The purpose of this study was to compare the electromyographic (EMG) amplitude and mean power frequency (MPF) versus power output relationships for the three superficial quadriceps muscles during incremental cycle (CE) and knee-extensor (KE) ergometry in the same subjects. Eight men performed incremental CE and KE tests to exhaustion. Surface EMG signals were recorded simultaneously from the vastus lateralis (VL), rectus femoris (RF), and vastus medialis (VM). Polynomial regression analyses on a subject-by-subject basis indicated that the relationship between EMG amplitude versus power output was best-fit with either a linear, quadratic, or cubic model for CE, whereas the relationship was best-fit with a linear model for all subjects for the KE test. No consistent relationship was found for EMG MPF within subjects and between muscle groups for CE or KE. Compared with CE, however, the EMG amplitude during KE exercise was, on average, approximately 87% and 30% higher for the RF and VM muscles, respectively. These results suggest that KE exercise may be a better mode of examining EMG amplitude in the quadriceps muscle during incremental exercise than traditional CE.

Endogenous estrogens likely increase blood flow and subsequently shear stress but have also been associated with improved endothelial function and cardiovascular protection. In contrast, a high-fat meal is thought to reduce endothelial function and increase cardiovascular risk. Therefore, we tested the hypotheses that fluctuating hormones across the menstrual cycle (1) facilitate an increase in shear rate and explain phase-specific differences in flow-mediated dilation (FMD) and (2) provide vascular protection against the insult of a high-fat meal. Flow-mediated dilation was determined at baseline and 4 hours following a high-fat meal in young women during the menses (M), follicular (F), and luteal (L) phases of the menstrual cycle. Male control participants were studied once. 17β-Estradiol was elevated (P < .05) during the F (5.3 ± 0.7 pg/mL) and L (5.2 ± 0.6 pg/mL) phases when compared to the M (3.9 ± 0.5 pg/mL) phase, and this was accompanied by an elevated FMD in the F and L phases (12.4 ± 1.4% and 11.2 ± 0.9%, respectively) compared to M (8.0 ± 0.9) with no change in shear rate. Female postprandial FMD was similar throughout the menstrual cycle, while men exhibited a 50% reduction (6.4 ± 1 to 3.3 ± 1%; P < .05). Interestingly, the postprandial FMD response was not associated with concentrations of either 17β-estradiol or progesterone. Despite acutely changing ovarian hormones across the menstrual cycle, shear stress is invariant and therefore does not account for the changes in FMD. Additionally, young women appear to have an inherent vascular protection from the insult of a high-fat meal, perhaps helping to explain sex-specific differences in cardiovascular risk.

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Key points Endurance trained athletes exhibit enhanced cardiovascular function compared to non‐athletes, although it is considered that exercise training does not enhance lung structure and function.An increased pulmonary capillary blood volume at rest is associated with a higher V˙O2 max .In the present study, we compared the diffusion capacity, pulmonary capillary blood volume and diffusing membrane capacity responses to exercise in endurance‐trained males compared to non‐trained males.Exercise diffusion capacity was greater in athletes, secondary to an increased membrane diffusing capacity, and not pulmonary capillary blood volume.Endurance‐trained athletes appear to have differences within the pulmonary membrane that facilitate the increased O2 demand needed for high‐level exercise. AbstractEndurance‐trained athletes exhibit enhanced cardiovascular function compared to non‐athletes, allthough it is generally accepted that exercise training does not enhance lung structure and function. Recent work has shown that an increased resting pulmonary capillary blood volume (V C) is associated with a higher maximum oxygen consumption (V˙O2 max ), although there have been no studies to date examining how aerobic fitness affects the V C response to exercise. Based on previous work, we hypothesized that endurance‐trained athletes will have greater V C compared to non‐athletes during cycling exercise. Fifteen endurance‐trained athletes (HI: V˙O2 max 64.6 ± 1.8 ml kg−1 min−1) and 14 non‐endurance trained males (LO: V˙O2 max 45.0 ± 1.2 ml kg−1 min−1) were matched for age and height. Haemoglobin‐corrected diffusion capacity (DLCO), V C and diffusing membrane capacity (D M) were determined using the Roughton and Forster (1957) multiple fraction of inspired O2 (FIO2)‐DLCO method at baseline and during incremental cycle exercise up to 90% of peak O2 consumption. During exercise, both groups exhibited increases in DLCO, D M and V C with exercise intensity. Athletes had a greater DLCO and greater D M at 80 and 90% of V˙O2 max compared to non‐athletes. However, V C was not different between groups during exercise. In contrast to our hypothesis, exercise V C was not greater in endurance‐trained subjects compared to controls; rather, the increased DLCO in athletes at peak exercise was secondary to an enhanced D M. These findings suggest that endurance‐trained athletes appear to have differences within the pulmonary membrane that facilitate the increased O2 demand needed for high‐level exercise.

Chronic obstructive pulmonary disease (COPD) patients have increased central arterial stiffness and muscle sympathetic nervous activity (MSNA), both of which contribute to cardiovascular (CV) dysfunction and increased CV risk. Previous work suggests that COPD patients have elevated carotid chemoreceptor (CC) activity/sensitivity, which may contribute to the elevated MSNA and arterial stiffness. Accordingly, the effect of CC inhibition on central arterial stiffness, MSNA and CV function at rest in COPD patients was examined in a randomized placebo-controlled study. Thirteen mild-moderate COPD patients (forced expired volume in 1 s (FEV ) predicted ± SD: 83 ± 18%) and 13 age- and risk-matched controls completed resting CV function measurements with either i.v. saline or i.v. dopamine (2 μg kg min ) while breathing normoxic or hyperoxic air (100% O ). On a separate day, a subset of COPD patients and controls completed MSNA measurements while breathing normoxic or hyperoxic air. Arterial stiffness was determined by pulse-wave velocity (PWV) and MSNA was measured by microneurography. Brachial blood flow was determined using Doppler ultrasound, cardiac output was estimated by impedance cardiography, and vascular conductance was calculated as flow/mean arterial pressure (MAP). CC inhibition with dopamine decreased central and peripheral PWV, and MAP (P < 0.05) while increasing vascular conductance in COPD. No change in CV function was observed with dopamine in controls. CC inhibition with hyperoxia decreased peripheral PWV and MSNA (P < 0.05) in COPD, while no change was observed in controls. CC inhibition decreased PWV and MSNA, and improved vascular conductance in COPD, suggesting that tonic CC activity is elevated at rest and contributes to the elevated arterial stiffness in COPD.