Elevated baseline V̇o2 per se does not slow O2 uptake kinetics during work-to-work exercise transitions

2010 ◽  
Vol 109 (4) ◽  
pp. 1148-1154 ◽  
Author(s):  
Fred J. DiMenna ◽  
Stephen J. Bailey ◽  
Anni Vanhatalo ◽  
Weerapong Chidnok ◽  
Andrew M. Jones

We investigated whether the characteristic slowing of pulmonary oxygen uptake (V̇o2) kinetics during “work-to-work” exercise is attributable to elevations in baseline metabolic rate (V̇o2) as opposed to the elevated baseline work rate, per se. We hypothesized that a step transition to a higher work rate from “unloaded” cycling, but with elevations in V̇o2 [and heart rate (HR)] reflective of a work-to-work transition, would result in a lengthened phase II time constant (τp). Seven male subjects (mean ± SD age 27 ± 10 yr) completed 1) transitions to a high-intensity work rate from a moderate-intensity work rate (M→H) and 2) two consecutive bouts of high-intensity exercise (U→H and E→H, respectively) initiated from unloaded cycling, with the time separating the exercise bouts chosen such that the baseline V̇o2 for the second transition was similar to the baseline V̇o2 for the M→H transition. The τp for M→H (48 ± 16 s) was significantly greater ( P < 0.05) than the τp for U→H (28 ± 8 s) and E→H (27 ± 6 s), which did not differ significantly. These findings suggest that the altered V̇o2 dynamics that are observed during work-to-work exercise are not related to the elevated baseline V̇o2 (or HR) per se; rather, these effects appear to be linked to the elevated baseline work rate, which would be expected to dictate the subsequent muscle fiber recruitment profile.

2008 ◽  
Vol 33 (1) ◽  
pp. 107-117 ◽  
Author(s):  
Nicola Lai ◽  
Melita M. Nasca ◽  
Marco A. Silva ◽  
Fatima T. Silva ◽  
Brian J. Whipp ◽  
...  

The dynamics of the pulmonary oxygen uptake (VO2) responses to square-wave changes in work rate can provide insight into bioenergetic processes sustaining and limiting exercise performance. The dynamic responses at the onset of exercise and during recovery have been investigated systematically and are well characterized at all intensities in adults; however, they have not been investigated completely in adolescents. We investigated whether adolescents display a slow component in their VO2 on- and off-kinetic responses to heavy- and very heavy-intensity exercise, as demonstrated in adults. Healthy African American male adolescents (n = 9, 14–17 years old) performed square-wave transitions on a cycle ergometer (from and to a baseline work rate of 20 W) to work rates of moderate (M), heavy (H), and very heavy (VH) intensity. In all subjects, the VO2 on-kinetics were best described with a single exponential at moderate intensity (τ1, on = 36 ± 11 s) and a double exponential at heavy (τ1, on = 29 ± 9 s; τ2, on = 197 ± 92 s) and very heavy (τ1, on = 36 ± 9 s; τ2, on = 302 ± 14 s) intensities. In contrast, the VO2 off-kinetics were best described with a single exponential at moderate (τ1, off = 48 ± 9 s) and heavy (τ1, off = 53 ± 7 s) intensities and a double exponential at very heavy (τ1, off = 51 ± 3 s; τ2, off = 471 ± 54 s) intensity. In summary, adolescents consistently displayed a slow component during heavy exercise (on- but not off- transition) and very heavy exercise (on- and off-transitions). Although the overall response dynamics in adolescents were similar to those previously observed in adults, their specific characterizations were different, particularly the lack of symmetry between the on- and off-responses.


2013 ◽  
Vol 304 (3) ◽  
pp. R238-R247 ◽  
Author(s):  
Matthew D. Spencer ◽  
Braden M. R. Gravelle ◽  
Juan M. Murias ◽  
Livio Zerbini ◽  
Silvia Pogliaghi ◽  
...  

The present study was designed to investigate whether absolute work rate (WR) affects Phase I pulmonary oxygen uptake (V̇o2p) duration during moderate-intensity (Mod) exercise and to compare two methods for estimating Phase I V̇o2p duration (PI-Dur). Fourteen males (24 ± 5 yr) each completed 4–8 repetitions of Mod transitions from 20 W to 50, 70, 90, 110, and 130 W. PI-Dur was identified by 1) a marked decrease in both respiratory exchange ratio and end-tidal partial pressure of O2 following exercise onset [i.e., visual inspection of three independent reviewers, and the average (Avg) of the two most similar values]; or 2) the intersection (time delay, TD) of the first and second components in a biexponential nonlinear regression of the entire V̇o2p response from exercise onset. PI-Dur did not differ among WRs ( P > 0.05), regardless of the estimation method used. No differences were detected between Avg and TD (time in s) at any of the five WRs (50 W, 21 ± 6 vs. 23 ± 10 s; 70 W, 23 ± 9 vs. 23 ± 7 s; 90 W, 24 ± 3 vs. 22 ± 5 s; 110 W, 23 ± 6 vs. 22 ± 6 s; 130 W, 21 ± 6 vs. 21 ± 7 s; P > 0.05 for Avg and TD, respectively). Broad limits of agreement within Bland-Altman plots revealed relatively weak agreement among reviewers for individual estimation of PI-Dur. A nonsignificant correlation coefficient ( r = 0.13) and broad limits of agreement suggest disparity between individual Avg and TD estimates of PI-Dur. The present data do not support a role for Mod WR in determining PI-Dur per se. Furthermore, this study illustrated a poor agreement of PI-Dur estimates derived from two different, but accepted methods.


2016 ◽  
Vol 120 (11) ◽  
pp. 1319-1327 ◽  
Author(s):  
Peter M. Christensen ◽  
Robert A. Jacobs ◽  
Thomas Bonne ◽  
Daniela Flück ◽  
Jens Bangsbo ◽  
...  

The aim of the present study was to examine whether improvements in pulmonary oxygen uptake (V̇o2) kinetics following a short period of high-intensity training (HIT) would be associated with improved skeletal muscle mitochondrial function. Ten untrained male volunteers (age 26 ± 2 yr; mean ± SD) performed six HIT sessions (8-12 × 60 s at incremental test peak power; 271 ± 52 W) over a 2-wk period. Before and after the HIT period, V̇o2 kinetics was modeled during moderate-intensity cycling (110 ± 19 W). Mitochondrial function was assessed with high-resolution respirometry (HRR), and maximal activities of oxidative enzymes citrate synthase (CS) and cytochrome c oxidase (COX) were accordingly determined. In response to HIT, V̇o2 kinetics became faster (τ: 20.4 ± 4.4 vs. 28.9 ± 6.1 s; P < 0.01) and fatty acid oxidation (ETFP) and leak respiration (LN) both became elevated ( P < 0.05). Activity of CS and COX did not increase in response to training. Both before and after the HIT period, fast V̇o2 kinetics (low τ values) was associated with large values for ETFP, electron transport system capacity (ETS), and electron flow specific to complex II (CIIP) ( P < 0.05). Collectively, these findings support that selected measures of mitochondrial function obtained with HRR are important for fast V̇o2 kinetics and better markers than maximal oxidative enzyme activity in describing the speed of the V̇o2 response during moderate-intensity exercise.


1997 ◽  
Vol 77 (05) ◽  
pp. 0839-0844 ◽  
Author(s):  
Vittorio Pengo ◽  
Fabio Barbero ◽  
Alberto Banzato ◽  
Elisabetta Garelli ◽  
Franco Noventa ◽  
...  

SummaryBackground. The long-term administration of oral anticoagulants to patients with mechanical heart valve prostheses is generally accepted. However, the appropriate intensity of oral anticoagulant treatment in these patients is still controversial.Methods and Results. From March 1991 to March 1994, patients referred to the Padova Thrombosis Center who had undergone mechanical heart valve substitution at least 6 months earlier were randomly assigned to receive oral anticoagulants at moderate intensity (target INR = 3) or moderate-high intensity (target INR = 4). Principal end points were major bleeding, thromboembolism and vascular death. Minor bleeding was a secondary end-point.A total of 104 patients were assigned to the target 3 group and 101 to the target 4 group; they were followed for from 1.5 years to up 4.5 years (mean, 3 years). Principal end-points occurred in 13 patients in the target 3 group (4 per 100 patient-years) and in 20 patients in the target 4 group (6.9 per 100 patient-years). Major hemorrhagic events occurred in 15 patients, 4 in the target 3 group (1.2 per 100 patient-years) and 11 in the target 4 group (3.8 per 100 patient-years) (p = 0.019). The 12 recorded episodes of thromboembolism, 4 of which consisted of a visual deficit, were all transient ischemic attacks, 6 in the target 3 group (1.8 per 100 patient-years) and 6 in the target 4 group (2.1 per 100 patient- years). There were 3 vascular deaths in each group (0.9 and 1 per 100 patient-years for target 3 and target 4 groups, respectively). Minor bleeding episodes occurred 85 times (26 per 100 patient-years) in the target 3 group and 123 times (43 per 100 patient-years) in the target 4 group (p = 0.001).Conclusions. Mechanical heart valve patients on anticoagulant treatment who had been operated on at least 6 months earlier experienced fewer bleeding complications when maintained on a moderate intensity regimen (target INR = 3) than those on a moderate-high intensity regimen (target INR = 4). The number of thromboembolic events and vascular deaths did not differ between the two groups.


2018 ◽  
Vol 24 (4) ◽  
pp. 427-441 ◽  
Author(s):  
Marija Vavlukis ◽  
Sasko Kedev

Background: Diabetic dyslipidemia has specifics that differ from dyslipidemia in patients without diabetes, which contributes to accelerated atherosclerosis equally as dysglycemia. The aim of this study was to deduce the interdependence of diabetic dyslipidemia and cardiovascular diseases (CVD), therapeutic strategies and the risk of diabetes development with statin therapy. Method: We conducted a literature review of English articles through PubMed, PubMed Central and Cochrane, on the role of diabetic dyslipidemia in atherosclerosis, the antilipemic treatment with statins, and the role of statin therapy in newly developed diabetes, by using key words: atherosclerosis, diabetes mellitus, diabetic dyslipidemia, CVD, statins, nicotinic acid, fibrates, PCSK9 inhibitors. Results: hyperglycemia and dyslipidemia cannot be treated separately in patients with diabetes. It seems that dyslipidemia plays one of the key roles in the development of atherosclerosis. High levels of TG, decreased levels of HDL-C and increased levels of small dense LDL- C particles in the systemic circulation are the most specific attributes of diabetic dyslipidemia, all of which originate from an inflated flux of free fatty acids occurring due to the preceding resistance to insulin, and exacerbated by elevated levels of inflammatory adipokines. Statins are a fundamental treatment for diabetic dyslipidemia, both for dyslipidemia and for CVD prevention. The use of statin treatment with high intensity is endorsed for all diabetes-and-CVD patients, while a moderate - intensity treatment can be applied to patients with diabetes, having additional risk factors for CVD. Statins alone are thought to possess a small, although of statistical significance, risk of incident diabetes, outweighed by their benefits. Conclusion: As important as hyperglycemia and glycoregulation are in CVD development in patients with diabetes, diabetic dyslipidemia plays an even more important role. Statins remain the cornerstone of antilipemic treatment in diabetic dyslipidemia, and their protective effects in CVD progression overcome the risk of statin- associated incident diabetes.


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