Differences in cardiovascular function between sexes have been documented at rest and maximal exercise. The purpose of this study was to examine the sex differences in cardiovascular function during submaximal constant-load exercise, which is not well understood.Thirty-one male and 33 female subjects completed nine minutes moderate and nine minutes vigorous intensity submaximal exercise (40 and 75% of peak watts determined by maximal exercise test). Measurements included: intra-arterial blood pressure (SBP and DBP), cardiac index (QI), heart rate (HR), oxygen consumption (VO2) and arterial catecholamines (epinephrine = EPI and norepinephrine = NE), and blood gases. Mean arterial pressure (MAP), stroke volume index (SVI), systemic vascular resistance index (SVRI), arterial oxygen content (CaO2), arterial to venous O2 difference (AVO2) and systemic oxygen transport (SOT) were calculated.At rest and during submaximal exercise QI, SVI, SBP, MAP, NE, CaO2, and SOT were lower in females compared to males. VO2, AVO2, EPI were lower in females throughout exercise. When corrected for wattage, females had a higher Q, HR, SV, VO2 and AVO2 despite lower energy expenditure and higher mechanical efficiency.This study demonstrates sex differences in the cardiovascular response to constant-load submaximal exercise. Specifically, females presented limitations in cardiac performance in which they are unable to compensate for reductions in stroke volume through increases in HR, potentially a consequence of a female’s blunted sympathetic response and higher vasodilatory state. Females demonstrated greater cardiac work needed to meet the same external work demand, and relied on increased peripheral oxygen extraction, lower energy expenditure and improvements in mechanical efficiency as compensatory mechanisms.

BackgroundExercise immunology has become a growing field in the past 20 years, with an emphasis on understanding how different forms of exercise affect immune function. Mechanistic studies are beginning to shed light on how exercise may impair the development of cancer or be used to augment cancer treatment. The beneficial effects of exercise on the immune system may be exploited to improve patient responses to cancer immunotherapy.MethodsWe investigated the effects of acute exercise on the composition of peripheral blood leukocytes over time in a male population of varying fitness. Subjects performed a brief maximal intensity cycling regimen and a longer less intense cycling regimen at separate visits. Leukocytes were measured by multi-parameter flow cytometry of more than 50 immunophenotypes for each collection sample.ResultsWe found a differential induction of leukocytosis dependent on exercise intensity and duration. Cytotoxic natural killer cells demonstrated the greatest increase (average of 5.6 fold) immediately post-maximal exercise whereas CD15+ granulocytes demonstrated the largest increase at 3 h post-maximal exercise (1.6 fold). The longer, less intense endurance exercise resulted in an attenuated leukocytosis. Induction of leukocytosis did not differ in our limited study of active (n = 10) and sedentary (n = 5) subjects to exercise although we found that in baseline samples, sedentary individuals had elevated percentages of CD45RO+ memory CD4+ T cells and elevated proportions of CD4+ T cells expressing the negative immune regulator programmed death-1 (PD-1). Finally, we identified several leukocytes whose presence correlated with obesity related fitness parameters.ConclusionsOur data suggests that leukocytes subsets are differentially mobilized into the peripheral blood and dependent on the intensity and duration of exercise. Pre-existing compositional differences of leukocytes were associated with various fitness parameters.Electronic supplementary materialThe online version of this article (doi:10.1186/s40425-017-0231-8) contains supplementary material, which is available to authorized users.

During peak exercise HR, stroke volume and cardiac output were not different between the groups with and without diabetes; however, forced expiratory flow at 50% of the forced vital capacity was lower in subjects with diabetes (P < 0.05). Within the group with diabetes, HbA1c was lower in the low-HbA1c versus high-HbA1c group (6.5 +/- 0.3 vs 7.8 +/- 0.4, respectively; P < 0.05), but training volume was not different. At rest, the low-HbA1c group had greater cardiac output and lower systemic vascular resistance than the high-HbA1c group, and all pulmonary function measurements were greater in the low-HbA1c group (P < 0.05). During peak exercise, the VO2, workload, HR, stroke volume, and cardiac output were greater in the low-HbA1c versus the high-HbA1c group (P < 0.05). In addition, all indices of pulmonary function were higher in the low-HbA1c group (P < 0.05). Finally, within the subjects with diabetes, there was a weak inverse correlation between HbA1c and exercise training volume (r2 = -0.352) and stroke volume (r2 = -0.339). These data suggest that highly trained individuals with type I diabetes can achieve the same cardiopulmonary exercise responses as trained subjects without diabetes, but these responses are reduced by poor glycemic control.

These results suggest a limitation in exercise-mediated increases in membrane conductance in CF which may contribute to a drop in SaO(2) and that resting DLNO can account for a large portion of the variability in SaO(2).

Lung diffusing capacity (DLCO) is influenced by alveolar-capillary membrane conductance (D (M)) and pulmonary capillary blood volume (V (C)), both of which can be impaired in sedentary type 1 diabetes mellitus (T1DM) subjects due to hyperglycemia. We sought to determine if T1DM, and glycemic control, affected DLNO, DLCO, D (M), V (C) and SaO(2) during maximal exercise in aerobically fit T1DM subjects. We recruited 12 T1DM subjects and 18 non-diabetic subjects measuring DLNO, DLCO, D (M), and V (C) along with SaO(2) and cardiac output (Q) at peak exercise. The T1DM subjects had significantly lower DLCO/Q and D (M)/Q with no difference in Q, DLNO, DLCO, D (M), or V (C) (DLCO/Q = 2.1 ± 0.4 vs. 1.7 ± 0.3, D (M)/Q = 2.8 ± 0.6 vs. 2.4 ± 0.5, non-diabetic and T1DM, p < 0.05). In addition, when considering all subjects there was a relationship between DLCO/Q and SaO(2) at peak exercise (r = 0.46, p = 0.01). Within the T1DM group, the optimal glycemic control group (HbA1c <7%, n = 6) had higher DLNO, DLCO, and D (M)/Q than the poor glycemic control subjects (HbA1c ≥ 7%, n = 6) at peak exercise (DLCO = 38.3 ± 8.0 vs. 28.5 ± 6.9 ml/min/mmHg, DLNO = 120.3 ± 24.3 vs. 89.1 ± 21.0 ml/min/mmHg, D (M)/Q = 3.8 ± 0.8 vs. 2.7 ± 0.2, optimal vs. poor control, p < 0.05). There was a negative correlation between HbA1c with DLCO, D (M) and D (M)/Q at peak exercise (DLCO: r = -0.70, p = 0.01; D (M): r = -0.70, p = 0.01; D (M)/Q: r = -0.68, p = 0.02). These results demonstrate that there is a reduction in lung diffusing capacity in aerobically fit athletes with T1DM at peak exercise, but suggests that maintaining near-normoglycemia potentially averts lung diffusion impairments.

Aging is associated with a fall in maximal aerobic capacity as well as with a decline in lean body mass. The purpose of the study was to investigate the influence of aging on the relationship between aerobic capacity and lean body mass in subjects that chronically train both their upper and lower bodies. Eleven older rowers (58±5 yrs) and 11 younger rowers (27±4 yrs) participated in the study. Prior to the VO2max testing, subjects underwent a dual energy X-ray absorptiometry scan to estimate total lean body mass. Subsequently, VO2max was quantified during a maximal exercise test on a rowing ergometer as well as a semi-recumbent cycle ergometer. The test protocol included a pre-exercise stage followed by incremental exercise until VO2max was reached. The order of exercise modes was randomized and there was a wash-out period between the two tests. Oxygen uptake was obtained via a breath-by-breath metabolic cart (Vmax™ Encore, San Diego, CA). Rowing VO2max was higher than cycling VO2max in both groups (p<0.05). Older subjects had less of an increase in VO2max from cycling to rowing (p<0.05). There was a significant relationship between muscle mass and VO2max for both groups (p<0.05). After correcting for muscle mass, the difference in cycling VO2max between groups disappeared (p>0.05), however, older subjects still demonstrated a lower rowing VO2max relative to younger subjects (p<0.05). Muscle mass is associated with the VO2max obtained, however, it appears that VO2max in older subjects may be less influenced by muscle mass than in younger subjects.

Background Individuals with cystic fibrosis (CF) have reduced pulmonary function and exercise tolerance. Additionally, these individuals may develop abnormal cardiac function. The implications of abnormal cardiac function on exercise tolerance are unclear in CF. Objective Study relationships between exercise cardiac hemodynamics and exercise tolerance in CF. Methods 17 CF and 25 controls participated in cardiopulmonary exercise testing to measure exercise duration and peak workload (PW). Cardiac index (QI) was measured using acetylene rebreathe and oxygen uptake (VO2) breath-by-breath. Forced expiratory volume 1-second (FEV1) was performed at rest. Results Peak QI was 6.7±0.5 vs. 9.1±0.3 mL/min/m2, CF vs. controls, respectively (p<0.05). Linear regressions between QI (R2=0.63 and 0.51) and exercise duration or PW were stronger than VO2 (R2=0.35 and 0.37) or FEV1 (R2=0.34 and 0.36) in CF, respectively (p<0.05). Conclusion These data are clinically relevant as they suggest attenuated cardiac function in addition to low airway function relate to exercise tolerance in CF.

In these healthy subjects, administration of a nebulized β(2)-agonist resulted in enhanced ventricular function and a decrease in SVR, suggesting peripheral vasodilation. In addition, the increase in norepinephrine level with albuterol, but not placebo, may have important implications in patients with known cardiovascular disease.