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Background: Reduced heart rate variability (HRV), a marker of autonomic system dysfunction, has been reported in patients with chronic obstructive pulmonary disease (COPD). Yet, limited data exists on the reliability of HRV measurement in this population. Here we investigated the reliability of short-term HRV measurement performed during spontaneous breathing in patients with COPD. Methods: Thirteen individuals (8 males) with moderate-to-severe COPD (FEV1 46 ± 16% predicted; FEV1/FVC 49 ± 13) underwent standard time and frequency domain HRV measurements derived from 5-minute electrocardiograms collected on two separate days using a SphygmoCor device. Absolute and relative reliability was assessed by a number of coefficients including within-subject random variation, systematic change in the mean, and retest correlations. Results: Within-subject coefficients of variation (CV) ranged from 4.3% to 193.4%. The intraclass correlation coefficients (ICC) ranged from 0.72 to 0.93 for parameters related to overall HRV, and from 0.57 to 0.59 for those related to parasympathetic tone in both time and frequency domains. Mean heart rate was the only parameter that showed excellent absolute and relative reliability (CV = 4.3%, ICC = 0.93). Conclusion: The HRV parameters showed overall moderate-to-substantial reliability during spontaneous breathing in COPD population. Our findings support the use of HRV parameters for diagnosis and cardiac risk assessment, but only mean heart rate can be used reliably for monitoring changes in autonomic status following rehabilitation intervention in this population.

Background: Myocardial infarction (MI) remains under-recognized in chronic lung disease (CLD) patients. Rehabilitation health professionals need accessible clinical measurements to identify the presence of prior MI in order to determine appropriate training prescription. Objectives: We aimed to estimate prior MI in CLD patients entering a pulmonary rehabilitation program, as well as its association with heart rate parameters such as resting heart rate and chronotropic response index. Design: Retrospective cohort design.Setting: Pulmonary rehabilitation outpatient clinic in a tertiary care university-affiliated hospital. Patients: Eighty-five CLD patients were studied. Methods: Electrocardiograms at rest and peak cardiopulmonary exercise testing, performed before pulmonary rehabilitation, were analyzed. Electrocardiographic evidence of prior MI, quantified by the cardiac infarction injury score (CIIS), was contrasted with reported myocardial events and then correlated with resting heart rate and chronotropic response index parameters. Main outcome measurements: Cardiac infarction injury score, resting heart rate and 40 chronotropic response index. Results: Sixteen CLD patients (19%) demonstrated electrocardiographic evidence of prior MI, but less than half (8%) had a reported MI history (p 20. Conclusions: CLD patients entering pulmonary rehabilitation are at risk of unreported prior MI. Elevated resting heart rate seems to be an indicator of prior MI in CLD patients; therefore, careful adjustment of training intensity such as intermittent training is recommended under these circumstances. Level of evidence: III

The consensus in the literature is that exercise-induced hypoxemia (EIH) occurs secondary to ventilation-perfusion (VA/Q) inequalities and diffusion limitations resulting from elevated pulmonary pressures causing the development of interstitial pulmonary edema, or decreased pulmonary transit time in the pulmonary vasculature. Endogenously produced pulmonary nitric oxide (NO) has been hypothesized to have several physiological functions including VA/Q matching and maintenance of low pulmonary vascular resistance. Respiratory derived NO is detectable in exhaled gases. Inhaled NO, a selective pulmonary vasodilator is used in the treatment of diseases characterized by pulmonary hypertension and hypoxemia. Short-term inhalation of NO causes selective pulmonary vasodilation without any systemic effects. Given that athletes with EIH are thought to have altered pulmonary hemodynamics during exercise, the relationship between endogenously produced and exogenously delivered NO and EIH was examined in two separate studies. It was hypothesized that subjects with EIH would have a decreased production rate of NO (VNO) compared to subjects who maintained normal oxyhemoglobin saturation (SaO2) and that SaO2 would be correlated with VNO. A group of highly-trained male cyclists (n = 18), some of whom develop EIH performed a maximal cycle test. VNO was determined during the cycle test. No significant differences were observed between those with and those without EIH. There was also no observed linear relationship between delta SaO2 and delta VNO. It can be concluded that NO present in exhaled air is not related to the etiology o f EIH. In a subsequent study, delivery of NO was accomplished using highly trained male cyclists (n = 7) with EIH who performed four 5-min cycle tests at VO2max under conditions of normoxia (N), normoxia + 20 ppm nitric oxide (N/NO), hypoxia (H), and hypoxia + 20 ppm nitric oxide (H/NO). It was hypothesized that: (i) inhaled NO would reverse EIH during normoxia, and (ii) inhaled NO would improve arterial oxygenation during hypoxia. Inhalation of NO during normoxic or hypoxic conditions did not significantly affect gas exchange, cardiorespiratory variables, or power output. These findings imply that pulmonary capillary blood volume reaches a maximal morphological limit during exercise and further dilation is not possible.

Pulmonary gas transport has not been typically recognized as a limiting factor to physical exercise. Dempsey et al. (1984; 1986) have suggested that the pulmonary system remains unchanged despite chronic aerobic training. Adaptations to other physiological systems may impose metabolic demands which the respiratory system can not meet. In essence, the lung's capacity for gas exchange becomes surpassed by other training adaptations. Supporting evidence is seen as decreases in arterial oxygenation at near maximal work rates in highly trained male endurance athletes (Dempsey et al., 1984; Powers et al., 1988; 1989; Hopkins and McKenzie 1989). Decreased arterial oxygenation has been termed exercise-induced arterial hypoxemia (EIH), and has direct consequences on VO₂max (Lawler et al., 1988; Powers et al., 1989; Martin and O'Kroy, 1993) and maximal performance capacity (Koskolou and McKenzie, 1994). It is estimated that approximately fifty percent of highly trained male endurance athletes exhibit EIH (Powers et al., 1988; 1993; Martin et al., 1992b). One mechanism that has been advanced to explain this phenomenon is a diffusion limitation. Diffusion capacity of the lung (DL) may be depressed during exercise and not allow for complete gas equilibrium to occur. If a structural alteration were present during exercise, it would continue to depress DL during recovery. To investigate the time course of change in pulmonary diffusion capacity for carbon monoxide (DL[sub co]) ten (N=10) highly trained male cyclists (HT) and ten (N=10) moderately (MT) male subjects were selected for this study. Subjects cycled to exhaustion to determine maximal oxygen consumption (VO₂max) on an electronically braked cycle ergometer (Mijnhardt KEM-3) (mean ± SD; HT VO₂max = 68.0 ± 4.9; MT VO₂max = 51.6 ± 4.7 mL-kg⁻¹Emin⁻¹). Percent arterial oxygen saturation (%SaO₂) was monitored by a pulse oximeter (Ohmeda Biox 3740) to determine if subjects demonstrated exercise-induced arterial hypoxemia (defined as %SaO₂ ≤ 91%) (%SaO₂min HT = 91.4 ± 1.6; MT = 94.6 ± 1.1). At a second data collection period, pulmonary function testing was performed. All subjects demonstrated normal pulmonary function. Initial diffusion measurements were made to obtain resting DL[sub CO]. diffusion capacity of the alveolar membrane (DM), and pulmonary capillary blood volume (Vc). Both spirometry and diffusion measurements were made using the same apparatus (Collins PLUS DS II). DM and Vc were calculated by measuring DL[sub CO] at two inspired O₂ concentrations using the technique of Roughton & Forster (1957). Subjects then cycled to fatigue at a workrate that corresponded to the highest workrate attained during the VO₂max test. Expired gases and %SaO₂ data were collected during the time to fatigue cycle test. Five additional measurements of pulmonary diffusion were made at 1, 2, 4, 6 and 24 hours following the cycle test. One hour post-exercise, DL[sub CO] was significantly decreased in both groups compared to baseline. The decrease reached a minimum value at 6 hrs and approached normal values 24 hrs after the exercise. Only HT subjects exhibited EIH yet both groups experienced similar changes in DL[sub CO] The correlation between %SaO₂min and change in DL[sub CO] was low (r=-0.3), implying that EIH can not be explained by post exercise decrease in DL[sub CO]. The change in DL[sub CO] can be explained primarily by a parallel decrease in Vc. Vc decreased below baseline values in both groups, perhaps indicating a compensatory shunting mechanism. A smaller degree of change was observed in DM, and played less of a role in the decreased DL[sub CO]- The results of this study are the first to compare diffusion capacity in two separate groups, based on training status, following maximal exercise. Both moderately trained and highly trained subjects exhibited similar decreases in pulmonary diffusing capacity. This supports the theory that the lung may not adapt to aerobic training and behaves in a similar manner regardless of training status.