II26 



HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY II 



pattern; it is constantly being inhibited or facilitated 

 through central nervous, reflex or humoral influences. 

 Actually, the number of factors which can influence 

 respiration in the intact animal is so great that 

 virtually the entire organism can be said to con- 

 tribute something to the control of respiration. 



The complexity of the problem is best illustrated 

 when one attempts to uncover the origin of the hy- 

 perpnea associated with muscular effort. This type of 

 hyperpnea has commanded the interest of investi- 

 gators for many years since very large respiratory 

 minute volumes can be measured. Yet this increase 

 in respiration cannot arise merely from a change in 

 composition of the blood gases — in the steady state, for 

 example, the arterial pCOa is lowered rather than 

 increased. From the very beginning of research on 

 this problem, four theories for the occurrence of 

 increased ventilation with muscular activity were 

 suggested. These have often been advocated even by 

 more recent investigators. 



a) The assumption was made that working muscles 

 produce unknown metabolic products which stimu- 

 late the respiratory center, either directly or through 

 a reflex mechanism (9, 73, 79). .Such substances have 

 occasionally been designated as 'hyperneine,' but 

 their existence seems questionable (109). 



b) It was suggested that 'work hyperpnea' could be 

 elicited, through a reflex mechanism, by afferent 

 impulses from active muscles and joints (61, 62, 82). 

 In the dog, for example, leg movements evoked by 

 stimulation of the ventral roots lead immediately to 

 hyperpnea. This fails to occur when the spinal cord 

 has been cut at the level of the tenth thoracic verte- 

 bra, or appears later in a weaker form — similar to the 



reaction in the cat before spinal cord section. In a 

 similar manner, the hyperpnea produced in man 

 through passive mo\ements of the legs ma\' be 

 abolished by spinal anesthesia (45). The increased 

 ventilation elicited by electrical stimulation of affer- 

 ent fibers from joints and muscles (45, 60, 71, 210) also 

 argues for the possibility of a reflex activation of 

 respiration. 



c) From the sudden onset of hyperpnea at the 

 beginning of increased voluntary activity, a direct 

 cortical influence on the respiratory center has been 

 inferred (117, 134). 



(/) On the basis of excitability studies with carbon 

 dioxide, the assumption has been made that muscular 

 activity gives rise to a general enhancement in the 

 sensitivity of the respiratory center to chemical and 

 other stimuli (115, 117, 140). The more easily ex- 

 citable respiratory center could then be activated in 

 the presence of a lower pCOi in arterial blood. But 

 the nature of this increase in sensitivity is as little 

 understood as that of the greater sensitivity of the 

 respiratory center towards carbon dioxide which 

 occurs with acclimatization to high altitudes. 



Considered alone, none of these suggested mech- 

 anisms entirely explains the occurrence of hyperpnea 

 in connection with muscular activity. Therefore, one 

 must assume that, in this case at least, chemical and 

 nervous influences are laoth in\olved. From a teleo- 

 logical point of view, such a complex method of 

 regulating respiration must be considered the more 

 suitable, for only in this way can a ventilation be 

 maintained which is capable of meeting widely 

 varving bodilv needs. 



REFERENCES 



1. AcHARD, O. .'iND V. M. BucHER. Hclvfl p/ivswl. el Pharma- 

 col, acta 12: 265, 1954. 



2. Adri.^n, E D. J . Physiol. 79: 332, 1933. 



3. Adrian, E. D. .and D VV. Bronk. j. Phvsiol. 66: 81 

 1928. 



4. Allen, W. F. .-im J. P/iyuol. 88: 117, 1929. 



5. Allen, W. F. Am. J. Physiol. 88: 620, 1929 



6. Allen, \V F. Am. J. Physiol. 115:579, 1936. 



7. Amoroso, E. C, F. R. Bell and H. Rosenberg. Pruc. Ruv. 

 Soc, London, ser. B 139: 128, 1951-52. 



8. .-^nderegcen, p., R. J. H. Oberholzer and O. .\. M. 

 Wyss. Helvet. physiot. et Pharmacol, acta ^^ 213, 1946. 



9. Asmussen, E. and M. Nielsen. Acta physiol. scandinav. 12: 

 1^71, 1946. 



10. AsTRAND, P. O. Acta physiol. scandinav. 30: 335, 1954. 



11. Aviado, D M., Jr. and C. F. .Schmidt. Physiol. Rev. 35: 

 247. 1955- 



12. Bach, L. M. N. .Am. J. Physiol. 171 : 417, 1952. 



13. B.-^ilev, p. and W. H. Sweet. J. j\'europhysiol. 3: 276, 

 1940. 



14 Banus, M. G., H. H. Gorman, V. P. Perlo and G. H. 

 PoPKlN. Am. J. Physiol. 142: 121, 1944. 



15. Bartels, H. and E. Witzleb Arch. ges. Physiol. 262: 466, 

 '956- 



16. B.AXTER, D. \V. .AND J. Olszewski. J. .Xeurophysiol. 18: 276, 



'955- 



17. Bean, J. \V. .4m. J. Physiol. 171: 522, 1952. 



18. Beaton, L. E. and H. VV. Magoun. Am. J. Physiol. 134: 



177, 1941. 



19. Beyer, H. G. Arch. Anat. Physiol. 261, 1901. 



20. BiNET, A. AND J. Courtier, .innce Psychol. 3: 65, 1897. 



21. Bjurstedt, .\. G. H .Ada phyiioL scandinav. 12: Suppl. 38, 

 1946. 



