Category: Home

Ac variability causes

Ac variability causes

BDNF Kettlebell and weightlifting exercises cauwes is associated with reduced hippocampal volume in healthy subjects. No studies evaluated HbA 1c variability in type 1 diabetes and mortality. Center of Registries.


AC Polarity Explained - Electricity 101

Ac variability causes -

In cities, the heat from running ACs at night can raise ambient temperatures by 1°C, or 1. Air conditioners pose another direct problem for the climate. Many of them use refrigerants that are also powerful heat-trapping gases.

Chemicals like hydrofluorocarbons HFCs can be upward of 12, times more potent at trapping heat in the atmosphere than carbon dioxide. Small coolant leaks multiplied by billions of AC units could be devastating for the climate.

The good news is, there is a lot that can be done. And some of that work is underway now. In current heat waves around the world, the priority must be saving as many lives as possible, even if the only options draw on fossil fuels.

However, taking the temperature down has to remain an urgent priority, even after the weather cools off. There are many ways to curb the climate impacts of ACs. With greater energy efficiency, air conditioners do more with less.

Also, homes and businesses need better insulation and sealing to prevent waste. Many countries, including the US, are phasing out HFCs. The US Senate will soon vote to ratify the Kigali Amendment to the Montreal Protocol , an international treaty that commits to cutting HFCs 85 percent by At the same time, there is going to be a massive market for sustainable cooling technologies.

Technology alone is not enough. ACs are only useful for people who work indoors, but millions still labor outside. Reducing outdoor air temperatures requires careful planning to ensure adequate shade and measures like cool roofs.

For some jobs, workers will have to take on schedules that keep them out of the sun during the hottest times of day. In some places, the only tolerable times to work outdoors are at night.

Cooling may also require a more collective approach. Rather than installing ACs on every individual home, some areas can use district cooling systems. And in emergencies, people will need public cooling centers. Regulators need to step in, too. Governments also need to enforce tougher standards for energy efficiency in cooling.

The countries that have historically burned the most fossil fuels now have the wealth to cope with rising temperatures, while those who contributed least to the problem are facing the most dangerous heat with the fewest resources.

Ergo, rich countries are obligated to help places facing dangerous heat deploy cooling, and to help pay for it. So while billions of people are facing more devastating and extreme heat, protecting them and avoiding as much warming as possible benefits everyone on Earth. Will you help keep Vox free for all?

Support our mission and help keep Vox free for all by making a financial contribution to Vox today. We accept credit card, Apple Pay, and Google Pay. You can also contribute via. Understand the world with a daily explainer plus the most compelling stories of the day.

Explainers Israel-Hamas war election Supreme Court. Animal welfare Climate change What to watch. Filed under: Science Explainers Technology. The air conditioning paradox. By Umair Irfan May 18, , am EDT.

Share this story Share this on Facebook Share this on Twitter Share this on Reddit Share All sharing options Share All sharing options for: The air conditioning paradox. Reddit Pocket Flipboard Email. A woman fans her child with a sheet of paper as a fan sits idle amid a power outage during a heat wave in Jacobabad, Pakistan, on May Irfan is also a regular contributor to the radio program Science Friday.

Part of The Vox guide to extreme heat. One study found that the response of wax esters to heat stress was delayed after bleaching, as that lipid class was not depleted at 0, 1. This is consistent with the role of wax esters class lipids as a long-term i.

Our samples were collected approximately 5 months after the peak heat stress, and this delayed response may explain the lack of difference between island groups studied here. However, more studies investigating changes in lipid class concentrations at different times after bleaching are needed.

Corals in South Tarawa experience similar year-to-year temperature variability to those at Abaiang and North Tarawa, but are subject to greater local human-induced stress due to the proximity to the population and administrative centre of Kiribati [47].

Previous studies have found that local stress reduces bleaching resistance with a given amount of heat stress [11] , [18]. However, the difference was not statistically significant, and the corals in South Tarawa were exposed to higher heat stress in than those in North Tarawa and Abaiang.

In addition, after the heat stress event, there were no significant differences between coral tissue and lipids measures between South Tarawa versus Abaiang and North Tarawa Figure 5.

The seeming resistance of corals in South Tarawa to bleaching may be due to the interaction of the local stressors with the effects of thermal history on the physiology of the corals.

The lack of significant differences in tissue thickness or lipids measures between South Tarawa versus Abaiang and North Tarawa, despite higher heat stress in at South Tarawa, suggests that the sampled corals may benefit energetically due to increased food availability from surface runoff, appearing healthier several months after the heat stress event.

For instance, one study found that corals in turbid, inshore environments actually had higher lipid stores than corals of the same species further offshore, probably due to higher rates of particle feeding [52].

The coral community on the outer reef in South Tarawa is different from that at the other outer reef sites studied; South Tarawa is dominated by the weedy encrusting species Porites rus , while at the other sites the coral community is dominated by massive Porites spp.

and Favia spp. The cover of P. rus in South Tarawa expanded after the bleaching event [47] ; by , P. One possibility is that the remaining massive Porites sp. corals we sampled at South Tarawa are highly resistant remnant colonies, and more susceptible massive Porites sp.

colonies have already died off. The results from South Tarawa underscore the need to compare corals from similar environments to isolate the effects of a certain stressor. These results suggest that the background temperature regime may affect coral resilience to bleaching, although the relationship may also depend on direct human stress on the coastal environment.

This finding could eventually be useful in refining methods of bleaching prediction [16] and developing methods for identifying coral reefs or habitats that are more resilient to future warming. For example, locations subject to high historical temperature variability are likely to be less affected by future heat stress, and may be considered priorities for protection.

Further data collection in the Gilbert Islands and other regions subject to ENSO-driven variability in temperature could help identify the effect of frequent heat stress events on the susceptibility of different taxa and different coral communities to bleaching and bleaching-related mortality.

Annual coral calcification rates. Annual average coral density. We thank Aranteiti Tekiau, Toaea Beiateuea, Iobi Arabua, the late Iranimwemwe Teingiia, the late Moiwa Erutarem, and Adam Young for help in the field.

Thanks go to Dale Bailey and the Royal North Shore Hospital for CT scanning, Mark Ohman for laboratory space and use of the Iatroscan MK-5, and Scott Heron of NOAA Coral Reef Watch for providing the satellite-derived SST data. Conceived and designed the experiments: JC SDD. Performed the experiments: JC SDD ACH.

Analyzed the data: JC SDD ACH. Wrote the paper: JC SDD ACH. Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field. Article Authors Metrics Comments Media Coverage Reader Comments Figures. Abstract Coral bleaching is the breakdown of symbiosis between coral animal hosts and their dinoflagellate algae symbionts in response to environmental stress.

Voolstra, King Abdullah University of Science and Technology, Saudi Arabia Received: September 20, ; Accepted: February 28, ; Published: March 30, Copyright: © Carilli et al. Introduction Coral bleaching is a stress response in which corals lose their symbiotic dinoflagellate algae [1].

Download: PPT. Methods We collected coral cores and tissue samples from several locations around three atolls in the central and northern Gilbert Islands: Tarawa, Abaiang, and Butaritari, with permission and assistance from the Republic of Kiribati's Ministry of Fisheries and Marine Resource Development Figure 1.

Coral core collection A total of 28 cores were collected during May, Measurement of coral growth rates and tissue thickness Cores were scanned whole using computerized tomography CT at the Royal North Shore Hospital in Sydney, Australia with a Siemens Biograph mCT [41].

Coral total lipid extractions Coral lipids were extracted using a modified Folch procedure [45]. Figure 3. Weekly sea surface temperature °C; black and degree heating weeks °C·week; gray from through Statistical analyses We measured the severity of bleaching in as 1 the percentage that extension rates were reduced in from the long-term average for the length of each coral core up to and 2 the proportion of cores that showed a partial mortality scar in Results Background thermal variability from — was lower at Butaritari than at Abaiang and North Tarawa as well as at South Tarawa Table 1.

Figure 4. Boxplots of temperature variability and reduction in coral extension rates in Figure 5. Boxplots of tissue thickness and lipid class concentrations for each island. Discussion Butaritari experiences lower year-to-year variability in SST than Abaiang and Tarawa, which are more directly influenced by current and wind reversals during ENSO events [16] , [47].

Supporting Information. Figure S1. s TIF. Figure S2. Table S1. s DOC. Acknowledgments We thank Aranteiti Tekiau, Toaea Beiateuea, Iobi Arabua, the late Iranimwemwe Teingiia, the late Moiwa Erutarem, and Adam Young for help in the field.

Author Contributions Conceived and designed the experiments: JC SDD. References 1. Brown B Coral bleaching: causes and consequences. Coral Reefs 16,: SupplS—S View Article Google Scholar 2.

Lesser M Oxidative stress causes coral bleaching during exposure to elevated temperatures. Coral Reefs — View Article Google Scholar 3.

Downs C, Fauth JE, Halas JC, Dustan P, Bemiss J, et al. Free Radic Biol Med 33 4 : — View Article Google Scholar 4. Ambio — View Article Google Scholar 5. Fitt W, Brown BE, Warner ME, Dunne RP Coral bleaching: interpretation of thermal tolerance limits and thermal threshold in tropical corals.

Coral Reefs 51— View Article Google Scholar 6. Strong A, Barrientos CS, Duda C, Sapper J Improved satellite techniques for monitoring coral reef bleaching. Proc 8th Intl Coral Reef Symp 2: — View Article Google Scholar 7. Harvell C, Kim K, Burkholder JM, Colwell RR, Epstein PR, et al.

Science — View Article Google Scholar 8. Lough J — Unprecedented thermal stress to coral reefs? Geophys Res Lett 27 23 : — View Article Google Scholar 9. McWilliams J, Côté IM, Gill JA, Sutherland WJ, Watkinson AR Accelerating impacts of temperature-induced coral bleaching in the Caribbean.

Ecology 86 8 : — View Article Google Scholar Halley R, Hudson JH Fidelity of annual growth in Montastraea faveolata and the recentness of coral bleaching in Florida.

In: Aronson R, editor. Geological Approaches to Coral Reef Ecology. New York: Springer. Carilli J, Norris RD, Black B, Walsh SW, McField M Century-scale records of coral growth rates indicate that local stressors reduce coral thermal tolerance threshold. Global Change Biol 16 4 : — Carilli JE, Godfrey J, Norris RD, Sandin SA, Smith JE Periodic endolithic algal blooms in Montastraea faveolata corals may represent periods of low-level stress.

Bull Mar Sci 86 3 : — Hoegh-Guldberg O Climate change, coral bleaching, and the future of the world's coral reefs. Mar Freshw Res — Donner SD, Skirving WJ, Little CM, Oppenheimer M, Hoegh-Guldberg O Global assessment of coral bleaching and required rates of adaptation under climate change.

Global Change Biol 11 12 : — Thompson DM, Van Woesik R Corals escape bleaching in regions that recently and historically experienced frequent thermal stress. In the North Atlantic the amplitude of the modeled SST anomalies generally decreases. This is because the modeled mixed layer depth is much deeper than 75 m so that the same flux anomalies generate smaller changes in SST.

The deeper modeled mixed layer depths are more realistic. The SST anomalies simulated in the far North Atlantic with the uniform depth layer were too large but, using the variable depth mixed layer, they are now too small, for example, in the region south and west of Iceland.

However, south of Greenland they remain too large. We compared the modeled mixed layer depths with those derived from the Levitus data and found that the model underestimates the depths over much of the Atlantic north of 40°N.

This difference explains why the model SST anomalies are too large south of Greenland, but the underestimated SST anomalies south and west of Iceland suggest that other processes, such as ocean advection, must be contributing to the SST anomalies there. In the subtropical South Atlantic, use of the variable depth mixed layer increases the size of the SST anomalies because the mixed layers in this region, where it is local summer, are shallower than 75 m.

The modeled SST anomalies would, however, appear to be too large. Comparing the modeled mixed layer depths with those derived from Levitus data reveals that this is because the model depths are somewhat too small.

Spatial and temporal variations in the mean mixed layer depth, which are hard to model correctly, nonetheless have an important effect on the the SST variability.

In order to see how changes in ocean heat transport impact the evolution of SST anomalies we integrated the Lamont ocean GCM Visbeck et al. The GCM spans the Atlantic Ocean from 30°S to 73°N with a resolution of 2° × 2°, and 30 fixed vertical levels, 13 of which are in the upper m. The model includes basin geometry and bathymetry consistent with the resolution.

Model temperatures, at all depths, are relaxed toward seasonally varying climatological values within 5° of the northern and southern ends of the domain only. Salinity is restored to observed values at all grid points so the influence of salinity variability is ignored. The model includes a simple 1½-layer thermodynamic sea ice model, a bulk wind-driven mixed layer model, convective adjustment, and isopycnal thickness diffusion.

The mixed layer depth is now computed and can deviate from its climatological values. Figure 7b shows the winds and modeled SST anomaly corresponding to the first mode of modeled SST variability in the GCM.

Figure 7c shows the corresponding time series. It is immediately apparent that the pattern is very similar to both the pattern derived by the ocean mixed layer models and to the observations. There are however a few differences. The GCM now more faithfully reproduces the magnitude of the SST anomalies in large areas of the far North Atlantic that were overestimated by the uniform depth ocean mixed layer model and underestimated by the variable depth model.

It is also apparent that the GCM faithfully reproduces the warm SST anomalies that occur south of the North Atlantic Current between 25° and 30°N.

However, the GCM has problems simulating the variability north of the Gulf Steam and off the coast of New England and Canada and, generally, it produces too much variability in this region.

To compare the roles of surface fluxes and ocean heat transport in determining the SST variability we performed two regressions of the modeled surface heat fluxes and anomalous ocean heat transports, integrated down to the base of the modeled ocean mixed layer, each against the time series of the SST anomalies of the first SVD mode.

These are shown in Fig. The anomalous ocean heat transport is defined positive if it warms the SST whereas the anomalous surface heat flux is positive if it cools the SST. The broad-scale features of the surface heat fluxes perfectly match the SST anomalies in the sense of the atmosphere forcing the ocean.

Ocean heat transport is important in the northern North Atlantic where it is the same magnitude as the surface fluxes. We broke the anomalous heat transport into two terms, advection of the mean SSTs by the anomalous currents and advection of the anomalous SSTs by the mean currents. Advection of the mean temperature by the anomalous currents was the most important term outside the Tropics.

During a high-index NAO year, stronger westerlies drive a southward Ekman drift over the high-latitude ocean that cools the SSTs. This amplifies the cooling due to enhanced surface fluxes. Luksch noted the same effect in her ocean model simulations of the —79 period.

This anomalous Ekman drift increases the simulated SST anomalies relative to the case with a variable depth mixed layer. Clearly, the reasonably sized SST anomalies simulated with a uniform mixed layer depth, and no anomalous ocean heat transport, were obtained for the wrong reason.

In reality, both ocean heat transport and surface fluxes are important in this area, and it is necessary to account for the fact that the surface fluxes impact the temperature of a deep wintertime mixed layer.

We also looked at the role of anomalous entrainment and found that it dampens the SST changes because of the altered difference in temperatures between the mixed layer and below.

This confirms the same result seen by Halliwell in a model integration. Farther south, stronger trades drive a northward Ekman drift that warms the subtropics and southern midlatitudes.

This weakly opposes the cooling of the subtropics by surface fluxes but enhances the warming to the south of the North Atlantic drift. In the latter region this causes a warming in the GCM that is realistic, but was missed by the ocean mixed layer models. The strong anomalies seen in the data in the region of the North Atlantic Current region are not reproduced by the mixed layer model or the GCM.

It is probable that ocean heat transport is responsible for some of the observed variability of SST in the North Atlantic Current region, but this low resolution GCM cannot capture this. The GCM also has an improved SST simulation in the Gulf of Guinea that may indicate a role for equatorial dynamics.

To further examine the role of ocean heat transport we looked at the heat budget of the ocean mixed layer averaged over different areas. An area average in the subpolar gyre shows a strong relationship between SST changes, surface fluxes, ocean heat transport, and the wind forcing.

Increased westerlies cause dynamical cooling of the ocean that is in phase with the cooling by surface fluxes. This is further evidence for our claim that changes in ocean heat transport are primarily associated with anomalous Ekman drifts that establish themselves instantaneously once the wind changes.

We also computed the time series of northward heat flux by the Gulf Stream off Cape Hatteras. This showed no decadal variability or trend in contrast with the coupled model runs of Grötzner et al.

We were unable to find any evidence for any lead or lag relationship involving ocean heat transports, confirming the earlier model result of Luksch While this is not a comprehensive examination of the possible roles for ocean heat transport, it is in contrast with model simulations of the tropical Pacific Ocean where it is easy to identify changes in ocean heat transport leading the development of SST anomalies e.

These can be compared with the observed SST anomalies for that period shown in Fig. The NAO-associated SST patterns of these individual winters are broadly the same as those derived by SVD or EOF analysis but show some interesting differences.

For example, during cold water did not stretch all the way across the North Atlantic from Newfoundland to the British Isles but, instead, warm waters lay west of Europe.

In the tropical SST anomalies were the same sign north and south of the equator. Neither winter showed a pattern of strong SST anomalies in the North Atlantic Current region. These differences give some idea of how individual winters can depart from the more typical patterns derived by SVD analysis.

Looking at Fig. The peculiarities of the SST patterns, in comparison with the SVD patterns, are also reproduced by the model. We also examined the higher modes of observed and modeled variability. The second and third modes together explain less variance of SST than the first mode alone.

Both higher modes are high-latitude features dominated by anomalous circulations at around 55°N, with that associated with the third mode being located much farther east than that associated with the second mode.

Both modes are dominated by interannual variability without any noticeable trend. The ocean GCM reasonably reproduces the patterns and time evolution of these modes. We regressed the ocean heat transport and surface fluxes onto the time series of the pattern of modeled SST revealed by the SVD analyses.

For the second mode, anomalous surface heat fluxes are the dominant forcing for SST variability with changes in ocean heat transport contributing in the North Atlantic Current region at about 40°N. Patterns of surface fluxes, ocean heat transport, and SST are not coherently linked for the third mode, which makes us wonder about its realism and we do not consider it further.

In this study we first examined why surface heat fluxes have varied over the Atlantic Ocean during the last four decades. We analyzed the different terms in the lowest-level thermodynamic energy budget using NCEP—NCAR reanalyzed data. In agreement with the results of others e.

Changes in wind speed and direction cause changes in surface fluxes that force SST changes. We also found that anomalous subsidence can create changes in surface fluxes that dampen SST anomalies.

Changes in atmospheric eddy fluxes also primarily dampen SST anomalies. Therefore, as far as the SST is concerned, it is changes in the mean atmospheric flow that create the SST anomalies while the eddies dampen them. Next we were able to show that a simple model of the atmospheric mixed layer AML that balances surface fluxes, radiation, subsidence, advection, and eddy transports was quite capable of reproducing the observed surface flux variability when forced by observed SSTs.

This suggests that it would be possible to simulate the SST variability with an ocean model coupled to the AML model. We used three different ocean models: two in which the ocean heat transports were held fixed at their seasonally varying climatological values, the first with a uniform 75 m depth and the second with a mixed layer model that allows the depth to vary and, third, a full ocean GCM in which ocean heat transports varied.

The SST variations simulated by the uniform depth mixed layer model were surprisingly similar to those observed. The model reproduces the familiar tripole-banded structure of SST anomalies associated with the NAO and also reproduces the long-term trend in that pattern toward the high-index state of the NAO Hurrell This result makes it clear that, to first order, the variations of Atlantic Ocean SSTs since can be explained as the response to variations in atmospheric circulation.

This is true at all timescales. By comparing this result with the SSTs simulated using a variable depth ocean mixed layer we were able to assess the role of mixing. The deep winter mixed layers of the far North Atlantic greatly restricted the amplitude of SST anomalies forced by surface fluxes and, in fact, they were too small.

In the South Atlantic the shallow summer mixed layers increase the SST anomalies. The full ocean GCM also includes the variable depth ocean mixed layer model and, in addition, allows the ocean heat transport to vary. Changes in ocean heat transport are important in the far North Atlantic.

Here, when anomalous westerlies cool the SSTs by surface fluxes, they also create an anomalous equatorward Ekman drift that enhances the cooling. The SST anomalies in this simulation were realistic suggesting that here surface fluxes, mixing of the influence of surface fluxes down to considerable depths, and changes in ocean heat transport are all important.

Anomalous entrainment at the base of the mixed layer dampens SST anomalies. In the region to the south of the North Atlantic Current anomalous easterly winds drive an anomalous poleward Ekman drift that warms the SST and greatly improves the realism of the SST simulation relative to the mixed layer models.

We were only able to identify a role for anomalous Ekman drifts. These are generated almost instantaneously and cannot provide any long-term memory that could lead to oscillatory behavior e.

Analyses of the heat budgets in various regions did not uncover any evidence that ocean heat transports systematically lead or lag the SSTs. Instead, where there was a clear signal in changes in ocean heat transport, e.

The results of an ocean modeling study alone cannot be used to fully explain climate variability in the Atlantic sector. We have demonstrated that changes in the surface fluxes forced by a changed atmospheric circulation and, to a much lesser extent, changes in ocean heat transport, can be successfully invoked to explain the variations of Atlantic SST.

However, we cannot explain why the atmospheric circulation changed in the first place. The current results are consistent with the atmosphere forcing the ocean at all timescales, including decadal, but this raises a particularly difficult question:where does the persistence from one winter to another, including the long-term trends, come from?

Atmospheric timescales appear to be too short to explain such low-frequency behavior while they may easily explain persistence during a winter. In nature, the ocean heat transport does in fact play the dominant role and the atmosphere responds constructively such that the surface flux anomalies reinforce the SST anomalies generated by ocean dynamics.

In our model, the reasoning would follow, we do not see the importance of the changes in ocean heat transport because, by fortuitous tuning, the surface fluxes account for almost all the SST change.

If this scenario was correct then the modeled flux anomalies in our models would be systematically too large. There is no evidence for this.

Further, we do not find that the ocean heat transport significantly leads or lags the SST or surface fluxes. This makes it hard to argue for changes in ocean heat transport driving Atlantic climate variability.

This conclusion appears at face value to contradict the recent atmosphere modeling results of Rodwell et al. They forced an atmospheric GCM with observed SSTs and, in an ensemble mean, reproduced much of the observed behavior of the NAO since , though with greatly reduced amplitude.

However, we note that their surface fluxes dampen the SST anomalies rather than force the SST anomalies as observed. Bretherton and Battisti argue that these features are the expected result of taking the mean of an ensemble of experiments in which an atmospheric GCM is forced by the time history of SSTs that were, in fact, created by atmospheric forcing.

The results, therefore, in their interpretation, do not indicate that the NAO behavior was in any way forced by the changes in SST.

In nature, changes in atmospheric circulation create SST anomalies but the atmospheric response to those SST anomalies is such as to reinforce the changes in circulation and fluxes that created the SST anomalies in the first place. Persistence from one winter to another would be aided if variations in ocean mixing could sequester thermal anomalies below the summer mixed layer to be reentrained the following winter Battisti et al.

Both this explanation and the previous one flounder in that they rely on a coherent atmospheric response to midlatitude SST anomalies, in the sense of high pressure downstream of warm water, that has been difficult to demonstrate.

Another explanation of North Atlantic variability is that it is driven from elsewhere, perhaps from the South Atlantic Robertson et al. In this scenario changes in South Atlantic SSTs would influence the strength and location of convection over the Amazon and in the ITCZ.

Atmospheric teleconnections, or changes in the Hadley cell, would then communicate this change to the North Atlantic circulation.

But why do the South Atlantic SSTs change? This explanation substitutes the problem of explaining the persistence of South Atlantic SSTs for the problem of explaining persistence in the North Atlantic.

However it is easier to demonstrate a constructive response of the tropical atmosphere to SST anomalies e. The causes of low-frequency variability in the Atlantic sector lie outside of the Atlantic basin. In particular the Pacific Ocean has strong decadal variability whose origin is unknown Zhang et al.

However, the NAO and Pacific variability have not been demonstrated to be well correlated. More generally, the influence of the Pacific on the high- and midlatitude Atlantic, which occurs via the Pacific—North American teleconnection pattern, is weak.

On the other hand, ENSO has a powerful and coherent impact on the tropical Atlantic Giannini et al. The final contender is greenhouse warming.

Shindell et al. In this scenario surface winds over the Atlantic will be altered as the Arctic Oscillation shifts to a high-index phase. This will then cause the SSTs to vary. Our modeling results are entirely consistent with this explanation but, obviously, cannot prove that it is correct.

Our ocean modeling experiments indicate that over the last four decades Atlantic Ocean climate variability can be adequately explained in terms of the ocean being forced by changes in atmospheric circulation.

Progress therefore requires understanding why the atmospheric circulation changed. We need to discover what can excite trends in the circulation and what can cause persistence from one winter to another.

Changes in the distribution of atmospheric convection in the tropical Atlantic sector are one possibility, greenhouse warming is another, and there are probably others. In terms of the persistence within a winter our observational analysis of the thermodynamic budget of the lower part of the atmosphere is revealing.

Clearly the mean flow creates SST anomalies that the atmospheric eddies dampen. This may not be a fortuitous arrangement. It is possible that the atmospheric eddies force changes in the mean flow via changes in eddy momentum fluxes.

These changes in the mean flow create surface flux and SST changes that the eddy heat fluxes then try to dampen. This three-way coupling between the eddies, the mean flow, and the SST may arrange itself in such a way as to allow persistence and will generally redden the spectrum of variability.

This will be the topic of future work. We would like to thank Tom Delworth for a useful critical reading of the manuscript. Discussions with Wilco Hazeleger, Chris Gordon, and Mark Rodwell are gratefully acknowledged.

Two anonymous reviewers provided helpful comments. Citation: Journal of Climate 13, 16; JOURNALS Artificial Intelligence for the Earth Systems Bulletin of the American Meteorological Society Community Science Earth Interactions Journal of Applied Meteorology and Climatology Journal of Atmospheric and Oceanic Technology Journal of Climate Journal of Hydrometeorology Journal of Physical Oceanography Journal of the Atmospheric Sciences Monthly Weather Review Weather and Forecasting Weather, Climate, and Society Meteorological Monographs.

Sign in Sign up. Advanced Search Help. Journal of Climate. Sections Abstract 1. Introduction 2. Observational analyses of atmospheric boundary layer thermodynamic budgets and SST forcing 3. Simulation of surface heat flux variability between and 4. Simulation of SST anomalies with a uniform depth ocean mixed layer coupled to the AML model a.

Simulation with a uniform depth ocean mixed layer b. Simulations with a variable depth ocean mixed layer 5. Simulation of SST variability with an ocean GCM 6.

Export References. ris ProCite. bib BibTeX. enw EndNote. Export Figures. Close View raw image Fig. View raw image Fig. All Time Past Year Past 30 Days Abstract Views 0 0 0 Full Text Views 11 PDF Downloads 9.

Authors: Wayne H. Joseph B. Kenneth F. Development and Application of a Physical Approach to Estimating Wind Gusts. Author: O. Evaluation of Turbulent Surface Flux Parameterizations for the Stable Surface Layer over Halley, Antarctica.

Authors: John J. Thomas R. John C. A Numerical Study of an Extreme Cold-Air Outbreak over the Labrador Sea: Sea Ice, Air—Sea Interaction, and Development of Polar Lows. Authors: Mariusz Pagowski. Authors: Dingchen Hou.

Eugenia Kalnay. Kelvin K. Next Article. Editorial Type: Article Article Type: Research Article. Causes of Atlantic Ocean Climate Variability between and Richard Seager Richard Seager Lamont-Doherty Earth Observatory of Columbia University, Palisades, New York Search for other papers by Richard Seager in Current site Google Scholar PubMed Close.

Yochanan Kushnir Yochanan Kushnir Lamont-Doherty Earth Observatory of Columbia University, Palisades, New York Search for other papers by Yochanan Kushnir in Current site Google Scholar PubMed Close. Martin Visbeck Martin Visbeck Lamont-Doherty Earth Observatory of Columbia University, Palisades, New York Search for other papers by Martin Visbeck in Current site Google Scholar PubMed Close.

Naomi Naik Naomi Naik Lamont-Doherty Earth Observatory of Columbia University, Palisades, New York Search for other papers by Naomi Naik in Current site Google Scholar PubMed Close.

Jennifer Miller Jennifer Miller Lamont-Doherty Earth Observatory of Columbia University, Palisades, New York Search for other papers by Jennifer Miller in Current site Google Scholar PubMed Close. Gerd Krahmann Gerd Krahmann Lamont-Doherty Earth Observatory of Columbia University, Palisades, New York Search for other papers by Gerd Krahmann in Current site Google Scholar PubMed Close.

Heidi Cullen Heidi Cullen Lamont-Doherty Earth Observatory of Columbia University, Palisades, New York Search for other papers by Heidi Cullen in Current site Google Scholar PubMed Close. CO;2 Page s : —

Catherine GorstChun Shing Variabi,itySaadia Aslam Replenishing after workout, Iain BuchanKettlebell and weightlifting exercises Kontopantelis variiability, Phyo K. MyintGrant Heatlie Kettlebell and weightlifting exercises, Yoon LokeMartin K. RutterMamas A. Mamas; Long-term Glycemic Variability and Risk of Adverse Outcomes: A Systematic Review and Meta-analysis. Diabetes Care 1 December ; 38 12 : — Glycemic variability is emerging as a measure of glycemic control, which may be a reliable predictor of complications. Ac variability causes

Ac variability causes -

J Am Coll Cardiol ; 73 : — Ceriello A , Monnier L , Owens D. Glycaemic variability in diabetes: clinical and therapeutic implications. Lancet Diabetes Endocrinol ; 7 : — Association of visit-to-visit variability of systolic blood pressure with cardiovascular disease and mortality in primary care Chinese patients with type 2 diabetes: a retrospective population-based cohort study.

Diabetes Care ; 40 : — Lee EY , Yang Y, Kim HS, Cho JH, Yoon KH, Chung WS Effect of visit-to-visit LDL-, HDL-, and non-HDL-cholesterol variability on mortality and cardiovascular outcomes after percutaneous coronary intervention. Atherosclerosis ; : 1 — 9.

Ceriello A , Lucisano G , Prattichizzo F , Eliasson Franzén S , Svensson AM , Nicolucci A. Variability in body weight and the risk of cardiovascular complications in type 2 diabetes: results from the Swedish National Diabetes Register. Uric acid variability as a predictive marker of newly developed cardiovascular events in type 2 diabetes.

Front Cardiovasc Med ; 8 : Rawshani A , Rawshani A , Franzén S Sattar N, Eliasson B, Svensson AM, et al.

Risk factors, mortality, and cardiovascular outcomes in patients with type 2 diabetes. Mahmood SS , Levy D , Vasan RS , Wang TJ. The Framingham Heart Study and the epidemiology of cardiovascular disease: a historical perspective.

Lancet ; : — Ceriello A , Lucisano G , Prattichizzo F , La Grotta R , Franzén S , Svensson AM , et al. Hba1c variability predicts cardiovascular complications in type 2 diabetes regardless of being at glycemic target.

Cardiovasc Diabetol ; 21 : Ciampi A , Negassa A , Lou Z. Tree-structured prediction for censored survival data and the Cox model.

J Clin Epidemiol ; 48 : — Durante C , Costante G , Lucisano G , Bruno R, Meringolo D, Paciaroni A, The natural history of benign thyroid nodules. JAMA ; : — Wright AK , Suarez-Ortegon MF , Read SH , Kontopantelis E , Buchan I , Emsley R , et al.

Risk factor control and cardiovascular event risk in people with type 2 diabetes in primary and secondary prevention settings. Circulation ; : — Impact of diabetes on coronary severity and cardiovascular outcomes in patients with heterozygous familial hypercholesterolaemia.

Eur J Prev Cardiol ; 28 : — Banerjee A , Chen S , Pasea L , Lai AG , Katsoulis M , Denaxas S , et al. Excess deaths in people with cardiovascular diseases during the COVID pandemic.

Prospective Studies Collaboration ; Lewington S , Whitlock G , Clarke R , Sherliker P , Emberson J , et al. Blood cholesterol and vascular mortality by age, sex, and blood pressure: a meta-analysis of individual data from 61 prospective studies with 55, vascular deaths.

Ceriello A , De Cosmo S , Rossi MC , Lucisano G , Genovese S , Pontremoli R , et al. Variability in HbA1c, blood pressure, lipid parameters and serum uric acid, and risk of development of chronic kidney disease in type 2 diabetes. Diabetes Obes Metab ; 19 : — Variability of body weight and health outcomes in the Framingham population.

Strohacker K , Carpenter KC , McFarlin BK. Consequences of weight cycling: an increase in disease risk? Int J Exerc Sci ; 2 : — Int J Cardiol Hypertens ; 6 : Strohacker K , McFarlin BK.

Influence of obesity, physical inactivity, and weight cycling on chronic inflammation. Front Biosci Elite Ed ; 2 : 98 — Yatsuya H , Tamakoshi K , Yoshida T , Hori Y, Zhang H, Ishikawa M, et al.

Association between weight fluctuation and fasting insulin concentration in Japanese men. Int J Obes Relat Metab Disord ; 27 : — Ceriello A , Motz E. Is oxidative stress the pathogenic mechanism underlying insulin resistance, diabetes, and cardiovascular disease?

The common soil hypothesis revisited. Arterioscler Thromb Vasc Biol ; 24 : — Prattichizzo F , Giuliani A , Sabbatinelli J , Matacchione G, Ramini D, Bonfigli AR, et al. Prevalence of residual inflammatory risk and associated clinical variables in patients with type 2 diabetes.

Diabetes Obes Metab ; 22 : — La Sala L , Prattichizzo F , Ceriello A. The link between diabetes and atherosclerosis. Eur J Prev Cardiol ; 26 : 15 — Sarin HV , Lee JH , Jauhiainen M , Joensuu A, Borodulin K, Männistö S, et al. Substantial fat mass loss reduces low-grade inflammation and induces positive alteration in cardiometabolic factors in normal-weight individuals.

Sci Rep ; 9 : Piening BD , Zhou W , Contrepois K , Röst H, Gu Urban GJ, Mishra T, et al. Integrative personal omics profiles during periods of weight gain and loss.

Cell Syst ; 6 : — The effect of blood pressure variability on coronary atherosclerosis plaques. Front Cardiovasc Med ; 9 : Taheri S , Zaghloul H , Chagoury O , Elhadad S, Ahmed SH, El Khatib N, et al.

Effect of intensive lifestyle intervention on bodyweight and glycaemiain early type 2 diabetes DIADEM-I : an open-label, parallel-group, randomised controlled trial. Lancet Diabetes Endocrinol ; 8 : — Wing RR , Lang W , Wadden TA , Safford M , Knowler WC , Bertoni AG , et al.

Benefits of modest weight loss in improving cardiovascular risk factors in overweight and obese individuals with type 2 diabetes. Diabetes Care ; 34 : — Costantino S , Paneni F , Battista R , Castello L, Capretti G, Chiandotto S, Impact of glycemic variability on chromatin remodeling, oxidative stress, and endothelial dysfunction in patients with type 2 diabetes and with target HbA1c levels.

Diabetes ; 66 : — Prattichizzo F , Giuliani A , Ceka A , Rippo MR , Bonfigli AR , Testa R , et al. Epigenetic mechanisms of endothelial dysfunction in type 2 diabetes.

Clin Epigenetics ; 7 : Hill AJ. Does dieting make you fat? Br J Nutr ; 92 : S15 — S Ceriello A , Prattichizzo F , Phillip M , Hirsch IB , Mathieu C , Battelino T. Glycaemic management in diabetes: old and new approaches.

Lancet Diabetes Endocrinol ; 10 : 75 — Hocht C , Del Mauro JS , Bertera FM , Taira CA. Drugs affecting blood pressure variability: an update. Curr Pharm Des ; 21 : — Ceriello A , Ofstad AP , Zwiener I , Kaspers S , George J , Nicolucci A. Empagliflozin reduced long-term HbA1c variability and cardiovascular death: insights from the EMPA-REG OUTCOME trial.

Cardiovasc Diabetol ; 19 : Brown E , Wilding JPH , Barber TM , Alam U , Cuthbertson DJ. Weight loss variability with SGLT2 inhibitors and GLP-1 receptor agonists in type 2 diabetes mellitus and obesity: mechanistic possibilities.

Obes Rev ; 20 : — Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide.

Sign In or Create an Account. Advertisement intended for healthcare professionals. Navbar Search Filter European Journal of Preventive Cardiology This issue ESC Publications Cardiovascular Medicine Books Journals Oxford Academic Mobile Enter search term Search. ESC Publications. Advanced Search.

Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents Abstract. Lay Summary. Supplementary material.

Author contributions. Data availability. Journal Article. Risk factor variability and cardiovascular risk among patients with diabetes: a nationwide observational study. Antonio Ceriello , Antonio Ceriello.

IRCCS MultiMedica. Corresponding author. ceriello hotmail. prattichizzo multimedica. Oxford Academic. Giuseppe Lucisano. Francesco Prattichizzo.

Rosalba La Grotta. Stefan Franzén. Health Metrics, Department of Public Health and Community Medicine, Sahlgrenska Academy, University of Gothenburg. Soffia Gudbjörnsdottir. Department of Medicine, Sahlgrenska University Hospital. Björn Eliasson. Center of Registries. Antonio Nicolucci.

Conflict of interest: None declared. Revision received:. Corrected and typeset:. PDF Split View Views. Select Format Select format. ris Mendeley, Papers, Zotero. enw EndNote. bibtex BibTex.

txt Medlars, RefWorks Download citation. Permissions Icon Permissions. Close Navbar Search Filter European Journal of Preventive Cardiology This issue ESC Publications Cardiovascular Medicine Books Journals Oxford Academic Enter search term Search.

Abstract Aims. Graphical Abstract. Open in new tab Download slide. Lay Summary The variability of multiple risk factors is associated with an increased risk of cardiovascular events and mortality in patients with Type 2 diabetes. Type 2 diabetes , Variability , Oscillations , Risk factors , Cardiovascular diseases , Mortality , Weight , Blood pressure , HbA1c , Cholesterol.

Figure 1. Figure 2. Table 1 Patient characteristics by recursive partitioning and amalgamation classes and in the overall cohort. Class 6 High weight and systolic blood pressure variability.

Class 5 High weight and low systolic blood pressure variability. Class 4 Intermediate weight and high HbA1c variability. Class 3 Intermediate weight and low HbA1c variability. Class 2 Low weight and high total cholesterol variability. Class 1 Low weight and total cholesterol variability.

Overall cohort. Open in new tab. Figure 3. Figure 4. Google Scholar Crossref. Search ADS. Effect of visit-to-visit LDL-, HDL-, and non-HDL-cholesterol variability on mortality and cardiovascular outcomes after percutaneous coronary intervention.

Google Scholar PubMed. OpenURL Placeholder Text. Body weight variability is not associated with changes in risk factors for cardiometabolic disease. Impact of glycemic variability on chromatin remodeling, oxidative stress, and endothelial dysfunction in patients with type 2 diabetes and with target HbA1c levels.

Published by Oxford University Press on behalf of the European Society of Cardiology. Issue Section:. Download all slides. Supplementary data. Comments 0. Add comment Close comment form modal. I agree to the terms and conditions. You must accept the terms and conditions. Add comment Cancel.

Submit a comment. Comment title. You have entered an invalid code. Submit Cancel. Thank you for submitting a comment on this article. Anderson, J. Timing is everything. Age differences in the cognitive control network are modulated by time of day. Aging 29, — Ando, S.

The interactive effects of acute exercise and hypoxia on cognitive performance: a narrative review. Sports 30, — Anokhin, A. Genetic influences on frontal brain function: WCST performance in twins. Neuroreport 14, — Genetic influences on dynamic complexity of brain oscillations.

Atkinson, G. True and false interindividual differences in the physiological response to an intervention.

Statistical methods for assessing measurement error reliability in variables relevant to sports medicine. Exercise training response heterogeneity: statistical insights. Diabetologia 61, — Issues in the determination of 'responders' and 'non-responders' in physiological research.

Barha, C. Sex differences in exercise efficacy to improve cognition: a systematic review and meta-analysis of randomized controlled trials in older humans. A systematic review and meta-analysis of randomized controlled trials in older humans. Personalising exercise recommendations for healthy cognition and mobility in aging: time to address sex and gender part 1.

Personalising exercise recommendations for brain health. Considerations and future directions. Biological sex: a potential moderator of physical activity efficacy on brain health. Aging Neurosci. Exercise and the aging brain: considerations for sex differences.

Brain Plast. Sex differences in exercise efficacy: is midlife a critical window for promoting healthy cognitive aging? FASEB J. Barnett, A. Regression to the mean: what it is and how to deal with it. Basso, J. Acute exercise improves prefrontal cortex but not hippocampal function in healthy adults.

Beedie, C. Consensus statement on placebo effects in sports and exercise: the need for conceptual clarity, methodological rigour, and the elucidation of neurobiological mechanisms. Sport Sci. Bento-Torres, J. Associations between cardiorespiratory fitness, physical activity, intraindividual variability in behavior, and cingulate cortex in younger adults.

Sport Health Sci. Blatter, K. Circadian rhythms in cognitive performance: methodological constraints, protocols, theoretical underpinnings. Blokland, G. Quantifying the heritability of task-related brain activation and performance during the N-back working memory task: a twin fMRI study.

Bonafiglia, J. An appraisal of the SDIR as an estimate of true individual differences in training responsiveness in parallel-arm exercise randomized controlled trials.

Examining interindividual differences in select muscle and whole-body adaptations to continuous endurance training. CrossRef Full Text Google Scholar. Moving beyond threshold-based dichotomous classification to improve the accuracy in classifying non-responders. Exploring differences in cardiorespiratory fitness response rates across varying doses of exercise training: a retrospective analysis of eight randomized controlled trials.

Inter-individual variability in the adaptive responses to endurance and sprint interval training: a randomized crossover study. PLoS One e Boot, W. The pervasive problem with placebos in psychology: why active control groups are not sufficient to rule out placebo effects.

Bouchard, C. Genomic predictors of trainability. DNA sequence variations contribute to variability in fitness and trainability. Sports Exerc. Familial aggregation of VO 2max response to exercise training: results from the HERITAGE family study.

Personalized preventive medicine: genetics and the response to regular exercise in preventive interventions. Bourdon, P. Monitoring athlete training loads. Consensus statement. Sports Physiol. Bratland-Sanda, S. Large inter-individual differences in responses to a block of high intensity aerobic interval training: a case series in national-level cyclists and triathletes.

PubMed Abstract Google Scholar. Budde, H. The impact of an exercise training intervention on cortisol levels and post-traumatic stress disorder in juveniles from an Ugandan refugee settlement: study protocol for a randomized control trial.

Trials Intermittent maximal exercise improves attentional performance only in physically active students. Acute coordinative exercise improves attentional performance in adolescents. Steroid hormones in the saliva of adolescents after different exercise intensities and their influence on working memory in a school setting.

Psychoneuroendocrinology 35, — Bueller, J. BDNF Val66Met allele is associated with reduced hippocampal volume in healthy subjects. Psychiatry 59, — Burgess, D.

Practical solutions to evidence-based training-load monitoring in elite team sports. Burke, T. Sleep inertia, sleep homeostatic and circadian influences on higher-order cognitive functions.

Sleep Res. Byun, K. Positive effect of acute mild exercise on executive function via arousal-related prefrontal activations: an fNIRS study.

NeuroImage 98, — Calamia, M. Scoring higher the second time around: meta-analyses of practice effects in neuropsychological assessment. Caspersen, C. Physical activity, exercise, and physical fitness. Definitions and distinctions for health-related research. Public Health Rep.

Google Scholar. Cermakova, P. Socioeconomic position in childhood and cognitive aging in Europe. Neurology 91, e—e Chan, M. Chang, Y. The effects of acute exercise on cognitive performance: a meta-analysis. Brain Res. Effects of acute exercise on executive function: a study with a tower of London task.

Sport Exerc. Chapman, R. The individual response to training and competition at altitude. Individual variation in response to altitude training. Chiolero, A. Assessing the relationship between the baseline value of a continuous variable and subsequent change over time.

Public Health Chrzanowski-Smith, O. Variability in exercise physiology: can capturing intra-individual variation help better understand true inter-individual responses? Costa, A. Genetic inheritance effects on endurance and muscle strength: an update. Cui, J. Does cardiorespiratory fitness influence the effect of acute aerobic exercise on executive function?

Dankel, S. A method to stop analyzing random error and start analyzing differential responders to exercise. Authors' reply to Tenan et al.

de Roos, B. Personalised interventions-a precision approach for the next generation of dietary intervention studies. Nutrients Dijk, D. Divert, V. Individual-typological assessment of cardiorespiratory responses to hypoxia and hypercapnia in young healthy men.

Donath, L. Absolute and relative reliability of acute effects of aerobic exercise on executive function in seniors. BMC Geriatr. Draheim, C. A toolbox approach to improving the measurement of attention control.

Drollette, E. Acute exercise facilitates brain function and cognition in children who need it most: an ERP study of individual differences in inhibitory control capacity. Elliott-Sale, K.

Methodological considerations for studies in sport and exercise science with women as participants: a working guide for standards of practice for research on women. Farah, M. The neuroscience of socioeconomic status: correlates, causes, and consequences.

Neuron 96, 56— Friedman, N. Individual differences in executive functions are almost entirely genetic in origin. Friedmann, B. Individual variation in the erythropoietic response to altitude training in elite junior swimmers. Glahn, D.

Genetic control over the resting brain. Goldberg, T. Genes and the parsing of cognitive processes. Trends Cogn.

Green, S. Improving methodological standards in behavioral interventions for cognitive enhancement. Green, C. On methodological standards in training and transfer experiments. Greenham, G. Biomarkers of physiological responses to periods of intensified, non-resistance-based exercise training in well-trained male athletes: a systematic review and meta-analysis.

Gronwald, T. Commentary: physical exercise as personalized medicine for dementia prevention? Standardization of exercise intensity and consideration of a dose-response is essential. Correlation properties of heart rate variability during endurance exercise: a systematic review.

Noninvasive Electrocardiol. Fractal correlation properties of heart rate variability: a new biomarker for intensity distribution in endurance exercise and training prescription?

Perspective of dose and response for individualized physical exercise and training prescription. Increasing exercise's effect on mental health: exercise intensity does matter.

Gurd, B. Incidence of nonresponse and individual patterns of response following sprint interval training. Hackman, D. Socioeconomic status and the developing brain. Socioeconomic status and the brain: mechanistic insights from human and animal research.

Halson, S. Monitoring training load to understand fatigue in athletes. Hecksteden, A. How to construct, conduct and analyze an exercise training study?

Individual response to exercise training—a statistical perspective. Repeated testing for the assessment of individual response to exercise training. Herold, F. The contribution of functional magnetic resonance imaging to the understanding of the effects of acute physical exercise on cognition.

Brain Sci. New directions in exercise prescription: is there a role for brain-derived parameters obtained by functional near-infrared spectroscopy? Dose-response matters! A discussion on different approaches for prescribing physical interventions—four roads lead to Rome, but which one should we choose?

Hodyl, N. The cortisol awakening response is associated with performance of a serial sequence reaction time task. Hofmann, P. Special needs to prescribe exercise intensity for scientific studies. Hopkins, W. Measures of reliability in sports medicine and science.

Individual responses made easy. Howley, E. Type of activity. Resistance, aerobic and leisure versus occupational physical activity.

Hughes, R. A review of the role of the gut microbiome in personalized sports nutrition. Hwang, J. Acute high-intensity exercise-induced cognitive enhancement and brain-derived neurotrophic factor in young, healthy adults.

Iannetta, D. A critical evaluation of current methods for exercise prescription in women and men. Impellizzeri, F. Internal and external training load: 15 years on. Ishihara, T. Baseline cognitive performance moderates the effects of physical activity on executive functions in children.

JCMM Iskandar, S. Interacting effects of age and time of day on verbal fluency performance and intraindividual variability.

B Aging Neuropsychol. Islam, H. Repeatability of training-induced skeletal muscle adaptations in active young males. Jamnick, N. An examination and critique of current methods to determine exercise intensity.

Jiménez-Pavón, D. Are changes in telomerase activity and telomere length due to different exercise modalities, intensity, or methods: intermittency? Heart J. High-intensity intermittent training versus moderate-intensity intermittent training: is it a matter of intensity or intermittent efforts?

Response: commentary: high-intensity intermittent training vs. moderate-intensity intermittent training: is it a matter of intensity or intermittent efforts? Johnson, L. Experimental effects of acute exercise in attenuating memory interference: considerations by biological sex.

Medicina The effects of acute exercise on episodic memory function among young university students: moderation considerations by biological sex. Health Promot. Joyner, M. Genetic approaches for sports performance: how far away are we?

Limits to the evidence that DNA sequence differences contribute to variability in fitness and trainability. Concepts about V˙O2max and trainability are context dependent. Kao, S. Acute effects of aerobic exercise on response variability and neuroelectric indices during a serial n-back task.

Brain Cogn. Karavirta, L. Individual responses to combined endurance and strength training in older adults. Korous, K.

A systematic overview of meta-analyses on socioeconomic status, cognitive ability, and achievement: the need to focus on specific pathways. Lambourne, K. The effect of exercise-induced arousal on cognitive task performance: a meta-regression analysis.

Li, L. Fitness-dependent effect of acute aerobic exercise on executive function. Lightfoot, J. Commentary on viewpoint: perspective on the future use of genomics in exercise prescription.

Lindheimer, J. Advancing the understanding of placebo effects in psychological outcomes of exercise: lessons learned and future directions. Reconceptualizing the measurement of expectations to better understand placebo and nocebo effects in psychological responses to exercise.

Liu-Ambrose, T. Physical activity for brain health in older adults. Loprinzi, P. The role of sex in memory function: considerations and recommendations in the context of exercise.

Ludyga, S. An event-related potential investigation of the acute effects of aerobic and coordinative exercise on inhibitory control in children with ADHD. Acute effects of moderate aerobic exercise on specific aspects of executive function in different age and fitness groups: A meta-analysis.

Psychophysiology 53, — A combined EEG-fNIRS study investigating mechanisms underlying the association between aerobic fitness and inhibitory control in young adults.

Neuroscience , 23— MacDonald, S. Intra-individual variability in behavior: links to brain structure, neurotransmission and neuronal activity.

Trends Neurosci. Makris, N. Critical population density triggers rapid formation of vast oceanic fish shoals. Science , — Mann, T. Methods of prescribing relative exercise intensity. Physiological and practical considerations. Martin, K. The impact of environmental stress on cognitive performance: a systematic review.

Factors 61, — McClearn, G. Substantial genetic influence on cognitive abilities in twins 80 or more years old. McLaren, S. The relationships between internal and external measures of training load and intensity in team sports. A meta-analysis. McMorris, T. Effect of acute hypoxia on cognition: a systematic review and meta-regression analysis.

McSween, M. The immediate effects of acute aerobic exercise on cognition in healthy older adults: a systematic review.

Mehren, A. Intensity-dependent effects of acute exercise on executive function. Neural Plast. Metcalfe, R. Heterogeneity and incidence of non-response for changes in cardiorespiratory fitness following time-efficient sprint interval exercise training.

Meyler, S. Biological and methodological factors affecting V̇O2max response variability to endurance training and the influence of exercise intensity prescription. Montero, D.

Refuting the myth of non-response to exercise training: 'non-responders' do respond to higher dose of training. Moore, R. Aerobic fitness and intra-individual variability of neurocognition in preadolescent children.

Morand, C. Contribution of plant food bioactives in promoting health effects of plant foods: why look at interindividual variability?

Moreau, D. Assessing change in intervention research: the benefits of composite outcomes. Methods Pract. Nedelec, M. The variability of sleep among elite athletes. Open Netz, Y. Is there a preferred mode of exercise for cognition enhancement in older age? Nummela, A.

Variability in hemoglobin mass response to altitude training camps. Sports 31, 44— Oberste, M. Control group paradigms in studies investigating acute effects of exercise on cognitive performance—an experiment on expectation-driven placebo effects.

Effects and moderators of acute aerobic exercise on subsequent interference control: a systematic review and meta-analysis. Acute exercise-induced set shifting benefits in healthy adults and its moderators: a systematic review and meta-analysis.

Ordovas, J. Personalised nutrition and health. BMJ bmj. Padilla, J. Identifying responders versus non-responders: incorporation of controls is required for sound statistical inference. Peper, J.

Genetic influences on human brain structure: a review of brain imaging studies in twins. Brain Mapp. Pickering, C. Understanding personalized training responses: can genetic assessment help? Open Sports Sci. Do non-responders to exercise exist—and if so, what should we do about them? Piepmeier, A.

A preliminary investigation of acute exercise intensity on memory and BDNF isoform concentrations. Pontifex, M. The effect of acute aerobic and resistance exercise on working memory. A primer on investigating the after effects of acute bouts of physical activity on cognition.

Puthucheary, Z. Genetic influences in sport and physical performance. Rogers, B. A new detection method defining the aerobic threshold for endurance exercise and training prescription based on fractal correlation properties of heart rate variability.

Detection of the anaerobic threshold in endurance sports: validation of a new method using correlation properties of heart rate variability. From laboratory to roadside: Real-time assessment and monitoring of the aerobic threshold in endurance-typed sports.

Ross, R. Separate effects of intensity and amount of exercise on interindividual cardiorespiratory fitness response. Mayo Clin.

The different responses of humans vqriability an apparently equivalent stimulus are called interindividual response variability. This phenomenon has gained Thermogenic effects on appetite and more attention in research in recent years. The research Thermogenic effects on appetite of exercise-cognition has also taken Organic energy-boosting capsules this variabilith, as Combating depression naturally by Cauzes growing variabbility of studies published in the past decade. In this perspective article, we aim to prompt the progress of this research field by i discussing the causes and consequences of interindividual variability, ii critically examining published studies that have investigated interindividual variability of neurocognitive outcome parameters in response to acute physical exercises, and iii providing recommendations for future studies, based on our critical examination. The provided recommendations, which advocate for a more rigorous study design, are intended to help researchers in the field to design studies allowing them to draw robust conclusions.

Author: Kajas

5 thoughts on “Ac variability causes

  1. Ich meine, dass Sie den Fehler zulassen. Geben Sie wir werden besprechen. Schreiben Sie mir in PM.

Leave a comment

Yours email will be published. Important fields a marked *

Design by