The paper for this journal club was:
What was the aim of the paper?
The aim of the paper was to look at whether thermal strain that is associated with prolonged self-paced exercise in the heat contributed to increased cardiovascular strain and therefore limited performance. The researchers hypothesised that thermal strain would increase cardiovascular strain (increase heart rate, reduce stroke volume, cardiac output and mean arterial pressure). The research was carried out by researchers at the University of Sydney and Australian Catholic University. It was supported by the University of Sydney Faculty of Health Sciences.
What did the study involve?
This was a laboratory study that used eight male endurance trained cyclists. Prior to the main experimental trials, the researchers measured maximal oxygen uptake of the cyclists on a cycle ergometer. The subjects then attended the laboratory on two occasions and were randomly assigned to either hot (35°C 60% RH) or thermoneutral (20°C 40% RH) conditions. The participants completed a 40 km time trial and the researchers measured oxygen uptake every 10 minutes during the trial and during the final km. Cardiac output and stroke volume were calculated and heart rate was monitored continuously. Core temperature and skin temperature were taken at 1 minute intervals and blood glucose and lactate measured were taken at rest, 10, 30, 45 minutes and upon completion of the time trial. Ratings of perceived exertion and thermal comfort were taken at 10 minute intervals and at the end of the time trial.
What were the main results?
Time to completion was lower in the thermoneutral condition (59.8 min) than the hot condition (64.3 min). Power output was lower from 20 minutes onwards in the heat, compared with the thermoneutral condition (P= ˂0.05). From 5 minutes onwards core temperature increased significantly in the heat and skin temperature remained significantly higher throughout the hot trial.Oxygen uptake was significantly higher in the thermoneutral condition and heart rate was higher in the hot trial. Stroke volume, cardiac output and mean arterial pressure were signficantly lower compared with the thermoneutral condition. There were no differences in rating of perceived exertion between the two trials (the authors do not mention this in the abstract).
What can we take from it?
The methodology in this study seemed well thought through and was relevant for the specific research question, for example the choice of ergometer for the time trial was relevant as the participants were cyclists and the researchers used an area weighted mean to measure skin temperature and calibrated the loggers before and after the study. The authors also took extra measurements that are not usually taken in similar studies, such as intravenous blood sampling and using a skin blood flow laser sensor. However, it also feels like the authors left out some important details of the study, for example they didn’t explain how the participants were randomly assigned to each condition.
The research question was focused, but as Ben and Chris mention the study did not add anything to what we already know about this subject. The paper is one of many studies that have looked at exercise performance and thermal strain during exercise in the heat.
As with the last journal club, the researchers studied only well-trained athletes and did not look at different ages, sex or ethnic groups. Therefore the results may not apply to other groups of people.
The following points from the journal club comments are really interesting and sum up the research really well.
- I am unsure that the data specifically supports the conclusions made.
- It would also be interesting to see whether the initial resting period within the climate lab has an impact on the perception of thermal comfort and sensation.
- Clearly you can’t blind participants or researchers to this intervention, so did the performance look they way it did because participants just expected to perform at a lower level during the hot trial.
- I’m not sure if the authors fitted a story a bit more to what they expected to happen then what the data warrants. To a large extent I think the arguments presented are logical, and quite possibly correct, I’d just like to see other research before I’m convinced.
- Self-paced exercise, particularly in hot environments, requires familiarised participants. The variability increases the less familiar the participant is with the testing modality and/or environmental conditions.
Overall, although the research area is interesting, this study doesn’t add anything to what we already know.
Becky Canvin 
I think this area of research is very relevant because athletes are increasingly being asked to perform in thermally stressful environments. Exposure to thermal stress is generally considered to be a major threat to the heath and performance of athletes, particularly in the case of those athletes that may only be exposed to hot climates during brief a competition period when events are often scheduled at the hottest parts of the day. Anecdotal evidence of this was present during the 2008 Beijing Olympics and the 2011 World Athletics Championships in Daegu.
It is well established that during prolonged exercise, the cardiovascular system must address the competing demands of increased cardiac output to the skin and working muscles while maintaining arterial blood pressure. The resulting increase in heart rate towards maximum heart rate helps compensate for the decrease in stroke volume. As heart rate continues to drift towards HRmax there is an increasing inability to maintain cardiac output to the working muscles signalling the start of fatigue.
However, an alternative hypothesis for reduced performance is that exercise is self-paced with skeletal muscle power output regulated to prevent a catastrophic rise in deep body temperature (Tucker, Marle, Lambert & Noakes, 2006). It is suggested that anticipatory mechanisms regulate voluntary output from the beginning of exercise and continue to regulate the work rate during exercise to ensure that a critical core temperature is not reached.
The current paper sets out to look at whether an increase in cardiovascular strain and the subsequent decrease in power output is mediated by the central thermoregulatory response rather than the anticipatory feed-forward mechanism suggested by Tucker et al, 2006.
The experimental protocol seems very straightforward and similar to the Tucker study, although they have used one less exercise condition. Power output was maintained at similar level between both exercise conditions until 15 mins when power output declined significantly in the hot condition. This declined in power output was accompanied by decreases in stroke volume, cardiac output and mean arterial pressure as shown in figure 4. The study suggests that as power output remained similar in both conditions for 15 mins, the subsequent reduction in power output was as a result of increasing cardiovascular strain rather than the anticipatory feed-forward mechanism. On the face of it, this paper adds further weight to the more ‘established’ reasoning behind impaired performance in the heat.
However, a slightly later study by Schadler, Simmons, Stannard & Mundel, 2011 looked at the role of skin temperature during self paced exercise. Using a liquid perfused suit, they were able to manipulate skin temperature during exercise from hot to cold and cold to hot. The study found that power output was greater from the outset when skin temperature was manipulated from cold to hot when compared to the hot to cold condition. The authors concluded elevations in skin temperature and increased perception of thermal comfort and sensation prior to exercise are largely responsible for the initial self-selected exercise intensity.
This was supported by Lee et al, 2010 who reported an anticipatory reduction in pace amongst runners during a half marathon in warm and humid conditions.
It would be really interesting to see whether introducing a radiant heat source would have any impact on the findings from the curent paper and in particular whether a radiant heat load on a specific limb/muscle group (i.e quadriceps for runners) has any perceptual impact. It would also be interesting to see whether the initial resting period within the climate lab has an impact on the perception of thermal comfort and sensation. The current paper has a resting period of just ~5 mins whilst the study by Schadler et al, 2011 had a resting period of 15 mins.
Finally, could both forms of exercise regulation be utilised by different athlete populations and different times? Are recreational athletes more susceptible to the psychological affect of exercise in the heat and therefore more likely to regulate their work rate from commencement of exercise?
From a practical point of view, we know that heat and prolonged exercise don’t really go hand-in-hand! Depending on your viewpoint, there will either be an anticipatory regulation of exercise or a reduction in power output during exercise as a result of increased cardiovascular strain. Therefore, it is important that we are aware of this and take steps to mitigate the impact. Interventions such as pre-cooling prior and menthol sprays during exercise may also help to prolong exercise performance in the heat.
As a part-time undergraduate student, I would be really interested to hear from anyone who has practical experience of working with athletes in warm/hot environments.
References:
Tucker, R., Marle, T., Lambert, E. V., & Noakes, T. D. (2006). The rate of heat storage mediates an anticipatory reduction in exercise intensity during cycling at a fixed rating of perceived exertion. Journal of Physiology, 574, 905-915.
Schlader, Z. J., Simmons, S. E., Stannard, S. R., & Mundel, T. (2011). Skin temperature as a thermal controller of exercise intensity. European Journal of Applied Physiology, 111, 1631-1639.
Lee, J. K . W., Nio, A. Q. X., Lim, C. L., Teo, E. Y. N., & Byrne, C. ( 2010). Thermoregulation, pacing and fluid balance during mass participation distance running in a warm and humid environment. European Journal of Applied Physiology, 109, 887-898.
Let me start with a couple of disclaimers.
I’m not a thermal physiologist, but have done some work in the area.
I know all the authors, personally, and was completing my PhD in the lab when this data collection started. I was a participant for a couple of related projects, but not this particular one.
I think this is a neat simple project. Quite a few measures have been considered and taken to eliminates many of the potential confounders and limitations to this type of study. The paper reinforces many things we already know, and through the measurement of a few extra measures not often taken, it provides a little more insight into the mechanism(s) behind why performance decreases in a hot environment. This is important from a practical standpoint, because understanding the mechanisms provides greater potential to put in place interventions to improve performance in a hot environment.
I am unsure however that the data specifically supports the conclusions made. Perhaps it is my (limited) understanding of the area, but here are my concerns.
The main conclusion is that the rise in CV strain is associated (yep, they both happen, though causative?) with reduced performance. And that the changes in performance and CV strain happen in parallel. It appears to me that the data doesn’t show such a close temporal relationship though. When comparing the thermoneutral and hot trials, the following significantly different changes are observed.
At 10min – stroke volume, HR, skin blood flow, rectal temperature and thermal comfort
At 20min – cardiac output, mean arterial pressure,
At 30min – oxygen uptake.
RPE is the same between trials at all time points.
But performance (pacing) is different from 20min, so they all seem to change at different times. I’m not sure if there is a better statistical way to analyze temporal relationships, but if there is maybe its warranted.
There is a confusing issue also that all measures are taken at the same time point, yet the amount of work done at each time point will be different (from 20min at least). But maybe this is still the way to look at it, but given performance is normally about a set distance (not set time) it seems a little weird to talk about practical performance from the point of view taken.
Clearly you can’t blind participants or researchers to this intervention, so did the performance look they way it did because participants just expected to perform at a lower level during the hot trial. The authors suggest that in the hot trial the participants may have been working at a relatively higher oxygen uptake based on previous research. That may be true, but the data is funny here. The authors suggest the heat provides a higher CV strain, so why couldnt participants reach at least the same lactate (pseudo anaerobic effort measure) levels as during the cool trial at the “maximal'” end spurt? And why is the SD for lactate at 10min so large in the hot condition, is there an outlier confusing the data in what is already a small sample? (some of the weight loss/hydration data seems similarly scattered) It seems to me like there must be other regulatory mechanisms at place higher than just CV control centres.
So in the end, I’m not sure what to take from this paper. I’m not sure if the authors fitted a story a bit more to what they expected to happen then what the data warrants. To a large extent I think the arguments presented are logical, and quite possibly correct, I’d just like to see other research before I’m convinced. The recent article discussed on SweatScience may add some further fuel to this debate – http://sweatscience.com/does-heat-slow-you-down-if-you-dont-know-its-hot/
Hi Ben,
Julien has responed to some of your comments that you mention above. He says that it’s great that his paper has created some discussion.
“To first address some of Ben’s comments. Changes in cardiovascular function occur progressively with the development of thermal strain. As such, the point of statistical significance for each cardiovascular parameter may not be reached at the same time point. But as we demonstrated, they were temporally related with the rise in thermal strain and the development of cardiovascular strain. Another point is raised by Ben about the practicality of taking measures at specific time points rather than a set distance, which is fair and perhaps that is why we did not see a difference in all measure at the same time point. However given that the subjects completed a 40 km time trial with a mean difference of less than 5 min between trials in cool and hot conditions, the amount of work performed after 20 min of exercise would not have been hugely different. The strategy of taking these measures every 10 min was implemented to describe the change in cardiovascular parameters at consistent intervals of time. With respect to the higher blood lactate concentrations, these are not uncommon in the heat at lower power outputs and we propose an explanation for this in the paper. In brief, the final end spurt in the heat resulted in a lower power output than thermoneutral conditions, therefore less muscle recruitment and hence less lactate accumulation. A similar response occurs at altitude with lactate…a decrease in VO2max and the lactate paradox.
As for our trying to fit a story around the data, rather than interpreting the data, we feel that the data is what told the story. As with constant load exercise, the progressive decline in VO2max during self-paced exercise in the heat led to an inability to maintain the same absolute critical power (the power output that can be sustained during a prolonged time trial, balancing aerobic an anaerobic metabolism) as during exercise in the cool. This was due to the progressive increase in thermal strain increasing cardiovascular strain.”
I find myself largely agreeing with Ben on this article. I wanted to like it, I wanted it to give me something new but I couldn’t and it didn’t… If I had reviewed this the authors would have had to have worked hard to convince me that it offered something novel and important to the literature becasue as it stands I do not think that it does…
A few specifics off the top of my head:
Background
There is controversy surrounding the CCT and CG theories but both seems to over-lap to a large degree and appear modality-specific. CV drift is a commonly observed response to exercise in the heat and the subsequent reduction in efficiency and oxygen uptake may explain the impaired performance observed in both constant and self-paced exercise.
Aim
To see if exercise in the heat causes increases in CV strain and limits performance (what is the novelty of this study?)
Methods
Self-paced exercise, particularly in hot environments, requires familiarised participants. The variability increases the less familiar the participant is with the testing modality and/or environmental conditions so I would have requested much more information about the extent to which the participants were ‘experienced in time-trial efforts’ (because too-familiarised may also be an issue with regards to pacing!!).
Nowadays simply stating that skin-folds were taken is no longer sufficient. Many journals will specifically request an author to state which guidelines they were following and if the investigator was trained to take the measurements (e.g. ISAK qualified).
I know that the aim was specifically to look at the last 1km but the authors never really state why. By only encouraging the participants to produce maximal effort in the final km by blinding them to the distance covered (apart from 5km check points) limits the extent to which the participants could really self-pace.
What was the temperature of the water consumed? How was it provided?
(A side point: I think that consistency is needed with regards to thermal sensation scales. I was in touch with Sebastien Racinais and his group in Qatar about this. His group were working on this problem but for some reason have shelved it for the time being. A consistency in scale would allow for greater comparison between studies.)
Results
I would want to know how variable the 40 km TT times are with this group of participants. Presumably these data are available because they have been identified as experienced at doing this task. Participants completed the task ~7.5% quicker so how does that compare with the CV% of the TT?
CV strain and skin BF were increased in the heat (nothing new there!)
VO2 was lower in the heat (well they were doing less work so the linear relationship explains that)
Discussion
The authors claim that the novelty of the study lies in the relationship between CV strain and performance. I would argue that this is not novel and that many studies have demonstrated similar concurrent reductions/increases in CV related variables but perhaps this has not been a primary aim of the study and so the data has not been as publicized as widely as it may have been.
I am always wary of studies which seem to rely on correlation data for their conclusions when the number of data points in low and the correlations run are inter-related e.g. SV is a component of Q so it is unsurprising that if one is related that the other is too. Interesting the authors did not state in their statistical analyses section that they were running any regression/correlation.
I am not convinced by the confidence that VO2peak was achieved in the final km. The participants were cycling at lower PO than in the cool trial and increases in HR could be simply due to CV drift rather than demonstrating VO2peak. HR should be used with caution in the heat due to this CV drift and so for example coaches who set HR zones may need to consider that the HR may not represent intensity as closely in thermally stressful conditions.
All in all the study is well run but doesn’t really contribute to existing knowledge and like Ben says may be over-reaching somewhat on their conclusions.
Hi Chris,
Julien has replied to some of your comments above. He’s pleased it’s created some discussion.
“To respond some of Chris’s comments, it appears that the aim of the study was slightly overlooked. We agree that cardiovascular strain has been observed in previous studies, but during constant load or incremental exercise. This is what led us to conduct this study. The novelty of the study stems from having examined cardiovascular function during self-paced exercise in a serial manner during the development of hyperthermia. Furthermore, it is unclear to us how the ability to self-pace is limited when the subjects are aware of the distance to be covered, are informed of their progress every 5 km (12.5% of total distance), and with 2 km left. Finally, of course the increase in heart rate is mediated by cardiovascular drift, that is the point! Cardiovascular drift, or the increase in cardiovascular strain, mediated by the development of thermal strain, leads to the attainment of maximum heart rate at submaximal workloads during constant rate exercise. The attainment of maximum heart rate is accompanied with a lower cardiac output due to a reduction in end-diastolic volume and ultimately stroke volume, which results in the decline in VO2max. Perhaps we should have performed an incremental VO2max test immediately after the TT, but this would not have taken into consideration the accumulation of fatigue incurred during the final moments of the time trial. Regardless, the progressive decline in VO2max increases relative exercise intensity for given workloads in the hot compared with the cool conditions during prolonged exercise. This is the mechanism we associated with the decline in self-paced exercise performance. To highlight Chris’s point, that is why heart rate should be used with caution when wanting to exercise at relative intensities. In fact, an additional aim of the study was to refute the conclusions of Tucker et al. (2004, 2006) that anticipating the rate of heat storage leads to a reduction of external work to avoid thermal distress. These studies disregarded their cardiovascular data in this conclusion, whereas we show that cardiovascular strain increases in parallel with decreasing performance in the heat. In fact the subjects tried hard to maintain their performance for ~15min even though stroke volume was decreasing and heart rate increasing. At 20min the subjects eventually had to succumb to the decreasing VO2max and reduce their power output.
On a side note, Chris will be happy to know that I have passed on his comment about thermal sensation to Sebastien Racinais at Aspetar, who is a colleague of mine now and sitting next to me!”
It’s great that we’re passing on our thoughts to researchers, especially with regards to your comment about thermal sensation scales!
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Hi everyone,
I’ve been contacted by the author of this paper, Julien Periard, with some comments about his research. It’s great to see that the researchers are taking note of our comments! Julien is happy to see that his paper has stirred up some debate and without going into too much detail, himself and the other researchers would like to respond to some of the comments. He
believes that the main point is that the novelty of the study was missed by us. In my summary I state that “this study doesn’t add anything to what we already know”. Julien said this is somewhat surprising and he would tend to disagree, as they were the first to evaluate cardiovascular function during self-paced exercise in the heat and describe the changes that occur during such exercise. Previous research has looked at constant load exercise or incremental exercise in the heat, which is very different given the behavioral aspect that comes into play with pacing.
Julien has given me some individual responses to the points we make above, which I will write in reply to each post.
Thanks Julien,
Reminds me of our research group discussions. I just can’t get my head around how things appearing at different time points (based on common statistical tools on which all other conclusions have been based) can be claimed (or implied) to be causative. I’m also struggling with the lack of end race spurt being caused by the peripheral physiological strain. I reckon you need to do some more studies, perhaps you can just go outside and do it this time?