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Objective. Autonomic nervous system function and thereby bodily stress and recovery reactions may be assessed by wearable devices measuring heart rate (HR) and its variability (HRV). So far, the validity of HRV-based stress assessments has been mainly studied in healthy populations. In this study, we determined how psychosocial stress affects physiological and psychological stress responses in both young (18–30 years) and middle-aged (45–64 years) healthy individuals as well as in patients with arterial hypertension and/or either prior evidence of prediabetes or type 2 diabetes. We also studied how an HRV-based stress index (Relax-Stress Intensity, RSI) relates to perceived stress (PS) and cortisol (CRT) responses during psychosocial stress. Approach. A total of 197 participants were divided into three groups: (1) healthy young (HY, N = 63), (2) healthy middle-aged (HM, N = 61) and (3) patients with cardiometabolic risk factors (Pts, N = 73, 32–65 years). The participants underwent a group version of Trier Social Stress Test (TSST-G). HR, HRV (quantified as root mean square of successive differences of R–R intervals, RMSSD), RSI, PS, and salivary CRT were measured regularly during TSST-G and a subsequent recovery period. Main results. All groups showed significant stress reactions during TSST-G as indicated by significant responses of HR, RMSSD, RSI, PS, and salivary CRT. Between-group differences were also observed in all measures. Correlation and regression analyses implied RSI being the strongest predictor of CRT response, while HR was more closely associated with PS. Significance. The HRV-based stress index mirrors responses of CRT, which is an independent marker for physiological stress, around TSST-G. Thus, the HRV-based stress index may be used to quantify physiological responses to psychosocial stress across various health and age groups.

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 A

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.

RISSANEN, A-P. E., H. O. TIKKANEN, A. S. KOPONEN, J. M. AHO, and J. E. PELTONEN. Central and Peripheral Cardiovascular Impairments Limit VO2peak in Type 1 Diabetes. Med. Sci. Sports Exerc., Vol. 47, No. 2, pp. 223-230, 2015. Purpose: Cardiovascular risk, predicted by peak O2 uptake (VO2peak), is increased in type 1 diabetes. We examined the contribution of central and peripheral mechanisms to VO2peak 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 ex- change (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 VO2peak than controls (47 T 5v s 56T 7m LImin j1 Ikg j1 fat-free mass, P G 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 G 0.05). Leg muscle blood flow was reduced independently of CO in the group with diabetes at peak exercise (P G 0.05), whereas arterial-venous O2 difference was similar in the groups throughout the exercise (P 9 0.05). The group with diabetes had lower relative BV than controls (P G 0.01), and BV correlated positively with peak SV and peak CO (P G 0.001). In the group with diabetes, peak SV and peak CO correlated (P G 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 VO2peak in physically active adults with type 1 diabetes. Importantly, central limitations, and probably peripheral limitations as well, are asso

Type 1 diabetes is a metabolic disorder, which has been associated with decreased heart rate variability (HRV) and increased risk for adverse cardiac events. The aim of this paper was to examine HRV dynamics during a cardiorespiratory exercise test. 13 male subjects with type 1 diabetes (age 33.0±6.7 years) and 25 healthy male controls (age 33.7±7.6 years) participated the study. HRV was analysed from pre-exercise rest, warm-up, light exercise (40 W cycling), peak exercise, and recovery time periods. The main finding of the study was that subjects with diabetes had higher HRV complexity (higher multiscale entropy) during peak exercise when compared to healthy controls. HRV during rest, warm-up and light exercise was similar between the groups.

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%, P0.01; Δ[deoxyhemoglobin] 15.03 ± 8.57 μM vs. 3.73 ± 3.98 μM, P0.001). At peak exercise, oxygen uptake was associated both with QaO2 and leg muscle deoxygenation (both P0.01). 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.

In polycystic ovary syndrome (PCOS), cardiovascular risk is increased. Peak O2 uptake (Embedded Image) predicts the cardiovascular risk. We were the first to examine the contribution of systemic O2 delivery and arteriovenous O2 difference to Embedded Image 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 Embedded Image 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 Embedded Image in PCOS women during the exercise test: A ∆CO/∆Embedded Image slope was steeper in PCOS women than in controls (β = 5.84 vs. β = 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., published version, peerReviewed