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Type 1 diabetes may, in time, cause lung dysfunction including airflow limitation. We hypothesized that ventilatory flow morphology during a cardiopulmonary exercise test (CPET) would be altered in adult men with well-controlled type 1 diabetes. Thirteen men with type 1 diabetes [glycated hemoglobin A1c 59 (9) mmol/mol or 7.5 (0.8)%, duration of diabetes 12 (9) years, and age 33.9 (6.6) years] without diagnosed diabetes-related complications and 13 healthy male controls [age 37.2 (8.6) years] underwent CPET on a cycle ergometer (40 W increments every 3 min until volitional fatigue). We used a principal component analysis based method to quantify ventilatory flow dynamics throughout the CPET protocol. Last minute of each increment, peak exercise, and recovery were examined using linear mixed models, which accounted for relative peak oxygen uptake and minute ventilation. The type 1 diabetes participants had lower expiratory peak flow (P = 0.008) and attenuated slope from expiration onset to expiratory peak flow (P = 0.012) at peak exercise when compared with the healthy controls. Instead, during submaximal exercise and recovery, the type 1 diabetes participants possessed similar ventilatory flow dynamics to that of the healthy controls. In conclusion, men with relatively well-controlled type 1 diabetes and without clinical evidence of diabetes-related complications exhibited attenuated expiratory flow at peak exercise independently of peak oxygen uptake and minute ventilation. This study demonstrates that acute exercise reveals alterations in ventilatory function in men with type 1 diabetes but not until peak exercise.

Impaired cardiovascular autonomic nervous system (ANS) function has been reported in type 1 diabetes patients. ANS function, evaluated by heart rate variability (HRV), systolic blood pressure variability (SBPV) and baroreflex sensitivity (BRS), has been linked to aerobic capacity (VO2peak) in healthy subjects, but relationship is unknown in type 1 diabetes. We examined cardiovascular ANS function at rest and during function tests, and its relations to VO2peak in type 1 diabetes individuals. Ten type 1 diabetes patients (T1D) (34 ± 7 years) and 11 healthy control (CON) (31 ± 6 years) age and leisure-time physical activity-matched men were studied. Autonomic nervous system function was recorded at rest and during active standing and handgrip. Determination of VO2peak was obtained with graded cycle ergometer test. During ANS recordings SBPV, BRS, and resting HRV did not differ between groups, but alpha1 responses to manoeuvres in detrended fluctuation analyses were smaller in T1D (active standing; 32%, handgrip; 20%, medians) than in CON (active standing; 71%, handgrip; 54%, p < 0.05). VO2peak was lower in T1D (36 ± 4 ml ∙ kg-1 ∙ min-1) than in CON (45 ± 9 ml ∙ kg-1 ∙ min-1, p < 0.05). Resting HRV measures, RMSSD, HF and SD1 correlated with VO2peak in CON (p < 0.05) and when analysing groups together. These results suggest that T1D had lower VO2peak, weaker HRV response to manoeuvres, but not impaired cardiovascular ANS function at rest compared with CON. Resting parasympathetic cardiac activity correlated with VO2peak in CON but not in T1D. Detrended fluctuation analysis could be a sensitive detector of changes in cardiac ANS function in type 1 diabetes.

The magnitude and timing of oxygenation responses in highly active leg muscle, less active arm muscle, and cerebral tissue, have not been studied with simultaneous alveolar gas exchange measurement during incremental treadmill exercise. Nor is it known, if blood O2 carrying capacity affects the tissue-specific oxygenation responses. Thus, we investigated alveolar gas exchange and tissue (m. vastus lateralis, m. biceps brachii, cerebral cortex) oxygenation during incremental treadmill exercise until volitional fatigue, and their associations with blood O2 carrying capacity in 22 healthy men. Alveolar gas exchange was measured, and near-infrared spectroscopy (NIRS) was used to monitor relative concentration changes in oxy- (Δ[O2Hb]), deoxy- (Δ[HHb]) and total hemoglobin (Δ[tHb]), and tissue saturation index (TSI). NIRS inflection points (NIP), reflecting changes in tissue-specific oxygenation, were determined and their coincidence with ventilatory thresholds (anaerobic threshold (AT), respiratory compensation point (RC); V-slope method) was examined. Blood O2 carrying capacity (total hemoglobin mass (tHb-mass)) was determined with the CO-rebreathing method. In all tissues, NIPs coincided with AT, whereas RC was followed by NIPs. High tHb-mass associated with leg muscle deoxygenation at peak exercise (e.g., Δ[HHb] from baseline walking to peak exercise vs. tHb-mass: r = 0.64, p < 0.01), but not with arm muscle- or cerebral deoxygenation. In conclusion, regional tissue oxygenation was characterized by inflection points, and tissue oxygenation in relation to alveolar gas exchange during incremental treadmill exercise resembled previous findings made during incremental cycling. It was also found out, that O2 delivery to less active m. biceps brachii may be limited by an accelerated increase in ventilation at high running intensities. In addition, high capacity for blood O2 carrying was associated with a high level of m. vastus lateralis deoxygenation at peak exercise.