Acute Cardiopulmonary and Muscle Oxygenation Responses to Normocapnic Hyperpnea Exercise in COPD.

PURPOSE: This study aimed to investigate cardiorespiratory responses and intercostal muscle oxygenation during normocapnic hyperpnea exercise in chronic obstructive pulmonary disease (COPD). METHODS: Twenty-two patients with COPD performed a cardiopulmonary cycling exercise test to assess peak oxygen consumption (V˙O2peak) and minute ventilation (V˙Epeak). They also performed a normocapnic hyperpnea exercise alone, at 50%-60% of V˙Epeak to exhaustion, using a respiratory device (Spirotiger) connected to a gas analyzer to monitor V˙O2, V˙E, and end-tidal CO2 partial pressure. Cardiac output, and intercostal and vastus lateralis muscle oxygenation were continuously measured during exercise using finger photoplethysmography and near-infrared spectroscopy, respectively. Arterial blood gases (arterial PCO2) and inspiratory capacity were obtained at rest and at the end of hyperpnea exercise. RESULTS: The hyperpnea exercise lasted 576 ± 277 s at a V˙E of 34.5 ± 12.1 L·min-1 (58% ± 6% of V˙Epeak), a respiratory rate of 22 ± 4 breaths per minute, and a tidal volume of 1.43 ± 0.43 L. From rest to the end of hyperpnea exercise, V˙O2 increased by 0.35 ± 0.16 L·min-1 (P < 0.001), whereas end-tidal CO2 partial pressure and arterial PCO2 decreased by ~2 mm Hg (P = 0.031) and ~5 mm Hg (P = 0.002, n = 13), respectively. Moreover, inspiratory capacity fell from 2.44 ± 0.84 L at rest to 1.96 ± 0.59 L (P = 0.002). During the same period, heart rate and cardiac output increased from 69 ± 12 bpm and 4.94 ± 1.15 L·min-1 at rest to 87 ± 17 bpm (P = 0.002) and 5.92 ± 1.58 L·min-1 (P = 0.007), respectively. During hyperpnea exercise, intercostal deoxyhemoglobin and total hemoglobin increased by 14.26% ± 13.72% (P = 0.001) and 8.69% ± 12.49% (P = 0.003) compared with their resting value. However, during the same period, vastus lateralis oxygenation remained stable (P > 0.05). CONCLUSIONS: In patients with COPD, normocapnic hyperpnea exercise provided a potent cardiorespiratory physiological stimulus, including dynamic hyperinflation, and increased intercostal deoxyhemoglobin consistent with enhanced requirement for muscle O2 extraction.

Cardiorespiratory and Muscle Oxygenation Responses to Isokinetic Exercise in Chronic Obstructive Pulmonary Disease.

PURPOSE: This study aimed to describe cardiorespiratory, quadriceps oxygenation, and muscle fatigue responses during a one-legged quadriceps isokinetic endurance exercise in chronic obstructive pulmonary disease (COPD) and control subjects. METHODS: Fourteen patients with COPD and 14 control subjects performed a cardiopulmonary cycling exercise test to exhaustion to assess peak oxygen consumption (V˙O2peak), minute ventilation (V˙Epeak), and heart rate (HRpeak). They also performed a quadriceps isokinetic endurance exercise consisting in 30 maximal knee extensions at 90°·s with continuous monitoring of expired gases, cardiac output, and oxygenation of the quadriceps by near-infrared spectroscopy. Total muscle work and fatigue index were also quantified. RESULTS: The total muscle work developed during the quadriceps isokinetic endurance exercise was 2.25 ± 0.57 kJ in COPD and 3.12 ± 0.60 kJ in controls, P < 0.001. In absolute terms, there were no between-group differences in V˙O2, V˙E, cardiac output, and HR at the end of quadriceps isokinetic endurance exercise. However, V˙E and HR reported that a fraction of their respective peak values during cardiopulmonary cycling exercise test were higher in COPD (V˙E/V˙Epeak, 69% ± 3%; HR/HRpeak, 82% ± 15%) compared with controls (V˙E/V˙Epeak, 45% ± 2%; HR/HRpeak, 71% ± 13%), all P < 0.05. During quadriceps isokinetic endurance exercise, quadriceps deoxyhemoglobin increased by 47% ± 31% in patients versus 33% ± 41% in controls (P < 0.05 from rest values) with a significant between-group differences (P = 0.025). The fatigue index during the quadriceps exercise was higher in COPD compared with controls. CONCLUSIONS: Although one-legged quadriceps isokinetic endurance exercise resulted in substantial central cardiorespiratory demands in COPD, this exercise was nevertheless associated with muscle overload as evidenced by muscle deoxygenation and higher muscle fatigue index in COPD compared with controls. These findings may have implications of the design of exercise training programs in COPD.

Respiratory muscle strength is decreased after maximal incremental exercise in trained runners and cyclists.

The respiratory muscle fatigue seems to be able to limit exercise performance and may influence the determination of maximal oxygen uptake (V̇O2max) or maximum aerobic work rate during maximal incremental test. The aim of this study was therefore to investigate whether maximal incremental exercise decreases respiratory muscle strength. We hypothesized that respiratory muscle strength (maximal pressure) will decrease after maximal incremental exercise to exhaustion. 36 runners and 23 cyclists completed a maximal incremental test on a treadmill or a cycle ergometer with continuous monitoring of expired gases. Maximal inspiratory (MIP) and expiratory (MEP) pressure measurements were taken at rest and post- exercise. At rest, the MIP and MEP were 140±25 and 172±27 in runners vs. 115±26 and 146±33 in cyclists (p<0.05 between groups, respectively). The rest values of MIP and MEP were correlated to the V̇O2peak in all athletes, r=0.34, p<0.01 and r=0.36, p<0.01, respectively. At exhaustion, the MIP and MEP decreased significantly post- test by 13±7% and 13±5% in runners vs. 17±11% and 15±10% in cyclists (p>0.05), respectively. Our results suggest that respiratory muscle strength is decreased following maximal incremental exercise in trained runners and cyclists.

Respiratory and locomotor muscle implications on the VO2 slow component and the VO2 excess in young trained cyclists.

We investigated the impact of ramp and constant-load exercise on (i) respiratory muscle fatigue and locomotor muscle oxygenation, (ii) their relationship with the excess VO2 and VO2 slow component (SC). Fourteen male cyclists performed two tests to exhaustion: an incremental ramp and a constant-load exercise with continuous monitoring of expired gases and oxygenation of the vastus lateralis muscle on two separate days. Maximal inspiratory (MIP) and expiratory (MEP) pressure measurements were taken at rest and post- exercise. The VO2 excess represents the difference between VO2max observed and VO2max expected using linear equation between the VO2 and the intensity before gas-exchange threshold. During the ramp exercise, MIP and MEP declined by 13±8 and 19±10%, respectively (p<0.05). MIP and MEP were not correlated to the excess VO2 (0.09±0.05lmin-1). During the constant-load exercise, the VO2 SC (0.70±0.22lmin-1) was correlated (r=0.68, p<0.01) to deoxyhemoglobin SC (2.94±1.25AU) but not to the excess VO2 (r=0.30, p=0.2). Additionally, the significant decrease in MIP (20±9%) and MEP (23±11%) was correlated (r=0.55, p<0.05 and r=0.75, p<0.05, respectively) to the VO2 SC. Our results show that respiratory muscle fatigue was correlated to the VO2 SC in the constant-load exercise, whereas it was not correlated to the excess VO2 in ramp exercise may be because of our small excess VO2.

Excess VO2 during ramp exercise is positively correlated to intercostal muscles deoxyhemoglobin levels above the gas exchange threshold in young trained cyclists.

We assessed respiratory muscles oxygenation responses during a ramp exercise to exhaustion and further explored their relationship with the non-linear increase of VO2 (VO2 excess) observed above the gas-exchange threshold. Ten male cyclists completed a ramp exercise to exhaustion on an electromagnetically braked cycle-ergometer with a rate of increment of 30Wmin(-1) with continuous monitoring of expired gases (breath-by-breath) and oxygenation status of intercostal muscles. Maximal inspiratory and expiratory pressure measurements were taken at rest and at exhaustion. The VO2 excess represents the difference between VO2max observed and VO2max expected using linear equation between the VO2 and the intensity before gas-exchange threshold. The deoxyhemoglobin remained unchanged until 60% of maximal aerobic power (MAP) and thereafter increased significantly by 37±18% and 40±22% at 80% and 100% of MAP, respectively. Additionally, the amplitude of deoxyhemoglobin increase between 60 and 100% of MAP positively correlated with the VO2 excess (r=0.69, p<0.05). Compared to exercise start, the oxygen tissue saturation index decreased from 80% of MAP (-4.8±3.2%, p<0.05) onwards. At exhaustion, maximal inspiratory and expiratory pressures declined by 7.8±16% and 12.6±10% (both p<0.05), respectively. In summary, our results suggest a significant contribution of respiratory muscles to the VO2 excess phenomenon.

Respiratory muscle endurance, oxygen saturation index in vastus lateralis and performance during heavy exercise.

The purpose of this study was to investigate the relationships between respiratory muscle endurance, tissue oxygen saturation index dynamics of leg muscle (TSI) and the time to exhaustion (TTE) during high intensity exercise. Eleven males performed a respiratory muscle endurance test, a maximal incremental running field test (8 km h(-1)+0.5 km h(-1) each 60s) and a high-intensity constant speed field test at 90% VO2max. The TSI in vastus lateralis was monitored with near-infrared spectroscopy. The TSI remained steady between 20 and 80% of TTE. Between 80 and 100% of TTE (7.5 ± 6.1%, p<0.05), a significant drop in TSI concomitant with a minute ventilation increase (16 ± 10 l min(-1)) was observed. Moreover, the increase of ventilation was correlated to the drop in TSI (r=0.70, p<0.05). Additionally, respiratory muscle endurance was significantly correlated to TSI time plateau (20-80% TTE) (r=0.83, p<0.05) and to TTE (r=0.95, p<0.001). The results of the present study show that the tissue oxygen saturation plateau might be affected by ventilatory work and that respiratory muscle endurance could be considered as a determinant of performance during heavy exercise.