomena. Ventilation-perfusion and  perfusion  gravity do  the  then  the  of  bases  apices.  a  of  the  lung  recieve  and  and  could  there  perfusion  also  is  an  with  the  greater  homogenity  within different  intense  levels  exercise  perfusion are  not  of  u n e q u a i . i t.y,.. h a v e  sufficient  only  been  to account  a  of  the  the  as  flow  lung. in  et  changes  low  both  the  changes  passed  During  areas  of  than  increased  blood  result  (Gale  e f f e c t s of  blood  overall  found  ventilation  inequality  increase  the  to  greater  increase  minor  for  due  perfusion  v e n t i l a t e d segment  exercise  ventilation  are.non-uniform:  hypoxemia  poorly  intensity  lung  If ventilation  arterial  through  the  inequality: Generally  apical  tending  lung. in  At  to more  ventilation-  a l . ,  1985)  in P 0  which  seen  during  2 maximal  exercise.  Diffusion hypoxemia In  the  during  heavy  sedentary  time  f o r the  well  the  seconds). levels,  limitation:  red  time In  Another  exercise  individual blood  cell  required the  mean t r a n s i t  r e l a t e s to  during through  for complete  a t h l e t e capable time  possible  may  be 48  heavy the  e t i o l o g y of  diffusion exercise  pulmonary  reduced  reaching to  0.40  limitation. the  transit  circulation  equilibration of  arterial  very  is  (about  0.25  high  work  seconds  or  less,  secondary  to  increases  also  d i r e c t e d to  may  be  Diffusion  intravascular leak  Thus  underventilated  f u r t h e r reduced  1982).  fluid  i n pulmonary  and  an  of  arterial  uncertain.  In  demonstrating the  lowest  subjects  normal  the the  That  levels  of  lung,  second be  i n the  also  blood  (Dempsey  et a l . , high  .lead  interstitial the  times  i f  capillary  explain  is  transit  increased  •pulmonary  in fluid  hypoventilation plays  hypoxemia of  greatest  retain  i n the  the  I f the  to  space.  changes  in  observed.  study  not  of  also  the  may  flow.  0.25  seems l i k e l y ,  Dempsey degree  et  of  light  PCO  CO of  may  but  to  a role  t o what  a l . , 1984,  arterial  h y p e r v e n t i l a t o r y response  did  considered  within  increase  Hypoventilation: genesis  could  limitation  saturation  areas  l e s s than  distance  pressures  diffusion  arterial  to  blood  in  the  extent  is  the i n d i v i d u a l s  hypoxemia  exercise.  exhibited  While  these  above r e s t i n g levels, i t may be 2 s i g n i f i c a n t metabolic a c i d o s i s , that  be  inappropriate.  2 Non-apneic reported  arterial  during  pulmonary  sleep  disease.  described  of  patients  with  in  Some  diminished  desaturation  authors  during  compared  non-desaturating  or  to  non-REM  sleep  daytime  is  alterations  in  breathing  hypercapnia;  the  hypoxic  show some d e c r e a s e . is  well  maintained.  (Weil  and et  Thus  controls.  in In  with  pattern  49  to  have  hypoxia  and  individuals  subjects  be  ventilatory  seen  quiet  ventilation, hypoxia  normal  been  1980)  these  mild  In  has  obstructive  a l . ,  normal  and  a l . , 1984). can  more  decreased  hypercapnic  i t  et  responses  wakefulness  associated  of  chronic  (Littner  ventilatory,  hypercapnia  11%  responses  subjects  that  and  in  SaO 2 some  circumstances respiratory This  desaturation  is  review  has  focused  mechanisms  of  exercise.  Of  possible  either are  with  diminished  drives.  possible  arterial  associated  the four  desaturation,  due t o b l u n t e d  t h e a r e t h e most  on e x e r c i s e  arterial  desaturation  explainations  diffusion  50  and  during  the heavy  f o r the d e c l i n e  and i n a d e q u a c y  respiratory drive likely.  ventilation  in  of  ventilation  or mechanical  constraints  APPENDIX  rc  PH  ©  © -6.6  B  Po -OXYGEN SATURATIONS NOMOGRAM FOR WHOLE BLOOD 2  C O R R E C T I O N S F O R T E M P E R A T U R E A N D pH Sundvd DfccKlaMon C***m *£X*&rq to 1. W. ScwvrtnQhevl. 1903 t n w i w i an4 pH U W W P J H <eca>dtwg ta P. A«mo, 1065.  -6.7 -6.8  PQ2 own Hg  ©  -6.9  PQ_ mm Hg corraciad  ©  300 43 •  -7.0  •98.8  | T 230 -7.1  §_- 200  O2SATO/0 AT37'C A N D pH 7.40  p - 150  •7.2 40 • •7.3  > 100 90  •7.4  • 80 •7.3  M-4  • 70 • 60  •7.6 30 • 7.7  • 40  30-  90  • 7.8 30 •7.9 25-^  50-Eg  23  • 8.0  £-20  80 40•70  • 8.1  33 -  • 8.2  •60  30  20-3 • 10 9 •a  50 23-  7 15-  £ - 4 0  •6 • 5  10 3  20-  15 -  2.5  30  20  • 15  2X3  10-^  •10  9  0—=*  8  •6.5  To r e a d t h e c o r r e c t e d PC> ( s c a l e D) o r SaO ( s c a l e E) t h e measured temperature o r pH ' i s f o u n d o n s c a l e A o r B and a s t r a i g h t l i n e i s d r a w n t o t h e m e a s u r e d P0 on s c a l e C , 2  51  APPENDIX C SUBJECT PHYSIOLOGIC DATA  SUBJECT AGE (yrs)  HEIGHT (cms)  WEIGHT V02MAX (ml/kg/min) (kg)  HVR TREADMILL VELOCITY (l/%ASa02) (m/sec)  1  21  192.0  80.7  61.8  11.5  0.43  2  30  178.0  71.8  63.8  13.0  0.43  3  18  180.2  70.1  62,6  11.5  0.78  4  23  185.6  81.2  61.5  11.75  1.12  5  22  179.5  69.5  64.9  12.25  1.05  6  25  179.0  67.7  61.1  12.25  1.03  7  23  182.6  79.7  64.8  11.75  0.22  8  18  180.2  70.1  62.6  11.5  0.22  9  26  185.0  81.0  67.3 .  12.5  1.22  .10  24  169.0  61.4  66.8  12.5  0.87  11  28  179.5  74.3  61.7  11.75  0.43  12  27  184.8  73.6  61.8  11.75  0.26  52  APPENDIX D  SUBJECT FVC  PULMONARY FUNCTION TESTS  PRED. FVC MEASURED (1) (1)  %  FEV 1 (1)  % FVC  PEAK FLOW (1/min)  1  6.34  6.05  95.4  4.94  86.1  442  2  5.17  5.13  99.2  3.79  73.8  333  3  5.89  6.47  109.8  5.74  88.7  655  4  5.91  5.72  96.8  4.16  72.7  391  5  5.51  6.07  110.2  3.47  57.1  487  6  5.38  4.53  84.2  3.71  81.9  482  7  5.64  5.12  90.8  3.65  71.2  316  8  5.64  4.84  85.8  3.83  79.1  401  9  5.41  6.18  114.2  4.39  71.0  532  10  4.76  4.29  90.1  3.37  78.6  473  11  5.26  5.37  1.02  4.31  80.2  492  12  5.71  5.30  92.8  4.56  86.0  500  53  APPENDIX E HYPOXIC VFJCT1ATORY RESPONSE DATA 2 A and R for the line VE = A(Sa02) + Vo SUBJECT  TEST ONE A  R2  TEST TwO A  R2  TEST THREE HVR USED A R2  COMMENTS  0.41 0.80  0.45 0.82  0.43  mean of 1,2.  0.42 0.72  0.44 0.72  0.43  mean of 1,2.  0.78 0.70 1.25 0.  0.78 0.99 0.91  1.05 0.70  1.12  mean of 1,2.  1.05  1.10 0.89  0.% 0.93  1.03  0.15 0.29  0.08 0.25  0.28 0.40 0.22  mean of 1,3. poor 002 control i n 2.  0.22 0.63  0.07 0.12  0.21 0.81 0.22  mean of 1,3. two best f i t t i n g lines.  1.98 0.87  1.22 0.70  1.22  1 not used poor C02 control  10  0.87 0.77  11  0.43 0.77  0.14 0.45  0.43  12  0.18 0.49 -O.01 0.01  0.26 0.82 0.26  mean of 1,2.  0.87  VE i s observed ventilation, A = AVE/ l%ASa02, Vo i s calculated ventilation when Sa02 = 0  54  1 used as best f i t subject hyperventilatedat start of 1,2.  APPENDIX F SUBJECT DATA SUBJECT 1 TIME (min) pH  R  0:15 0:30 0:45 1:00 1:15 1:30 1:45 2:00 2:15 2:30 2:45 3:00 3:15 3:30 3:45 4:00 4:15 4:30 4:45 5:00  7.434 7.442 7.848 7.463 7.463 7.436 7.417 7.404 7.391 7.380 7.371 7.365 7.355 7.345 7.337 7.341 7.320 7.310 7.300 7.285 7.285  PC02 (torr)  36.5 35.3 37.7 37.7 36.0 36.1 39.3 34.1 36.1 35.4 36.9 34.6 37.2 36.7 36.4 32.9 32.6 37.3 30.3 31.7 30.5  P02 (torr)  91  106  100  92  93  93  98  92  93  87  89  87  85  86  87  86  88  81  85  80  84  97.4 98.3 98.2 97.6 97.7 97.5 97.7 97.3 97.2 96.5 96.7 96.4 96.0 96.0 96.0 96.1 96.1 94.8 95.4 94.4 95.0  Sa02 (%) V02(l/min)  1.33 2.78 3.95 4.52 4.20 4.58 4.32 4.65 4.28 4.62 4.64 4.42 4.82 4.77 4.62 4.87 4.78 4.78 4.70 4.86  VE(l/mixi BTR  58.0 88.0 107.5 130.3 131.5 146.4 142.5 157.1 146.8 161.3 162.7 156.3 167.4 169.0 167.9 164.1 169.1 169.1 166.9 170.9  SUBJECT 2 TIME (min) pH PC02 (torr)  R  7.442 7.465 7.451 7.431 7.408 7.380 7.353 7.353 7.337 7.319 7.279 7.260 7.242 7.230 7.213 7.201 7.183 7.165 7.146 7.137 7.122 36.5 34.1 38.7 35.8 39.4 40.4 40.6 40.9 40.0 36.4 39.4 39.9 40.0 38.5 39.3 38.6 38.5 38.4 38.4 38.5 38.1  P02 (torr) Sa02 (%)  0:15 0:30 0:45 1:00 1:15 1:30 1:45 2:00 2:15 2:30 2:45 3:00 3:15 3:30 3:45 4:00 4:15 4:30 4:45 5:00  113  131  113  97  97  97  94  97  99  98.6 99.2 98.6 97.8 97.6 97.4 97.0 97.2 97.3  95 Q8 f\  98  94  92  94  90  91  96.6 96.0 95.5 95.7 94.9 rv. n  88  87  1  93.7  Cll.  87 no  n  87  85 no  /  V02(l/min)  1.44 1.84 3.42 3.67 3.81 3.88 3.95 3.94 3.96 3.% 4.10 4.11 4.17 4.10 4.Z5 4.23 4.18 4.14 4.21 3.90  VE(l/miri BTR5)  57.6 67.4 88.9 99.4 107.1 117.4 125.9 129.9 129.5 130.0 135.7 136.2 139.7 135.9 139.0 144.5 141.3 138.4 138.2 124.7  SUBJECT 3 TIME (iron) pH RD2 (torr)  R  7.440 7.444 7.458 7.453 7.449 7.429 7.423 7.405 7.400 7.388 7.382 7.375 7.367 7.368 7.351 7.353 7.351 7.346 7.334 7.331 7.328 34.2 36.6 37.1 38.4 37.8 37.8 34.2 40.2 36.4 36.2 34.0 35.9 33.0 34.3 34.6 32.9 32.3 32.6 35.6 35.1 32.2  P02 (torr) Sa02 (%)  0:15 0:30 0:45 1:00 1:15 1:30 1:45 2:00 2:15 2:30 2:45 3:00 3:15 3:30 3:45 4:00 4:15 4:30 4:45 5:00  119  117  103  106  102  104  99  109  102  109  105  104  108  102  101  103  102  95  96  91  96  98.8 98.8 98.3 98.4 98.2 98.2 97.9 98.3 97.9 98.2 98.0 97.9 98.1 97.8 97.6 97.7 97.6 97.1 97.0 96.5 97.0  V02(l/ndn)  1.48 2.39 3.47 3.70 3.86 3.59 3.78 3.81 3.88 3.69 3.85 4.02 3.86 4.00 4.12 4.03 3.95 4.28 4.09 4.15  VE(l/min BTR5)  52.3 71.8 90.8 96.9 112.6 118.6 128.2 133.2 134.5 130.0 132.4 133.2 129.4 132.4 136.6 136.6 130.6 144.4 134.3 134.0  SUBJECT 4 TIME (min) pH KD2 (torr)  R  7.440 7.442 7.442 7.431 7.417 7.3% 7.384 7.368 7.335 7.338 7.322 7.311 7.295 7.282 7.272 7.266 7.256 7.244 7.230 7.221 7.207 38.4 38.1 39.2 37.0 37.9 40.2 37.4 37.9 38.1 38.0 40.9 39.6 37.3 36.8 39.4 38.7 37.3 36.3 37.2 37.4 35.7  P02 (torr) Sa02 (%)  0:15 0:30 0:45 1:00 1:15 1:30 1:45 2:00 2:15 2:30 2:45 3:00 3:15 3:30 3:45 4:00 4:15 4:30 4:45 5:00  100  107  88  83  83  86  86  86  93  89  83  84  84  83  84  86  86  85  84  82  85  98.0 98.4 97.1 96.5 96.4 96.5 96.4 96.3 96.8 96.3 95.3 95.2 95.1 94.7 94.8 95.0 94.9 94.5 94.1 93.0 94.0  V02(nti/min)  1.08 2.20 4.42 4.50 4.64 4.45 4.69 4.41 4.35 4.64 4.35 4.69 4.46 4.83 4.59 4.73 4.66 4.67 4.77 4.56  VE(l/niiii BTR5)  39.3 57.2 89.4 96.2 107.8 112.4 124.6 124.8 117.8 123.1 121.1 129.7 121.7 136.8 133.9 140.7 150.5 132.8 140.3 140.4  SUBJECT 5 TIME (nrLn) pH KD2 (torr)  R  7.437 7.404 7.439 7.430 7.404 7.376 7.366 7.347 7.330 7.320 7.313 7.295 7.282 7.275 7.255 7.250 7.234 7.223 7.205 7.194 7.179 40.3 40.2 39.1 38.8 40.4 42.9 41.2 39.0 41.5 39.6 38.7 38.3 37.3 39.5 38.3 35.4 38.7 36.9 36.4 36.1 37.7  P02 (torr) Sa02 (%)  0:15 0:30 0:45 1:00 1:15 1:30 1:45 2:00 2:15 2:30 2:45 3:00 3:15 3:30 3:45 4:00 4:15 4:30 4:45 5:00  105  107  105  96  92  93  95  92  89  88  87  86  86  83  82  82  80  80  81  81  79  98.2 98.2 98.2 97.6 97.2 97.0 97.1 96.7 96.1 96.0 95.8 95.5 95.2 94.6 94.1 94.0 93.4 93,1 93.1 92.9 91.7  V02(l/min)  0.60 1.38 2.44 3.64 3.93 3.93 4.02 3.89 4.22 4.01 4.07 4.24 4.10 4.24 4.33 4.35 4.19 4.46 4.19 4.36  vEQ/min BTR5).  22.8 55.2 76.3 96.3 107.4 114.1 123.6 124.1 134.7 129.5 134.6 139.8 131.6 137.9 139.0 140.2 137.8 145.7 139.6 144.7  SUBJECT 6 R  TIME (min) pH PC02 (torr)  7.400 7.424 7.413 7.390 7.371 7.348 7.332 7.315 7.300 7.266 7.238 7.235 7.213 7.194 7.178 7.160 7.149 7.132 39.2 34.9 38.0 40.8 41.5 40,6 39.6 39.4 40.1 41.3 42.5 40.0 41.4 39.5 41.8 39.2 38.6 40.6  P02 (torr) Sa02 (%)  0:15 0:30 0:45 1:00 1:15 1:30 1:45 2:00 2:15 2:30 2:45 3:00 3:15 3:30 3:45 4:00 4:15 4:30 4:45 5:00  106  122  101  94  95  95  92  93  90  87  84  88  83  83  81  84  81  81  98.1 98.8 97.9 97.2 97.1 97.0 96.6 96.5 96.0 95.1 94.3 94.8 93.5 93.3 92.5 92.9 92.1 91.4  V02(l/min)  1.69 2.04 3.12 3.86 3.48 3.93 3.89 3.77 4.00 3.62 4.11 3.94 4.08 3.94 4.15 4.25 3.59  VE(l/nun BTR5)  59.6 76.0 86.5 103.7 106.1 121.3 125.5 122.8 128.6 120.6 131.7 130.5 133.3 127.2 130.1 137.5 120.0  -  -  -  SUBJECT 7 R  TIME (min) pH  0:15 0:30 0:45 1:00 1:15 1:30 1:45 2:00 2:15 2:30 2:45 3:00 3:15 3:30 3:45 4:00 4:15 4:30 4:45 5:00  7.451 7.439 7.463 7.432 7.416 7.384 7.365 7.358 7.348 7.341 7.328 7.314 7.304 7.299 7.285 7.265 7.264 7.249 7.236 7.299 7.215 33.4 38.6 37.3 38.4 39.4 41.5 36.7 41.1 38.3 .41.2 41.2 39.7 36.6 39.5 41.5 38.5 39.9 40.3 41.3 40.9 41.1  PC02 (torr) P02 (torr)  100  112  107  96  86  86  85  84  89  84  87  80  78  79  85  86  77  76  75  79  75  91.8 98.5 98.5 97.7 96.7 96.4 96.2 95.8 96.3 95.6 95.9 94.7 94.1 94.2 95.0 95.1 93.1 92.6 92.1 93.1 91.5  Sa02 (%) V02(l/mLn)  2.84 3.14 4.41 4.98 4.79 4.88 5.00 5.20 4.90 5.07 5.22 5.07 4.96 5.19 4.95 5.23 5.10 5.15 5.15 4.96  VE(l/min BTR  92.6 103.3 111.8 128.5 127.8 129.3 132.3 143.9 137.5 143.0 148.1 143.6 143.0 150.0 142.6 150.1 146.4 150.7 150.3 145.1  SUBJECT 8 R  TIME (min) pH P002 (torr)  7.460 7.431 7.424 7.411 7.397 7.377 7.362 7.350 7.322 7.318 7.300 7.289 7.277 7.263 7.247 7.236 7.218 7.215 7.203 7.196 7.182 32.9 38.8 39.7 40.3 39.8 35.7 38.3 38.2 37.3 36.4 38.6 37.8 39.6 36.3 37.8 36.6 37.6 34.2 35.5 35.0 36.0  P02 (torr) Sa02 (%)  0:15 0:30 0:45 1:00 1:15 1:30 1:45 2:00 2:15 2:30 2:45 3:00 3:15 3:30 3:45 4:00 4:15 4:30 4:45 5:00  109  78  77  82  79  80 • 83  82  79  82  79  76  78  78  73  73  73  74  74  75  74  98.6 95.8 95.5 96.1 95.5 95.5 95.8 95.4 94.8 95.1 94.2 93.5 93.8 93.4 91.9 91.6 91.1 91.4 91.2 91.2 90.8  V02(l/min)  1.78 3.11 3.72 3.82 3.79 3.92 3.83 3.82 3.92 4.05 3.92 4.09 3.94 3.89 4.22 4.23 4.22 4.11 4.07 3.98  VE(l/nrin BTR5)  47.3 69.6 85.3 98.9 107.7 118.7 123.7 124.2 127.7 134.6 133.0.136.6 138.2 133.7 137.6 141.4 144.2 140.8 145.8 137.2  SUBJECT 9 R  TTME (min) PH F002 (torr)  7.431 7.473 7.472 7.469 7.437 7.422 7.392 7.384 7.368 7.355 7.335 7.327 7.312 7.298 7.284 7.277 7.259 7.248 7.233 7.219 7.208 38.3 31.4 34.4 35.4 36.2 36.0 36.6 36.6 36.6 36.4 36.7 36.8 36.7 36.6 35.9 36.9 36.9 34.7 36.1 35.9 35.6 107  P02 (torr) Sa02 (%)  0:15 0:30 0:45 1:00 1:15 1:30 1:45 2:00 2:15 2:30 2:45 3:00 3:15 3:30 3:45 4:00 4:15 4:30 4:45 5:00  123  122  103  91  91  84  87  83  82  78  78  77  76  73  72  72  73  70  70  71  98.3 99.9 99.0 98.3 97.4 97.3 96.3 96.5 95.9 95.6 94.7 94.4 94.1 93.7 92.7 92.3 91.7 91.9 90.6 90.2 90.1  V02(l/min)  1.09 2.30 4.15 4.94 4.74 4.67 5.10 5.07 5.13 5.18 5.24 5.43 4.32 5.44 5.52 5.37 5,45 5.58 5.43 5.59  VE(l/miii BDR5)  45.1 87.1 130.6 157.1 166.9 167.2 181.5 185.6 183.2 183.1 185.6 188.1 181.9 184.8 187.0 179.3 182.5 184.8 179.2 184.7  SUBJECT 10 TTME (min) pH P002 (torr)  R  7.434 7.475 7.478 7.430 7.417 7.405 7.373 7.360 7.331 7.313 7.286 7.280 7.273 7.254 7.236 7.226 7.209 7.198 7.187 7.190 7.161 27.4 30.3 32.7 31.4 35.2 35.2 36.8 35.8 36.2 35.8 33.6 37.4 34.1 33.8 35.4 34.5 35.5 34.6 35.4 33.0 35.7 125  P02 (torr) Sa02 (%)  0:15 0:30 0:45 1:00 1:15 1:30 • 1:45 2:00 2:15 2:30 2:45 3:00 3:15 3:30 3:45 4:00 4:15 4:30 4:45 5:00  117  103  91  89  91  89  87  86  86  83  81  84  84  78  81  77  77  76  75 75  99.0 98.9 98.4 97.4 97.1 97.2 96.7 96.3 95.9 95.7 94.9 94.5 94.8 94.7 93.1 93.6 92.1 92.0 91.5 91.4 90.6  V02(l/nrin)  1.61 2.11 3.57 3.88 3.65 3.85 3.87 4.13 4.07 4.17 4.30 4.21 4.15 4.36 4.13 4.35 4.40 4.35 4.40 4.14  VE(l/min BTR5)  66.8 90.2 114.5 128.0 129.8 134.4 139.2 148.3 145.9 151.2 155.7 151.5 148.2 154.5 147.4 151.2 156.2 151.2 152.5 141.4  SUBJECT 11  TIME (min) pH PG02 (torr)  R  7.443 7.470 7.480 7.455 7.439 7.436 7.395 7.379 7.357 7.340 7.331 7.317 7.298 7.285 7.268 7.260 7.244 7.242 7.123 7.213 7.207 44.1 40.3 43.4 36.3 35.8 38.7 39.2 39.2 42.6 41.3 39.8 40.8 41.2 41.3 42.3 41.0 40.8 40.4 40.6 38.9 41.8  P02 (torr) Sa02 (%)  0:15 0:30 0:45 1:00 1:15 1:30 1:45 2:00 2:15 2:30 2:45 3:00 3:15 3:30 3:45 4:00 4:15 4:30 4:45 5:00  101  126  106  98  88  83  89  77  75  74  73  73  70  70  69  70  70  71  69  68  66  98.0 99.1 98.4 98.0 97.1 96.6 96.9 95.0 94.3 93.8 93.4 93.2 92.0 91.6 90.9 91.0 90.5 91.0 89.7 89.1 88.1  VD2(l/nrin)  2.07 2.65 4.09 4.22 3.98 4.19 4.45 4.42 4.43 4.62 4.41 4.52 4.65 4.58 4.75 4.67 4.64 4.68 4.60 4.80  VE(l/min BTR  89.5 105.7 143.9 143.9 136.6 141.6 150.9 151.2 152.6 156.4 151.0 151.9 151.7 150.9 155.2 154.2 152.2 153.6 153.1 159.4  SUBJECT 12 TIME (min) pH FO02 (torr)  R  7.440 7.424 7.436 7.406 7.394 7.375 7.365 7.342 7.336 7.336 7.327 7.314 7.307 7.289 7.281 7.272 7.261 7.260 7.241 7.231 7.228 34.4 32.0 36.5 37.4 37.9 35.7 39.3 40.0 38.4 37.7 36.5 37.5 37.7 37.2 37.8 37.0 37.2 36.1 36.1 35.4 35.7  P02 (torr) Sa02 (%)  0:15 0:30 0:45 1:00 1:15 1:30 1:45 2:00 2:15 2:30 2:45 3:00 3:15 .3:30 3:45 4:00 4:15 4:30 4:45 5:00  113  98  94  75  76  76  76  76  75  74  75  71  71  71  67  69  68  68  70  68  71  98.6 97.9 97.6 95.0 95.0 94.9 94.7 94.2 94.0 93.8 94.0 93.7 92.5 92.0 90.7 91.3 90.6 90.7 90.7 90.0 90.9  V02(l/rtrLn)  1.31 2.08 4.61 3.93 4.13 4.13 4.37 4.38 4.44 4.07 4.38 4.30 4.26 4.44 4.45 4.63 4.22 4.58 4.56 4.62  VE(l/ndn BTR5)  62.3 70.0 103.8 102.7 109.5 108.7 116.0 125.8 138.9 131.0 133.6 129.7 125.9 129.5 128.9 136.0 129.6 136.2 140.3 145.4  APPENDIX G EQUIPMENT AND  SUPPLIES:  Equipment: 1. C a r d i a c m o n i t o r 2. B e c k m a n M e t a b o l i c M e a s u r e m e n t c a r t 3. H e w l e t t - P a c k a r d data a q u i s i t i o n system 4. s p i r o m e t e r 5 . C02 s e n s o r 6. 02 s e n s o r 7. b r e a t h i n g b a g a n d c i r c u i t 8. n i t r o g e n g a s a n d t w o way R u d o l p h v a l v e 9. c a r b o n d i o x i d e g a s 10. b l o o d g a s a n a l y z e r 11. t r e a d m i l l 12. c l o c k 1 3 . pneumo t a c h 14. e a r o x i m e t e r Supplies: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15.  A r t e r i a l cannulas plastic syringes # 22 g a u g e n e e d l e s # 18 g a u g e n e e d l e s 20 c c s y r i n g e s 5 cc s y r i n g e s #20 b u t t e r f l y i . v heparin locks OP-site compression tape h e p a r i n 1000 u/ml 10ml n o r m a l s a l i n e 5 0 0 ml bandages a l c o h o l swabs 2x2 g a u z e  20 100 100 20 20 20 20 20 20 1 roll 5 bottles 16 b a g s  Personnel: Day o n e : 1- p u l m o n a r y f u n c t i o n t e s t s 2- t r e a d m i l l r u n a n d B e c k m a n Day t w o : E x e r c i s e 1-timer 1-sampler  test 1-laboratory  Day t h r e e : 1-recorder 1-gas mixture  61  assistant  APPENDIX H EXERCISE  VENTILATION  STUDY  The purpose of t h i s study i s to r e l a t e the changes i n a r t e r i a l oxygen c o n c e n t r a t i o n and b r e a t h i n g d u r i n g heavy p h y s i c a l work. The subjects a r e r e c r u i t e d on a v o l u n t e e r basis and a r e n o r m a l h e a l t h y m a l e s who a r e h i g h l y t r a i n e d . On t h e f i r s t t e s t i n g s e s s i o n y o u w i l l h a v e m e a s u r e s o f y o u r l u n g f u n c t i o n s a n d maximum voluntary ventilation. This entails breathing through a m o u t h p i e c e s o t h a t y o u r v o l u m e o f e x p i r a t i o n a n d f l o w r a t e c a n be measured. These procedures are not associated with any significant risk. Following t h e s e d e t e r m i n a t i o n s you w i l l be asked to breathe through another apparatus. During t h i s measure t h e c o n c e n t r a t i o n o f o x y g e n i n t h e i n s p i r e d g a s w i l l be g r a d u a l l y be d e c r e a s e d a n d t h e c h a n g e i n y o u r b r e a t h i n g i n r e s p o n s e t o t h i s will be measured. T h i s p r o c e d u r e w i l l be done under medical supervision and your heart will be monitored through out. Extremely rarely irregularities i n heart rhythm have been reported with t h i s procedure. O t h e r c o m p l i c a t i o n s have n o t been reported. On the next t e s t i n g s e s s i o n , you w i l l have your maximal oxygen uptake according to e s t a b l i s h e d study protocol on a treadmill. The w o r k l o a d on t h e t r e a d m i l l w i l l be i n c r e a s e d , in stages until you a r e u n a b l e to continue, while the gas concentrations a r e d e t e r m i n e d i n your e x p i r e d gas as you b r e a t h e through a mouthpiece. The r i s k s o f t h i s p r o c e d u r e a r e minimal; some minor d i s c o m f o r t i n t h e jaw muscles and some increased a w a r e n e s s o f y o u r b r e a t h i n g may be n o t i c e d . Once your maximal oxygen uptake i s determined,you will be b r o u g h t b a c k on a n o t h e r d a y a n d w i l l p e r f o r m a f i v e m i n u t e r u n a t 100% o f y o u r V02 max. D u r i n g t h i s r u n you w i l l again breathe through t h e m o u t h p i e c e s o t h a t y o u r r a t e o f v e n t i l a t i o n c a n be m e a s u r e d . A l s o a t t h i s t i m e you w i l l have an i n d w e l l i n g c a n u l a i n y o u r r a d i a l a r t e r y . T h i s p r o c e d u r e i n v o l v e s some m i n o r d i s c o m f o r t s i m i l a r to t h a t of having a c o n v e n t i o n a l blood sample taken. The risks of t h i s procedure w i l l be m i n i m i z e d by using trained physician with s p e c i a l expertise i n this procedure. These risks include a s m a l l chance of i n f e c t i o n or i n c r e a s e d b l e e d i n g a t the s i t e of the puncture. I n e x t r e m e l y r a r e i n s t a n c e s an a n e u r i s m o r d i l a t i o n a t t h e s i t e o f t h e c a t h e t e r i n s e r t i o n c o u l d o c c u r . Spasm of t h e a r t e r y c a u s i n g i m p a i r e d b l o o d s u p p l y t o t h e hand could also occur r a r e l y a n d you. w i l l be c h e c k e d to insure adequate a l t e r n a t e blood supply p r i o r to i n s e r t i o n of the cannula. The benefits of the study include the opportunity to participate i n physiologic research, and t h e o p p o r t u n i t y t o have a V02 max d e t e r m i n a t i o n . I F YOU HAVE ANY QUESTIONS ABOUT THE STUDY PROCEDURES WE W I L L BE HAPPY TO ANSWER THEM NOW OR AT ANY TIME. I have read and understand t h e above and agree to p a r t i c i p a t e i n the study. I u n d e r s t a n d t h a t I have t h e r i g h t to w i t h d r a w a t any t i m e , w i t h o u t question. DATE :  "  SIGNATURE: WITNESS: 62  

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