SUMMARY1. The influence of pedal rate on ventilatory response and breathing pattern during cycle exercise was studied in twelve untrained female subjects performing 15 W/min incremental work on a bicycle at 30 and 60 r.p.m. Comparisons were made within the range of aerobic work rate to avoid additional influences of a developing lactic acidosis.2. At each pedal rate, CO2 excretion (VC702) increased progressively to a level of

During incremental exercise in normal humans, pulmonary ventilation (V E) linearly increases with increasing O 2 uptake (V O 2 ), but the increment of V E against V O 2 becomes steeper at two V O 2 points [1]. The first inflection point, occurring at a lower V O 2 , is termed the ventilatory threshold (VT) [2], above which various kinds of ventilatory stimuli such as a fall in arterial pH due to lactic acidosis, hyperkalemia and augumentation of arterial PCO 2 oscillation are newly induced [3][4][5][6]. With further increases in the ventilatory stimuli as exercise becomes heavier, a steeper increase in V E against V O 2 occurs. The V O 2 point of the onset of this V E augmentation is termed the respiratory compensation point (RCP), above which the V E augmentation (hyperventilation) induces a fall in arterial PCO 2 , with resulting constraint of further falls of arterial pH due to severer lactic acidosis [7]. Peripheral chemoreceptors have been implicated as the site at which the ventilatory stimuli act because of the absence of compensatory hyperventilation and subsequent fall in PCO 2 during heavy exercise in carotid body-resected patients [8,9]. Japanese Journal of Physiology, 50, 449-455, 2000 Key words: heavy exercise, respiratory compensation point, exercise hyperpnea, carotid body, lactic acidosis. Abstract:The pulmonary ventilation-O 2 uptake (V E-V O 2 ) relationship during incremental exercise has two inflection points: one at a lower V O 2 , termed the ventilatory threshold (VT); and another at a higher V O 2 , the respiratory compensation point (RCP). The individuality of RCP was studied in relation to those of the chemosensitivities of the central and peripheral chemoreceptors, which were assessed by resting estimates of hypercapnic ventilatory response (HCVR) and hypoxic ventilatory response (HVR), respectively, and the rate of lactic acid increase during exercise, which was estimated as a slope difference (⌬slope) between a lower slope of V CO 2 -V O 2 relationship (V CO 2 : CO 2 output) obtained at work rates below VT and a higher slope at work rates between VT and RCP. Twenty-two male and sixteen female subjects underwent a 1 min incremental exercise test until exhaustion, in which VT, RCP and ⌬slope were determined. All measures were normalized for body surface area. In the males, the individual difference in RCP was inversely correlated with those of HVR and ⌬slope (pϽ0.05), and in the females, similar tendencies persisted, while the correlation did not reach statistically significant levels (0.05ϽpϽ 0.1). There was no significant correlation between RCP and HCVR in either sex. A multiple linear regression analysis showed that 40 to 50% of the variance of RCP was accounted for by those of HVR and ⌬slope, both of which were related linearly and additively to RCP, this relation being manifested in the males but not in the females without consideration of the menstrual cycle. These results suggest that the individuality of RCP depends partly on the chemosensitivity of the carotid bodies and th...

Differential effects of uphill and downhill running on phase relation between locomotor and respiratory cycles were studies in nine experienced runners who were instructed to run uphill and downhill on a sloped surface at comfortable and constant speeds (actually 1.7-4.4 m s-1). Timings of footstrike and onsets of inspiration and expiration were measured to compute respiratory cycle duration (Ttot), inspiratory time (Ti), duty cycle (Ti/Ttot), and stride time (Ts). Incidence of locomotor/respiratory coupling (LRC) was determined based on steadiness of Ttot and Ts (within +/- 0.1 s in SD) and Ttot/Ts (LRC ratio, integer or a half-integer multiples). Both in the uphill and downhill running, LRC ratio observed was 1:1, 2:1, and 2.5:1. Ti/Ttot during LRC was 0.41-0.49, which depended on the combinations of Ts and LRC ratio but not on the running conditions. In the uphill running, the onset of inspiration subsequent to footstrike was seen during the first half period (corresponding to the support phase) of the step interval (Ts/2, the time interval between the right and left footstrikes) in 7 of the 9 subjects, while in the downhill running it occurred during the last half period of the step interval (the floating phase) in all subjects. For onset of expiration, no consistent relation to footstrike was observed. These results suggest that the mechanical constraints of running on the respiratory system affect the phase relation between locomotor and respiratory cycles but not Ti/Ttot during LRC.

We attempted to analyze how PACO2 is regulated during progesterone-induced hyperventilation in the luteal phase. A model for the CO2 control loop was constructed, in which the function of the CO2 exchange system was described as PACO2 = 0.863 x VCO2/VA (gain H = dPACO2/dVA) and that of the CO2 sensing system as VA = S (PACO2 - B). Using this model, we estimated (1) the primary increase in VA (delta VA (op)) produced by progesterone stimulation and (2) the effectiveness (E) of the loop to regulate PACO2, defined as delta PACO2 (op)/delta PACO2 (cl) in which op signifies open-loop and cl, closed-loop. These respiratory variables were investigated throughout the menstrual cycle in 8 healthy women. During the luteal phase, on average, VA increased by 9.4% and PACO2, B and H decreased by 0.33 kPa (2.5 mm Hg), 0.47 kPa (3.5 mm Hg) and 13.6%, respectively, while S and VCO2 did not change significantly. Delta VA (op) increased progressively on successive days of the luteal phase while E remained unchanged at a value of 7.9, thus there was a progressive decrease in PACO2. The decrease in H was considered to lessen delta PACO2 (op) and so reduce the final deviation of PACO2 (delta PACO2 (cl) during the luteal phase. The decrease in B was found to be dependent on delta VA (op).

The conscious entrainment of respiratory rhythm to exercise rhythm (ENT) has been hypothesized to alleviate breathing discomfort and reduce the oxygen (O2) cost of ventilation with a resulting decrease in total O2 uptake (VO2) during rhythmic exercise. This hypothesis has been tested in the study reported here. Eight female subjects performed cycle exercise at 50 rpm under two work load conditions of 40% and 60% of maximal VO2. During a 30-min exercise period at each work load, each subject was asked to breathe under two conditions for 15 min each: (1) spontaneously (non-ENT run), and (2) deliberately entraining the breathing rhythm to the cycling rhythm at preferred coupling ratios of the two rhythms (ENT run). In the ENT run, most subjects chose a ratio of 1:2. In each run, pulmonary ventilation (VE), total VO2 and the breathlessness sensation (BS) were measured at 4-5 min. BS was assessed according to a Borg category scale. The remaining 10 min of each 15-min run were allotted for measurement of the O2 cost of ventilation (delta VO2/delta VE), assessed by a hypercapnia-induced hyperventilation method in which the VO2 of the respiratory muscles (VO2RM) was calculated by multiplying delta VO2/delta VE by the prevailing VE. On average, there were no significant differences in any of the variables, VO2, delta VO2/delta VE, VO2RM and BS, between the non-ENT and ENT runs performed at any work load. However, there were wide variations among the subjects in the differences (delta) between the two runs, and significant correlations were found between delta VO2 vs delta VE, delta VO2 vs delta VO2RM, and delta BS vs delta VO2RM of individual subjects. These results indicate that reductions of the total VO2 and BS with ENT could occur in subjects in whom the VO2RM decreased during ENT.