Hemoglobin mass and performance responses during 4 weeks of normobaric "live high-train low and high".

PURPOSE: To investigate whether 4 weeks of normobaric "live high-train low and high" (LHTLH) causes different hematological, cardiorespiratory, and sea-level performance changes compared to living and training in normoxia during a preparation season. METHODS: Nineteen (13 women, 6 men) cross-country skiers competing at the national or international level completed a 28-day period (∼18 h day-1 ) of LHTLH in normobaric hypoxia of ∼2400 m (LHTLH group) including two 1 h low-intensity training sessions per week in normobaric hypoxia of 2500 m while continuing their normal training program in normoxia. Hemoglobin mass (Hbmass ) was assessed using a carbon monoxide rebreathing method. Time to exhaustion (TTE) and maximal oxygen uptake (VO2max ) were measured using an incremental treadmill test. Measurements were completed at baseline and within 3 days after LHTLH. The control group skiers (CON) (seven women, eight men) performed the same tests while living and training in normoxia with ∼4 weeks between the tests. RESULTS: Hbmass in LHTLH increased 4.2 ± 1.7% from 772 ± 213 g (11.7 ± 1.4 g kg-1 ) to 805 ± 226 g (12.5 ± 1.6 g kg-1 ) (p < 0.001) while it was unchanged in CON (p = 0.21). TTE improved during the study regardless of the group (3.3 ± 3.4% in LHTLH; 4.3 ± 4.8% in CON, p < 0.001). VO2max did not increase in LHTLH (61.2 ± 8.7 mL kg-1 min-1 vs. 62.1 ± 7.6 mL kg-1 min-1 , p = 0.36) while a significant increase was detected in CON (61.3 ± 8.0-64.0 ± 8.1 mL kg-1 min-1 , p < 0.001). CONCLUSIONS: Four-week normobaric LHTLH was beneficial for increasing Hbmass but did not support the short-term development of maximal endurance performance and VO2max when compared to the athletes who lived and trained in normoxia.

Cardiac output and arteriovenous oxygen difference contribute to lower peak oxygen uptake in patients with fibromyalgia.

BACKGROUND: Patients with fibromyalgia (FM) exhibit low peak oxygen uptake ([Formula: see text]O2peak). We aimed to detect the contribution of cardiac output to ([Formula: see text]) and arteriovenous oxygen difference [Formula: see text] to [Formula: see text] from rest to peak exercise in patients with FM. METHODS: Thirty-five women with FM, aged 23 to 65 years, and 23 healthy controls performed a step incremental cycle ergometer test until volitional fatigue. Alveolar gas exchange and pulmonary ventilation were measured breath-by-breath and adjusted for fat-free body mass (FFM) where appropriate. [Formula: see text] (impedance cardiography) was monitored. [Formula: see text] was calculated using Fick's equation. Linear regression slopes for oxygen cost (∆[Formula: see text]O2/∆work rate) and [Formula: see text] to [Formula: see text]O2 (∆[Formula: see text]/∆[Formula: see text]O2) were calculated. Normally distributed data were reported as mean ± SD and non-normal data as median [interquartile range]. RESULTS: [Formula: see text]O2peak was lower in FM patients than in controls (22.2 ± 5.1 vs. 31.1 ± 7.9 mL∙min-1∙kg-1, P < 0.001; 35.7 ± 7.1 vs. 44.0 ± 8.6 mL∙min-1∙kg FFM-1, P < 0.001). [Formula: see text] and C(a-v)O2 were similar between groups at submaximal work rates, but peak [Formula: see text] (14.17 [13.34-16.03] vs. 16.06 [15.24-16.99] L∙min-1, P = 0.005) and C(a-v)O2 (11.6 ± 2.7 vs. 13.3 ± 3.1 mL O2∙100 mL blood-1, P = 0.031) were lower in the FM group. No significant group differences emerged in ∆[Formula: see text]O2/∆work rate (11.1 vs. 10.8 mL∙min-1∙W-1, P = 0.248) or ∆[Formula: see text]/∆[Formula: see text]O2 (6.58 vs. 5.75, P = 0.122) slopes. CONCLUSIONS: Both [Formula: see text] and C(a-v)O2 contribute to lower [Formula: see text]O2peak in FM. The exercise responses were normal and not suggestive of a muscle metabolism pathology. TRIAL REGISTRATION: ClinicalTrials.gov, NCT03300635. Registered 3 October 2017-Retrospectively registered. https://clinicaltrials.gov/ct2/show/NCT03300635 .

Variability in hemoglobin mass response to altitude training camps.

The present study investigated whether athletes can be classified as responders or non-responders based on their individual change in total hemoglobin mass (tHb-mass) following altitude training while also identifying the potential factors that may affect responsiveness to altitude exposure. Measurements were completed with 59 elite endurance athletes who participated in national team altitude training camps. Fifteen athletes participated in the altitude training camp at least twice. Total Hb-mass using a CO rebreathing method and other blood markers were measured before and after a total of 82 altitude training camps (1350-2500 m) in 59 athletes. In 46 (56%) altitude training camps, tHb-mass increased. The amount of positive responses increased to 65% when only camps above 2000 m were considered. From the fifteen athletes who participated in altitude training camps at least twice, 27% always had positive tHb-mass responses, 13% only negative responses, and 60% both positive and negative responses. Logistic regression analysis showed that altitude was the most significant factor explaining positive tHb-mass response. Furthermore, male athletes had greater tHb-mass response than female athletes. In endurance athletes, tHb-mass is likely to increase after altitude training given that hypoxic stimulus is appropriate. However, great inter- and intra-individual variability in tHb-mass response does not support classification of an athlete permanently as a responder or non-responder. This variability warrants efforts to control numerous factors affecting an athlete's response to each altitude training camp.

The effects of skin and core tissue cooling on oxygenation of the vastus lateralis muscle during walking and running.

Skin and core tissue cooling modulates skeletal muscle oxygenation at rest. Whether tissue cooling also influences the skeletal muscle deoxygenation response during exercise is unclear. We evaluated the effects of skin and core tissue cooling on skeletal muscle blood volume and deoxygenation during sustained walking and running. Eleven male participants walked or ran six times on a treadmill for 60 min in ambient temperatures of 22°C (Neutral), 0°C for skin cooling (Cold 1), and at 0°C following a core and skin cooling protocol (Cold 2). Difference between oxy/deoxygenated haemoglobin ([diffHb]: deoxygenation index) and total haemoglobin content ([tHb]: total blood volume) in the vastus lateralis (VL) muscle was measured continuously. During walking, lower [tHb] was observed at 1 min in Cold 1 and Cold 2 vs. Neutral (P˂0.05). Lower [diffHb] was seen at 1 and 10 min in Cold 2 vs. Neutral by 13.5 ± 1.2 µM and 15.3 ± 1.4 µM and Cold 1 by 10.4 ± 3.1 µM and 11.1 ± 4.1 µM, respectively (P˂0.05). During running, [tHb] was lower in Cold 2 vs. Neutral at 10 min only (P = 0.004). [diffHb] was lower at 1 min in Cold 2 by 11.3 ± 3.1 µM compared to Neutral and by 13.5 ± 2.8 µM compared to Cold 1 (P˂0.001). Core tissue cooling, prior to exercise, induced greater deoxygenation of the VL muscle during the early stages of exercise, irrespective of changes in blood volume. Skin cooling alone, however, did not influence deoxygenation of the VL during exercise.

Wagner diagram for modeling O2pathway-calculation and graphical display by the Helsinki O2Pathway Tool.

Objective.Maximal O2uptake (V˙O2max) reflects the individual's maximal rate of O2transport and utilization through the integrated whole-body pathway composed of the lungs, heart, blood, circulation, and metabolically active tissues. As such,V˙O2maxis strongly associated with physical capacity as well as overall health and thus acts as one predictor of physical performance and as a vital sign in determination of status and progress of numerous clinical conditions. Quantifying the contribution of single parts of the multistep O2pathway toV˙O2maxprovides mechanistic insights into exercise (in)tolerance and into therapy-, training-, or disuse-induced adaptations at individual or group levels. We developed a desktop application (Helsinki O2Pathway Tool-HO2PT) to model numerical and graphical display of the O2pathway based on the 'Wagner diagram' originally formulated by Peter D. Wagner and his colleagues.Approach.The HO2PT was developed and programmed in Python to integrate the Fick principle and Fick's law of diffusion into a computational system to import, calculate, graphically display, and export variables of the Wagner diagram.Main results.The HO2PT models O2pathway both numerically and graphically according to the Wagner diagram and pertains to conditions under which the mitochondrial oxidative capacity of metabolically active tissues exceeds the capacity of the O2transport system to deliver O2to the mitochondria. The tool is based on the Python open source code and libraries and freely and publicly available online for Windows, macOS, and Linux operating systems.Significance.The HO2PT offers a novel functional and demonstrative platform for those interested in examiningV˙O2maxand its determinants by using the Wagner diagram. It will improve access to and usability of Wagner's and his colleagues' integrated physiological model and thereby benefit users across the wide spectrum of contexts such as scientific research, education, exercise testing, sports coaching, and clinical medicine.

Combined intermittent hypoxic exposure at rest and continuous hypoxic training can maintain elevated hemoglobin mass after a hypoxic camp.

Athletes use hypoxic living and training to increase hemoglobin mass (Hbmass), but Hbmass declines rapidly upon return to sea level. We investigated whether Intermittent Hypoxic Exposure (IHE) + Continuous Hypoxic Training (CHT) after return to sea level maintained elevated Hbmass, and if changes in Hbmass were transferred to changes in maximal oxygen uptake (V̇O2max) and exercise performance. Hbmass was measured in 58 endurance athletes before (PRE), after (POST1), and 30 days after (POST2) a 27 ± 4-day training camp in hypoxia (n=44, HYP) or at sea level (n=14, SL). After return to sea level, 22 athletes included IHE (2 h rest) + CHT (1 h training) into their training every third day for one month (HYPIHE+CHT), whereas the other 22 HYP athletes were not exposed to IHE or CHT (HYPSL). Hbmass increased from PRE to POST1 in both HYPIHE+CHT (4.4 ± 0.7%, mean ± SEM) and HYPSL (4.1 ± 0.6%) (both p<0.001). Compared to PRE, Hbmass at POST2 remained 4.2 ± 0.8% higher in HYPIHE+CHT (p<0.001) and1.9 ± 0.5% higher in HYPSL (p=0.023), indicating a significant difference between the groups (p=0.002). In SL, no significant changes were observed in Hbmass with mean alterations between -0.5% and 0.4%. V̇O2max and time to exhaustion during an incremental treadmill test (n=35) were elevated from PRE to POST2 only in HYPIHE+CHT (5.8 ± 1.2% and 5.4 ± 1.4%, respectively, both p<0.001). IHE+CHT possesses the potential to mitigate the typical decline in Hbmass commonly observed during the initial weeks after return to sea level.

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.

Effects of adenosine, exercise, and moderate acute hypoxia on energy substrate utilization of human skeletal muscle.

Glucose metabolism increases in hypoxia and can be influenced by endogenous adenosine, but the role of adenosine for regulating glucose metabolism at rest or during exercise in hypoxia has not been elucidated in humans. We studied the effects of exogenous adenosine on human skeletal muscle glucose uptake and other blood energy substrates [free fatty acid (FFA) and lactate] by infusing adenosine into the femoral artery in nine healthy young men. The role of endogenous adenosine was studied by intra-arterial adenosine receptor inhibition (aminophylline) during dynamic one-leg knee extension exercise in normoxia and acute hypoxia corresponding to ∼3,400 m of altitude. Extraction and release of energy substrates were studied by arterial-to-venous (A-V) blood samples, and total uptake or release was determined by the product of A-V differences and muscle nutritive perfusion measured by positron emission tomography. The results showed that glucose uptake increased from a baseline value of 0.2 ± 0.2 to 2.0 ± 2.2 µmol·100 g(-1)·min(-1) during adenosine infusion (P < 0.05) at rest. Although acute hypoxia enhanced arterial FFA levels, it did not affect muscle substrate utilization at rest. During exercise, glucose uptake was higher (195%) during acute hypoxia compared with normoxia (P = 0.058), and aminophylline had no effect on energy substrate utilization during exercise, despite that arterial FFA levels were increased. In conclusion, exogenous adenosine at rest and acute moderate hypoxia during low-intensity knee-extension exercise increases skeletal muscle glucose uptake, but the increase in hypoxia appears not to be mediated by adenosine.

Altered Expiratory Flow Dynamics at Peak Exercise in Adult Men With Well-Controlled Type 1 Diabetes.

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.

Identifying Personality Characteristics and Indicators of Psychological Well-Being Associated With Attrition in the Motivation Makes the Move! Physical Activity Intervention: Randomized Technology-Supported Trial.

BACKGROUND: Data attrition has been a common problem in longitudinal lifestyle interventions. The contributors to attrition in technology-supported physical activity interventions have not been thoroughly studied. OBJECTIVE: The present study examined the roles of personality characteristics and indicators of psychological well-being in data attrition within a technology-supported, longitudinal intervention study with overweight adults. METHODS: Participants (N=89) were adults from the Motivation Makes the Move! intervention study. Data attrition was studied after a 3-month follow-up. Participants' personality characteristics were studied using the Short Five self-report questionnaire. Psychological well-being indicators were assessed with the RAND 36-item health survey, Positive and Negative Affect Schedule, and Beck Depression Inventory. Logistic regression analyses were conducted to assess the risk of discontinuing the study. The analyses were adjusted for sex, age, study group, and educational status. RESULTS: At the 3-month follow-up, 65 of 89 participants (73% of the initial sample) had continued in the study. Participants' personality characteristics and indicators of psychological well-being were not associated with the risk of dropping out of the study (all P values >.05). The results remained the same after covariate controls. CONCLUSIONS: Participant attrition was not attributable to personality characteristics or psychological well-being in the Motivation Makes the Move! study conducted with overweight adults. As attrition remains a challenge within longitudinal, technology-supported lifestyle interventions, attention should be paid to the potentially dynamic natures of personality and psychological well-being, as well as other elements beyond these. TRIAL REGISTRATION: ClinicalTrials.gov NCT02686502; https://clinicaltrials.gov/ct2/show/NCT02686502.

Regulation of human skeletal muscle perfusion and its heterogeneity during exercise in moderate hypoxia.

Although many effects of both acute and chronic hypoxia on the circulation are well characterized, the distribution and regulation of blood flow (BF) heterogeneity in skeletal muscle during systemic hypoxia is not well understood in humans. We measured muscle BF within the thigh muscles of nine healthy young men using positron emission tomography during one-leg dynamic knee extension exercise in normoxia and moderate physiological systemic hypoxia (14% O(2) corresponding to approximately 3,400 m of altitude) without and with local adenosine receptor inhibition with femoral artery infusion of aminophylline. Systemic hypoxia reduced oxygen extraction of the limb but increased muscle BF, and this flow increment was confined solely to the exercising quadriceps femoris muscle. Exercising muscle BF heterogeneity was reduced from rest (P = 0.055) but was not affected by hypoxia. Adenosine receptor inhibition had no effect on capillary BF during exercise in either normoxia or hypoxia. Finally, one-leg exercise increased muscle BF heterogeneity both in the resting posterior hamstring part of the exercising leg and in the resting contralateral leg, whereas mean BF was unchanged. In conclusion, the results show that increased BF during one-leg exercise in moderate hypoxia is confined only to the contracting muscles, and the working muscle hyperemia appears not to be directly mediated by adenosine. Increased flow heterogeneity in noncontracting muscles likely reflects sympathetic nervous constraints to curtail BF increments in areas other than working skeletal muscles, but this effect is not potentiated in moderate systemic hypoxia during small muscle mass exercise.

Association Between Implementation of the Athlete Biological Passport and Female Elite Runners' Performance.

The purpose of this research was to evaluate the performances of female middle- and long-distance runners before and after the implementation of a new antidoping strategy (the Athlete Biological Passport [ABP]) in a country accused of systematic doping. A retrospective analysis of the results of Russian National Championships from 2008 to 2017 was performed. The 8 best female performances for the 800-m, 1500-m, 3000-m steeplechase, 5000-m, and 10,000-m events from the semifinals and finals were analyzed. The yearly number of athletes fulfilling standard qualifications for international competitions was also evaluated. Overall, numbers of athletes banned for doping in 2008-2017 were calculated. As a result, 4 events (800, 1500, 5000 [all P < .001], and 10,000 m [P < .01]) out of 5 showed statistically significant deterioration in the performances when comparing before and after the introduction of the ABP. The 3000-m steeplechase was the only event that did not show statistically significant change. The highest relative decrease in the number of runners who met standard qualification for international competition was for the 5000-m event (46%), followed by 1500-m (42%), 800-m (38%), 10,000-m (17%), and 3000-m steeplechase (1%). In conclusion, implementation of the ABP was followed by a significant reduction in the performance of female runners in a country accused of systematic doping. It can be reasonably speculated that more stringent antidoping testing, more specifically the introduction of the ABP, is a key reason for this reduction.

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.

Cerebral and muscle tissue oxygenation in acute hypoxic ventilatory response test.

Eight men were exposed to progressive isocapnic hypoxia for 10 min to test the hypothesis that (i) cerebral and muscle tissue would follow similar deoxygenation profiles during an acute hypoxic ventilatory response (AHVR) test; and (ii) strong cerebrovascular responsiveness to hypoxia would be related to attenuated cerebral deoxygenation. End-tidal O(2) concentration was reduced from normoxia (approximately 102 mmHg) to approximately 45 mmHg while arterial oxygen saturation (SpO2 %) declined from 98+/-1% to 77+/-7% (P<0.001). Near-infrared spectroscopy (NIRS)-derived local cerebral tissue (frontal lobe) deoxyhemoglobin increased 5.55+/-2.22 microM, while oxyhemoglobin and tissue oxygenation index decreased 2.57+/-1.99 microM and 6.2+/-3.4%, respectively (all P<0.001). In muscle (m. vastus lateralis) the NIRS changes from the initial normoxic level were non-significant. Cerebral blood velocity (V(mean), transcranial Doppler) in the middle cerebral artery increased from 53.4+/-10.4 to 60.6+/-11.6 cms(-1) (P<0.001). In relation to the decline in SpO2 % the mean rate of increase of V(mean) and AHVR were 0.33+/-0.19 cms(-1)%(-1) and 0.52+/-0.20l min(-1)%(-1), respectively. We conclude that cerebral, but not muscle, tissue shows changes reflecting a greater deoxygenation during acute hypoxia. However, the changes in NIRS parameters were not related to cerebrovascular responsiveness or ventilatory chemosensitivity during graded hypoxia.

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.

Ventilatory chemosensitivity, cerebral and muscle oxygenation, and total hemoglobin mass before and after a 72-day mt. Everest expedition.

BACKGROUND: We investigated the effects of chronic hypobaric hypoxic acclimatization, performed over the course of a 72-day self-supported Everest expedition, on ventilatory chemosensitivity, arterial saturation, and tissue oxygenation adaptation along with total hemoglobin mass (tHb-mass) in nine experienced climbers (age 37±6 years, [Formula: see text] 55±7 mL·kg(-1)·min(-1)). METHODS: Exercise-hypoxia tolerance was tested using a constant treadmill exercise of 5.5 km·h(-1) at 3.8% grade (mimicking exertion at altitude) with 3-min steps of progressive normobaric poikilocapnic hypoxia. Breath-by-breath ventilatory responses, Spo2, and cerebral (frontal cortex) and active muscle (vastus lateralis) oxygenation were measured throughout. Acute hypoxic ventilatory response (AHVR) was determined by linear regression slope of ventilation vs. Spo2. PRE and POST (<15 days) expedition, tHb-mass was measured using carbon monoxide-rebreathing. RESULTS: Post-expedition, exercise-hypoxia tolerance improved (11:32±3:57 to 16:30±2:09 min, p<0.01). AHVR was elevated (1.25±0.33 to 1.63±0.38 L·min(-1.)%(-1) Spo2, p<0.05). Spo2 decreased throughout exercise-hypoxia in both trials, but was preserved at higher values at 4800 m post-expedition. Cerebral oxygenation decreased progressively with increasing exercise-hypoxia in both trials, with a lower level of deoxyhemoglobin POST at 2400, 3500 and 4800 m. Muscle oxygenation also decreased throughout exercise-hypoxia, with similar patterns PRE and POST. No relationship was observed between the slope of AHVR and cerebral or muscle oxygenation either PRE or POST. Absolute tHb-mass response exhibited great individual variation with a nonsignificant 5.4% increasing trend post-expedition (975±154 g PRE and 1025±124 g POST, p=0.17). CONCLUSIONS: We conclude that adaptation to chronic hypoxia during a climbing expedition to Mt. Everest will increase hypoxic tolerance, AHVR, and cerebral but not muscle oxygenation, as measured during simulated acute hypoxia at sea level. However, tHb-mass did not increase significantly and improvement in cerebral oxygenation was not associated with the change in AHVR.

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.