Acute exercise improves postprandial lipemia, glucose tolerance, and insulin sensitivity, all of which are risk factors for cardiovascular disease. However, recent research suggests that prolonged sedentary behavior might abolish these healthy metabolic benefits. Accordingly, this study aimed to elucidate the impact of an acute bout of exercise on postprandial plasma triglyceride, glucose, and insulin concentrations after 4 days of prolonged sitting (~13.5 h/day). Ten untrained to recreationally active men ( n = 5) and women ( n = 5) completed a counterbalanced, crossover study. Four days of prolonged sitting without exercise (SIT) were compared with 4 days of prolonged sitting with a 1-h bout of treadmill exercise (SIT + EX; 63.1 ± 5.2% V̇o2max) on the evening of the fourth day. The following morning, participants completed a high-fat/glucose tolerance test (HFGTT), during which plasma was collected over a 6-h period and analyzed for triglycerides, glucose, and insulin. No differences between trials ( P > 0.05) were found in the overall plasma triglyceride, glucose, or insulin responses during the HFGTT. This lack of difference between trials comes with similarly low physical activity (~3,500–4,000 steps/day) on each day except for the 1-h bout of exercise during SIT + EX the day before the HFGTT. These data indicate that physical inactivity (e.g., sitting ~13.5 h/day and <4,000 steps/day) creates a condition whereby people become “resistant” to the metabolic improvements that are typically derived from an acute bout of aerobic exercise (i.e., exercise resistance). NEW & NOTEWORTHY In people who are physically inactive and sitting for a majority of the day, a 1-h bout of vigorous exercise failed to improve lipid, glucose, and insulin metabolism measured the next day. It seems that something inherent to inactivity and/or prolonged sitting makes the body resistant to the 1 h of exercise preventing the normally derived metabolic improvements following exercise.

High altitude‐induced hypoxaemia is often associated with peripheral vascular dysfunction. However, the basic mechanism(s) underlying high‐altitude vascular impairments remains unclear. This study tested the hypothesis that oxidative stress contributes to the impairments in endothelial function during early acclimatization to high altitude. Ten young healthy lowlanders were tested at sea level (344 m) and following 4–6 days at high altitude (4300 m). Vascular endothelial function was determined using the isolated perfused forearm technique with forearm blood flow (FBF) measured by strain‐gauge venous occlusion plethysmography. FBF was quantified in response to acetylcholine (ACh), sodium nitroprusside (SNP) and a co‐infusion of ACh with the antioxidant vitamin C (ACh+VitC). The total FBF response to ACh (area under the curve) was ∼30% lower at high altitude than at sea level (P = 0.048). There was no difference in the response to SNP at high altitude (P = 0.860). At sea level, the co‐infusion of ACh+VitC had no influence on the FBF dose response (P = 0.268); however, at high altitude ACh+VitC resulted in an average increase in the FBF dose response by ∼20% (P = 0.019). At high altitude, the decreased FBF response to ACh, and the increase in FBF in response to ACh+VitC, were associated with the magnitude of arterial hypoxaemia (R2 = 0.60, P = 0.008 and R2 = 0.63, P = 0.006, respectively). Collectively, these data support the hypothesis that impairments in vascular endothelial function at high altitude are in part attributable to oxidative stress, a consequence of the magnitude of hypoxaemia. These data extend our basic understanding of vascular (mal)adaptation to high‐altitude sojourns, with important implications for understanding the aetiology of high altitude‐related vascular dysfunction. Key points Vascular dysfunction has been demonstrated in lowlanders at high altitude (>4000 m). However, the extent of impairment and the delineation of contributing mechanisms have remained unclear. Using the gold‐standard isolated perfused forearm model, we determined the extent of vasodilatory dysfunction and oxidative stress as a contributing mechanism in healthy lowlanders before and 4–6 days after rapid ascent to 4300 m. The total forearm blood flow response to acetylcholine at high altitude was decreased by ∼30%. Co‐infusion of acetylcholine with the antioxidant vitamin C partially restored the total forearm blood flow by ∼20%. The magnitude of forearm blood flow reduction, as well as the impact of oxidative stress, was positively associated with the individual severity of hypoxaemia. These data extend our basic understanding of vascular (mal)adaptation to high‐altitude sojourns, with important implications for understanding the aetiology of high altitude‐related changes in endothelial‐mediated vasodilatory function.

Previous studies have demonstrated that African-American (AA) individuals have heightened vasoconstrictor and reduced vasodilator responses under resting conditions, as compared to Caucasian-American (CA) individuals. However, potential differences in vascular responses to exercise remain unclear. Therefore, we tested the hypothesis that, compared to CA, AA would present an attenuated increase in forearm vascular conductance (FVC) during rhythmic handgrip exercise. Forearm blood flow (FBF; duplex Doppler ultrasound), and mean arterial pressure (MAP; finger photoplethysmography) were measured in healthy young CA (N = 10) and AA (N = 10) men during six trials of rhythmic handgrip performed at workloads of 4, 8, 12, 16, 20, and 24 kg. FVC (calculated as FBF/MAP), FBF, and MAP were similar between groups at rest (FVC: CA: 63 ± 7 vs. AA: 62 ± 7 mL min 100 mmHg; P = 0.862). There was an intensity-dependent increase in FVC during exercise in both groups; however, AA presented lower FVC (interaction P < 0.001) at 8, 12, 16, 20, and 24 kg workloads ( e.g., 24 kg: CA: 324 ± 20 vs. AA: 241 ± 21 mL min 100 mmHg; P < 0.001). FBF responses to exercise were also lower in AA (interaction P < 0.001), whereas MAP responses did not differ between groups ( e.g., ∆MAP at 24 kg: CA: +19 ± 2 vs. AA: +19 ± 2 mmHg; interaction P = 0.950). These findings indicate lower hyperemic responses to rhythmic handgrip exercise in AA men, compared to CA men.

It is well known that hyperthermia lowers stroke volume (SV) during moderate-intensity prolonged exercise, yet the underlying mechanism is inconclusive, especially when skin temperature (Tsk) is hot (≥38°C). Purpose In the present study, HR was independently lowered by a low dose of β1-blockade (βB) to investigate its effect on SV during exercise when skin is hot. The effect of rapid skin cooling on reversing cardiovascular responses was also examined. Methods Nine men cycled at 62% V˙O2peak wearing a water-perfused suit for 20 min during three conditions: (a) moderate Tsk (~33°C) (MOD), (b) hot Tsk (~38°C) (HOT), and (c) hot Tsk (38°C) with βB (HOT-βB). Skin temperature was then rapidly cooled at 20 min in all trials by cold water (0°C–2°C) perfusion while subjects continued cycling for another 20 min. Results When HR was lowered during HOT-βB (152 ± 4 bpm) to the same level as MOD (150 ± 4 bpm; P = 0.30), SV in HOT-βB (132 ± 8 mL) was also restored to the same level as MOD (129 ± 7 mL, P = 0.37) even with a significantly higher cutaneous blood flow (CBF) and lower mean arterial blood pressure. When Tsk was rapidly cooled, cardiac output, HR, and CBF significantly decreased while SV remained lower in HOT. Forearm venous volume was not different between trials during heating and cooling. Conclusions The increase in HR rather than an increase in CBF or forearm venous volume was responsible for the decrease in SV during moderate-intensity exercise when Tsk was held at 38°C.

Non-Hispanic black (BL) individuals have the greatest prevalence of cardiovascular disease (CVD), relative to other racial/ethnic groups (e.g., non-Hispanic white population; WH) which may be secondary to blunted vascular function. While women typically present with reduced CVD relative to men of the same racial/ethnic group, the prevalence is similar between BL women and men though the mechanisms differ. This study hypothesized that reduced microvascular function in young, BL women is associated with endothelin-1 (ET-1) overactivity or insufficient L-arginine bioavailability. Nine BL and 9 WH women participated (age: 20 ± 2 vs. 22 ± 2 y). Cutaneous microvascular function was assessed during 39°C local heating, while Lactated Ringer's (control), BQ-123 (ET-1 receptor type A antagonist), BQ-788 (ET-1 receptor type B antagonist), or L-arginine was infused via intradermal microdialysis to modify cutaneous vascular conductance (CVC). Subsequent infusion of Nω-nitro-L-arginine methyl ester allowed for quantification of the nitric oxide (NO) contribution to vasodilation, while combined sodium nitroprusside and 43°C heating allowed for normalization to maximal CVC (%CVCmax). BL women had blunted %CVCmax and NO contribution to dilation during the 39°C plateau (P < 0.027 for both). BQ-123 improved thisresponse through augmented NO-mediated dilation (P < 0.048 for both). BQ-788 and L-arginine, did not alter the CVC responses (P > 0.835 for both) or the NO contribution (P > 0.371 for both). Cutaneous microvascular function is reduced in BL women, and ET-1 receptor type A may contribute to this reduced function. Further research is needed to better characterize these mechanisms in young, BL women.