Low total haemoglobin mass, blood volume and aerobic capacity in men with type 1 diabetes.

Blood O2 carrying capacity affects aerobic capacity (VO2max). Patients with type 1 diabetes have a risk for anaemia along with renal impairment, and they often have low VO2max. We investigated whether total haemoglobin mass (tHb-mass) and blood volume (BV) differ in men with type 1 diabetes (T1D, n = 12) presently without complications and in healthy men (CON, n = 23) (age-, anthropometry-, physical activity-matched), to seek an explanation for low VO2max. We determined tHb-mass, BV, haemoglobin concentration ([Hb]), and VO2max in T1D and CON. With similar (mean ± SD) [Hb] (144 vs. 145 g l(-1)), T1D had lower tHb-mass (10.1 ± 1.4 vs. 11.0 ± 1.1 g kg(-1), P < 0.05), BV (76.8 ± 9.5 vs. 83.5 ± 8.3 ml kg(-1), P < 0.05) and VO2max (35.4 ± 4.8 vs. 44.9 ± 7.5 ml kg(-1) min(-1), P < 0.001) than CON. VO2max correlated with tHb-mass and BV both in T1D (r = 0.71, P < 0.01 and 0.67, P < 0.05, respectively) and CON (r = 0.54, P < 0.01 and 0.66, P < 0.001, respectively), but not with [Hb]. Linear regression slopes were shallower in T1D than CON both between VO2max and tHb-mass (2.4 and 3.6 ml kg(-1) min(-1) vs. g kg(-1), respectively) and VO2max and BV (0.3 and 0.6 ml kg(-1) min(-1) vs. g kg(-1), respectively), indicating that T1D were unable to reach similar VO2max than CON at a given tHb-mass and BV. In conclusion, low tHb-mass and BV partly explained low VO2max in T1D and may provide early and more sensitive markers of blood O2 carrying capacity than [Hb] alone.

One-year unsupervised individualized exercise training intervention enhances cardiorespiratory fitness but not muscle deoxygenation or glycemic control in adults with type 1 diabetes.

Adaptations to long-term exercise training in type 1 diabetes are sparsely studied. We examined the effects of a 1-year individualized training intervention on cardiorespiratory fitness, exercise-induced active muscle deoxygenation, and glycemic control in adults with and without type 1 diabetes. Eight men with type 1 diabetes (T1D) and 8 healthy men (CON) matched for age, anthropometry, and peak pulmonary O2 uptake, completed a 1-year individualized training intervention in an unsupervised real-world setting. Before and after the intervention, the subjects performed a maximal incremental cycling test, during which alveolar gas exchange (volume turbine and mass spectrometry) and relative concentration changes in active leg muscle deoxygenated (Δ[HHb]) and total (Δ[tHb]) hemoglobin (near-infrared spectroscopy) were monitored. Peak O2 pulse, reflecting peak stroke volume, was calculated (peak pulmonary O2 uptake/peak heart rate). Glycemic control (glycosylated hemoglobin A1c (HbA1c)) was evaluated. Both T1D and CON averagely performed 1 resistance-training and 3-4 endurance-training sessions per week (∼1 h/session at ∼moderate intensity). Training increased peak pulmonary O2 uptake in T1D (p = 0.004) and CON (p = 0.045) (group × time p = 0.677). Peak O2 pulse also rose in T1D (p = 0.032) and CON (p = 0.018) (group × time p = 0.880). Training increased leg Δ[HHb] at peak exercise in CON (p = 0.039) but not in T1D (group × time p = 0.052), while no changes in leg Δ[tHb] at any work rate were observed in either group (p > 0.05). HbA1c retained unchanged in T1D (from 58 ± 10 to 59 ± 11 mmol/mol, p = 0.609). In conclusion, 1-year adherence to exercise training enhanced cardiorespiratory fitness similarly in T1D and CON but had no effect on active muscle deoxygenation or glycemic control in T1D.

Altered cardiorespiratory response to exercise in overweight and obese women with polycystic ovary syndrome.

In polycystic ovary syndrome (PCOS), cardiovascular risk is increased. Peak O2 uptake (V˙O2peak) predicts the cardiovascular risk. We were the first to examine the contribution of systemic O2 delivery and arteriovenous O2 difference to V˙O2peak in overweight and obese women with PCOS. Fifteen overweight or obese PCOS women and 15 age-, anthropometry-, and physical activity-matched control women performed a maximal incremental cycling exercise test. Alveolar gas exchange (volume turbine and mass spectrometry), arterial O2 saturation (pulse oximetry), and cardiac output (CO) (impedance cardiography) were monitored. Hb concentration was determined. Arterial O2 content and arteriovenous O2 difference (C(a-v)O2) (Fick equation) were calculated. Insulin resistance was evaluated by homeostasis model assessment (HOMA-IR). PCOS women had lower V˙O2peak than controls (40 ± 6 vs. 46 ± 5 mL/min/kg fat-free mass [FFM], P = 0.011). Arterial O2 content was similarly maintained in the groups throughout the exercise test (P > 0.05). Linear regression analysis revealed a pronounced response of CO to increasing V˙O2 in PCOS women during the exercise test: A ∆CO/∆V˙O2 slope was steeper in PCOS women than in controls (ß = 5.84 vs. ß = 5.21, P = 0.004). Eventually, the groups attained similar peak CO and peak CO scaled to FFM (P > 0.05). Instead, C(a-v)O2 at peak exercise was lower in PCOS women than in controls (13.2 ± 1.6 vs. 14.8 ± 2.4 mL O2/100 mL blood, P = 0.044). HOMA-IR was similar in the groups (P > 0.05). The altered cardiorespiratory responses to exercise in overweight and obese PCOS women indicate that PCOS per se is associated with alterations in peripheral adjustments to exercise rather than with limitations of systemic O2 delivery.

Central and peripheral cardiovascular impairments limit VO(2peak) in type 1 diabetes.

PURPOSE: Cardiovascular risk, predicted by peak O2 uptake (VO(2peak)), is increased in type 1 diabetes. We examined the contribution of central and peripheral mechanisms to VO(2peak) in physically active adults with type 1 diabetes. METHODS: Seven men with type 1 diabetes and 10 healthy age-, anthropometry-, and physical activity-matched men performed incremental cycling exercise until volitional fatigue. Alveolar gas exchange (turbine and mass spectrometry), cardiac function and systemic vascular resistance (impedance cardiography), and local active leg muscle deoxygenation and blood flow (near infrared spectroscopy) were monitored. Arterial-venous O2 difference was calculated (Fick principle). Blood volume (BV) (carbon monoxide rebreathing method) and glycemic control (glycosylated hemoglobin) were determined. RESULTS: The group with diabetes had lower VO(2peak) than controls (47 ± 5 vs 56 ± 7 mL·min·kg fat-free mass, P < 0.05). At peak exercise, fat-free mass-adjusted stroke volume (SV) and cardiac output (CO) were lower and systemic vascular resistance was higher in the group with diabetes than those in controls (P < 0.05). Leg muscle blood flow was reduced independently of CO in the group with diabetes at peak exercise (P < 0.05), whereas arterial-venous O2 difference was similar in the groups throughout the exercise (P > 0.05). The group with diabetes had lower relative BV than controls (P < 0.01), and BV correlated positively with peak SV and peak CO (P < 0.001). In the group with diabetes, peak SV and peak CO correlated (P < 0.05) and peak leg muscle blood flow tended to correlate (P = 0.070) inversely with glycosylated hemoglobin. CONCLUSIONS: Both central and peripheral cardiovascular impairments limit VO(2peak) in physically active adults with type 1 diabetes. Importantly, central limitations, and probably peripheral limitations as well, are associated with glycemic control.

Alveolar gas exchange, oxygen delivery and tissue deoxygenation in men and women during incremental exercise.

We investigated whether leg and arm skeletal muscle, and cerebral deoxygenation, differ during incremental cycling exercise in men and women, and if women's lower capacity to deliver O2 affects tissue deoxygenation. Men (n=10) compared to women (n=10), had greater cardiac output, which with greater hemoglobin concentration produced greater absolute (QaO2) and body size-adjusted oxygen delivery (QaO2i) at peak exercise. Despite women's lower peak QaO2, their leg muscle deoxygenation was similar at a given work rate and QaO2, but less than in men at peak exercise (Δtissue saturation index -27.1 ± 13.2% vs. -11.8 ± 5.7%, P<0.01; Δ[deoxyhemoglobin] 15.03 ± 8.57 µM vs. 3.73 ± 3.98 µM, P<0.001). At peak exercise, oxygen uptake was associated both with QaO2 and leg muscle deoxygenation (both P<0.01). Arm muscle and cerebral deoxygenation did not differ between sexes at peak exercise. Thus, both high O2 delivery and severe active muscle deoxygenation are determinants of good exercise performance, and active muscle deoxygenation responses are regulated partly in a sex-specific manner with an influence of exercise capacity.

Alveolar gas exchange and tissue oxygenation during incremental treadmill exercise, and their associations with blood O(2) carrying capacity.

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 O(2) 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 O(2) 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[O(2)Hb]), 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 O(2) 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 O(2) 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 O(2) carrying was associated with a high level of m. vastus lateralis deoxygenation at peak exercise.

Alveolar gas exchange and tissue deoxygenation during exercise in type 1 diabetes patients and healthy controls.

We used near-infrared spectroscopy to investigate whether leg and arm skeletal muscle and cerebral deoxygenation differ during incremental cycling exercise in men with type 1 diabetes (T1D, n=10, mean±SD age 33±7 years) and healthy control men (matched by age, anthrometry, and self-reported physical activity, CON, n=10, 32±7 years) to seek an explanation for lower aerobic capacity (˙VO2peak) often reported in T1D. T1D had lower ˙VO2peak (35±4mlkg(-1)min(-1) vs. 43±8mlkg(-1)min(-1), P<0.01) and peak work rate (219±33W vs. 290±44W, P<0.001) than CON. Leg muscle deoxygenation (↑ [deoxyhemoglobin]; ↓ tissue saturation index) was greater in T1D than CON at a given absolute submaximal work rate, but not at peak exercise, while arm muscle and cerebral deoxygenation were similar. Thus, in T1D compared with CON, faster leg muscle deoxygenation suggests limited circulatory ability to increase O(2) delivery as a plausible explanation for lower ˙VO2peak and earlier fatigue in T1D.

Cardiovascular autonomic nervous system function and aerobic capacity in type 1 diabetes.

Impaired cardiovascular autonomic nervous system (ANS) function has been reported in type 1 diabetes (T1D) patients. ANS function, evaluated by heart rate variability (HRV), systolic blood pressure variability (SBPV), and baroreflex sensitivity (BRS), has been linked to aerobic capacity (VO(2peak)) in healthy subjects, but this relationship is unknown in T1D. We examined cardiovascular ANS function at rest and during function tests, and its relations to VO(2peak) in T1D individuals. Ten T1D patients (34 ± 7 years) and 11 healthy control (CON; 31 ± 6 years) age and leisure-time physical activity-matched men were studied. ANS function was recorded at rest and during active standing and handgrip. Determination of VO(2peak) was obtained with a graded cycle ergometer test. During ANS recordings SBPV, BRS, and resting HRV did not differ between groups, but alpha1 responses to maneuvers 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). VO(2peak) 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 VO(2peak) in CON (p < 0.05) and when analyzing groups together. These results suggest that T1D had lower VO(2peak), weaker HRV response to maneuvers, but not impaired cardiovascular ANS function at rest compared with CON. Resting parasympathetic cardiac activity correlated with VO(2peak) in CON but not in T1D. Detrended fluctuation analysis could be a sensitive detector of changes in cardiac ANS function in T1D.