References: Tantucci et al, 1996
Tantucci C, Bottini P, Dottorini ML, Puxeddu E, Casucci G, Scionti L, Sorbini CA
Ventilatory response to exercise in diabetic subjects with autonomic neuropathy
J Appl Physiol 1996, 81(5): p.1978–1986.
Clinica di Semeiotica Metodologia Medica, University of Ancona, Ospedale Regionale Torrette, Ancona 60020; and Istituto di Medicina Interna e Scienze Endocrine e Metaboliche, University of Perugia, Perugia 06100, Italy
We have used diabetic autonomic neuropathy as a model of chronic pulmonary denervation to study the ventilatory response to incremental exercise in 20 diabetic subjects, 10 with (Dan1) and 10 without (Dan2) autonomic dysfunction, and in 10 normal control subjects. Although both Dan1and Dan2 subjects achieved lower O2 consumption and CO2 production (V˙ CO2) than control subjects at peak of exercise, they attained similar values of either minute ventilation (V˙ E) or adjusted ventilation (V˙ E/maximal voluntary ventilation). The increment of respiratory rate with increasing adjusted ventilation was much higher in Dan1 than in Dan2 and control subjects (P , 0.05). The slope of the linear V ˙ E/V˙ CO2 relationship was 0.032 6 0.002, 0.027 6 0.001 (P , 0.05), and 0.025 6 0.001 (P , 0.001) ml/min in Dan1, Dan2, and control subjects, respectively. Both neuromuscular and ventilatory outputs in relation to increasing V ˙ CO2 were progressively higher in Dan1 than in Dan2 and control subjects. At peak of exercise, end-tidal PCO2 was much lower in Dan1 (35.9 6 1.6 Torr) than in Dan2 (42.1 6 1.7 Torr; P , 0.02) and control (42.1 6 0.9 Torr; P , 0.005) subjects. We conclude that pulmonary autonomic denervation affects ventilatory response to stressful exercise by excessively increasing respiratory rate and alveolar ventilation. Reduced neural inhibitory modulation from sympathetic pulmonary afferents and/or increased chemosensitivity may be responsible for the higher inspiratory output.