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How to increase cardiovascular endurance by walking with restricted blood flow

This week for our sports science journal club Chris Brander looked at the paper below, which examined the effects of walking with blood flow restriction (BFR) on cardiovascular endurance in elite athletes.

Park S, Kim JK, Choi HM, Kim HG, Beekley MD, Nho H. Increase in maximal oxygen uptake following 2-week walk training with blood flow occlusion in athletes. European journal of applied physiology. 2010;109(4):591-600.

What was the aim of the paper?

Blood flow restriction (BFR) is a pretty novel exercise technique that is typically used in combination with strength exercise with light loads (20-30% of your predetermined 1 rep max). The benefit to applying a cuff or tourniquet around the limbs and reducing blood flow is an increase in muscle mass and strength similar to lifting much heavier loads (≥ 70% 1 rep max). This has huge implications for healthy populations including athletes, but also for populations that have limited strength capacities due to old age, musculoskeletal injuries, or muscle wasting due to inactivity or disease.

Alternatively, the use of BFR during aerobic modes of exercise such as walking and cycling has also been shown to be beneficial in improving gains in muscle strength and mass in both trained and untrained populations. While the research is not clear, the use of walk exercise with BFR may improve aspects of cardiovascular fitness; such as the maximal rate of oxygen consumption (VO2max), resting heart rate and resting blood pressure. So, the aim of this paper was to assess changes in cardiovascular fitness following a short duration training program in an athletic population.

What did the study involve?

Fourteen college male basketball players were recruited for the study and randomized into 2 training groups; walk training with BFR or walk training without BFR. The walk training consisted of 2 training sessions per day (morning and afternoon), 6 days per week, for 2 weeks (24 training sessions in total). Each training session involved walking for 5 sets of 3-minute bouts, interspersed with a 1-minute recovery period, at approximately 40% of their pre-determined VO2max.

For the BFR group a cuff was placed around the upper most portion of each leg and inflated to a pressure of 160-220 mmHg prior to each training session. The cuff remained inflated for the entire exercise bout including rest periods (22 minutes) and was immediately released at the end of the 5th set.

What were the main results?

The researchers found that following training, walking with BFR improved both VO2max (48.9 to 54.5 ml.kg.min – 11.6%) and VEmax (10.6%), whereas there was no change following walk training without BFR. Interestingly, unlike previous research, this study did not find any changes in either groups in lower body power (determined by a 30 second maximal Wingate sprint on a cycle ergometer), and no change in isokinetic knee extension strength.

What can we take from it?

This was the first study to show that a short period of low-intensity aerobic exercise with BFR improves cardiovascular endurance in elite athletes. What is really interesting about this study is that the improvement shown in VO2max was similar to other studies in athletes following high intensity exercise (i.e. 60-70% VO2max) over similar training periods.

From a coaching and practical point of view, research into the area of BFR is consistently demonstrating that we don’t have to train at high intensities or with heavy loads to induce changes in aerobic capacity and build muscle strength and mass. This doesn’t mean you should stop lifting those heavy weights or completing HIIT sessions, but perhaps provides an alternative stimulus to keep on improving once you reach a performance plateau or could be used as an in-season training modality to reduce the stress placed on you or your athletes’ body.

This study was well written and provided some nice images of the BFR walking if you are interested in how to set it up, as well as the important results in easy to read graphs and tables. One limitation of the study was that there was no reporting of any additional training (skills training, weights etc) that may have been completed during the study. This may have had a huge impact on the results if the athletes were completing any additional exercise. It also would have been a better study design if they directly compared the change in VO2max with a group that completed a similar volume of high intensity aerobic exercise.

Image of the journal article

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Sudden cardiac death in athletes: Outcomes in athletes with marked ECG repolarization abnormalities

This journal club looked at a paper related to sudden cardiac death in athletes. It’s a very topical subject at the moment, with the press reporting about cardiovascular events in the Boston marathon and the tragic death of a 30 year old lady at the London marathon.

Pelliccia A, Di Paolo FM, Quattrini FM, et al. Outcomes in athletes with marked ECG repolarization abnormalities. N Engl J Med 2008. 10: 152-61.

What was the aim of the paper?

It’s known that young athletes may have abnormal ECGs without evidence of cardiac disease. However, the question remains as to whether these abnormal ECG patterns represent the initial stage of cardiovascular disease, or are they just expressions of athletic conditioning? The researchers wanted to look at the long-term outcomes in athletes with ECGs characterised by abnormal repolarization.

What did the study involve?

This was a matched case-control study. The researchers reviewed ECG data from a database of 12,550 athletes evaluated at the Institute of Sports Medicine and Science in Italy. In Italy it is required by law for all athletes to undergo screening to rule out cardiovascular disease that could be associated with an increased risk during training and competition. The researchers identified 81 athletes that had abnormal ECGs (showing marked repolarization abnormalities) and excluded those that had evidence of structural heart disease. They compared this data with a control group of 229 athletes who had normal ECGs and no evidence of cardiovascular disease.

What were the main results?

Five of the 81 athletes with abnormal ECGs had a disease of the heart muscle called cardiomyopathy (one died suddenly at the age of 24 from undetected heart disease, three developed cardiomyopathy after an average of 12 years and one after 9 years of follow-up). None of the 229 control athletes had a cardiac event.

What can we take from it?

The researchers concluded that abnormal ECGs in apparently healthy athletes may show the initial expression of underlying heart disease that may be associated with adverse outcomes.

I really enjoyed reading this research paper and found it very informative. It addressed a very important topic and helped to add to what we already know about sudden cardiac death in athletes. The research question was well-developed, stating the population (young athletes), the parameter (abnormal ECGs) and the outcome (clinical outcomes). The study design was simple, with the researchers analysing data from a large number of athletes who were screened at the Institute of Sports Science and Medicine. We know that randomised controlled trials give the most robust evidence, however this was not ethically appropriate. The researchers didn’t state who analysed the ECGs but it was good to see that the control group were selected from the same database of athletes.

I’ve picked out the following comments about the research.

  • The article by Pelliccia and colleagues is a well written piece of work and identifies some ECG abnormalities that may contribute to sudden cardiac death in these athletes.
  • Is pre-screening really worth it if athletes continue to play on despite their awareness?!

Overall, this research shows that ECGs showing marked abnormalities can be useful for identifying those athletes who are at risk of subsequent development of heart disease. However, as Carla mentions in her comments, even if athletes knew that they were at risk of heart disease, would they give it all up to prevent such events?

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The effects of intermittent hypoxic training on aerobic capacity and endurance performance in cyclists

For this journal club we looked at the following journal article:

Czuba M, Waskiewicz Z, Zajac A, et al. The effects of intermittent hypoxic training on aerobic capacity and endurance performance in cyclists. Journal of Sports Science and Medicine 2011; 10: 175-183

What was the aim of the paper?

The aim of the paper was to look at the efficacy of intermittent hypoxic training at 95% of lactate threshold on endurance performance and aerobic capacity in cyclists. The authors did not include a hypothesis. The research was carried out by scientists at the Jerzy Kukuczka Academy of Physical Eduction in Poland.

What did the study involve?

The researchers recruited 20 male elite cyclists and randomly divided them into a hypoxia (H) group (who trained in a normobaric hypoxic environment, O2= 15.2%) and a control group (normoxia environment). The experiment consisted of baseline testing, followed by three weeks of progressive training and one week recovery in which the training load was significantly reduced, and then post-testing. The testing involved taking resting blood samples, body mass and body composition. This was then followed by a progressive cycle ergometer test to determine VO2max and lactate threshold and the researchers measured heart rate, minute ventilation, oxygen uptake and expired carbon dioxide. After 24 hour rest, the participants performed a 30km time trial and heart rate, blood lactate, speed, cadence and power were measured. The training programme was the same for both groups and involved three sessions per week with a 15 minute warm-up, 30-40 minutes of core training (30 min at 95% lactate threshold workload in 1st week, 35 min in second week and 40 min in third week) and a 15 minute cool down. Intensity for the control group was 100% of lactate threshold workload.

What were the main results?

The researchers results showed that after the three week training period, there was a significant increase in VO2max, maximum workload and lactate threshold workload during the incremental test in the hypoxia group compared to the control group. The results also indicated a significant reduction in the time of the trial and a significant increase in average generated power and speed during the time trial in the hypoxia group. However, there was no difference in red blood cell count, haemoglobin concentration and haematocrit value. The authors conclude that intermittent hypoxic training at lactate threshold intensity improves aerobic capacity and endurance performance at sea level.

What can we take from it?

I enjoyed reading this paper and agree with Ben that it had some very interesting points. The research question was focussed and the study design was suitable for the research question, but it was unfortunate that they did not include a hypothesis.

The main point that I want to highlight is that the researchers did not use a repeated measures, crossover design and therefore the participants did not serve as their own control, which means that the groups could have been unbalanced and it may have introduced bias to the results. The training period of three weeks was fairly short, but the training sessions were quite long (around an hour) and at a high intensity, which may not be suitable for the general population. However, as Carla mentions, a three week training programme that improves sea level performance could be appealing to athletes to gain a competitive edge.

I’ve picked out the following comments about the research.

  • The paper fails to find any changes to haematological parameters, suggesting that this intervention was not harsh enough to bring about significant erythropoiesis.
  • Future research should use the same intervention, but have more follow-up analysis and include muscle biopsies to measure for changes in skeletal muscle.
  • The only problem I can see with the present study is that the training only went for 3 weeks, it does not state what type of program the athletes come off, as a supercompensation effect could have accounted for the increases in power, lactate threshold and such.
  • This paper highlights that hypoxia is a complimentary tool to training and not the primary stimulus.

 

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Low-volume high-intensity interval training induces performance and metabolic adaptations that resemble ‘all-out’ sprint interval training

For journal club we looked at the following paper:

Bayati M, Farzad, B, Gharakhanlou R, et al. A practical model of low-volume high-intensity interval training induces performance and metabolic adaptations that resemble ‘all-out’ sprint interval training. Journal of Sports Science and Medicine, 2011; 10:571-76

What was the aim of the paper?

The researchers wanted to compare a sprint interval training (SIT) protocol (3-4 x 30 seconds ‘all out’ effort with 4 minutes recovery) versus a high intensity interval training (HIT) protocol (6-10 x 30 seconds with 125% Pmax with 2 minutes recovery) . They hypothesised that the training induced changes would be the same between the two protocols. The research was carried out by researchers from the Department of Physical Education and Sports Sciences at Tarbiat Modares University.

What did the study involve?

The researchers recruited 24 male graduate students who were habitually active. After a familiarisation trial, the participants carried out a graded exercise test on a cycle ergometer to measure VO2max and power at VO2 max (Pmax). They also did a test to determine the time to exhaustion at Pmax by cycling to fatigue at a self-selected cadence. Finally they carried out a 30 second Wingate test to analyse peak power output (PPO), mean power output (MPO) and total work (Wtot).

The researchers then assigned the participants to one of three groups; HIT, SIT or a control group. The participants trained 3 times a week for 4 weeks. Following the training intervention, the three tests above were repeated. Blood lactate was measured at rest and three and 20 minutes after the Wingate test only.

What were the main results?

The researchers found that following the four week training programme, Pmax, VO2 max and PPO were significantly increased in both training groups compared to the control group. MPO increased significantly with SIT compared with the control group, but MPO did not change significantly with the HIT group. Blood lactate was significantly different in both training groups compared to the control group.

What can we take from it?

I enjoyed reading this study because I am very interested in the research area, especially after watching it on BBC Horizon. It was an easy paper to read and had some good points to take away from it. The researchers clearly stated a research question and hypothesis, and used a simple study design to test the research question. They used a quick and easy training protocol that would be easy for the general population to carry out and because the researchers used participants that were not athletes, it made the results relevant for the general population. The use of a control group in the study helped to eliminate bias and they used a relatively large number of participants compared to similar research (although they did not state if they had used a power calculation for sample size).

Although the paper had many good points, there were a number of areas that I questioned. The training was only carried out over a period of four weeks and I would have liked to see the long-term effects of the training protocols. The study was not a repeated measures design and the researchers matched the subjects, but they did not state the criteria for this and also did not say how they randomised the participants into the groups. I would have liked to have seen how the diet and physical activity adherence was measured. I also wonder why the researchers only measured blood lactate. They could have measured other markers of fitness, such as heart rate and also perceptual measures, including rating of perceived exertion. Finally, this training protocol would not be suitable for people who had an existing medical condition.

The following points that Dan made about the research are very valid.

  • Are the two adequately distinctive enough to warrant such investigation? 125% Pmax for obese, unfit and/or unaccustomed individuals is still a big ask and questionably unsustainable for long-term exercise prescription. As well as being difficult to quantify this intensity in real life.
  • With regard to adding to current literature, relevant is the finding that lower intensity (125% Pmax vs. ‘all out’) but more repetitions (6-10 vs. 3-5) provide similar metabolic and performance gains.
  • Would be interesting if subjects were to see comparable improvements with the comparison of HIT and SIT protocols used in the current study against the utilisation of those rest periods to conduct low intensity recovery exercise (interval training)

Overall, I enjoyed reading this study but would have liked it to be a bit ‘meatier’ and feel like some important points were missing.

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The role of exercise intensity in the bone metabolic response to an acute bout of weight-bearing exercise

The paper we looked at for journal club was from the Journal of Applied Physiology and entitled ‘The role of exercise intensity in the bone metabolic response to an acute bout of weight-bearing exercise.’

What was the aim of the paper?

The researchers wanted to compare the effects of three different cardiovascular intensities on changes in bone turnover markers during and for 4 days after acute endurance running. They did not state a hypothesis, but previous research has shown that short-duration, high-impact exercise is beneficial for bone mass and endurance running exercise has been linked with detrimental effects on bone. The research was carried out by researchers in the UK.

What did the study involve?

The researchers recruited 10 men who performed at least one bout of endurance running a week. The study consisted of three counterbalanced 8-day experimental conditions, separated by at least a week. You can find out why the researchers carried out this design here. On days 1-3 of the trial, the participants did not carry out physical activity. Day 4 consisted of a single 60 minute bout of running at 55%,65% and 75% of VO2max, followed by 3 hours recovery. The researchers measured 60 seconds of expired air and RPE at 18,38 and 58 minute of exercise. They recorded heart rate continuously. Blood samples were taken at baseline, after 20,40 and 60 min of exercise and 0.5, 1,2 and 3 hours of recovery. The researchers measured the following markers: COOH-terminal telopeptide of procollagen type 1 (β-CTX), NH2-terminal propeptides of procollagen type 1 (P1NP), osteocalin (OC), bone-alkaline phosphatase (ALP), osteoprotegerin (OPG), parathyroid hormone (PTH), albumin-adjusted calcium (ACa), phosphate (PO4) and cortisol. The participants consumed a standardised meal in the lab 3 hours after exercise, and around 4.5 and 7 hours after exercise. On days 5-8 the participants did not carry out physical activity but followed a prescribed diet and went to the lab for analysis.

What were the main results?

The researchers found that β-CTX concentrations were higher in the first hour following exercise at 75% VO2max, compared to 55% and 65%. P1NP increased significantly during exercise only and ALP concentrations increased significantly at 3 and 4 days after exercise, but neither were effected by exercise intensity. PTH and cortisol increased signficiantly with exercise at 75% only. OPG, ACa and PO4 increased signficiantly with exercise but were not effected by exercise intensity.

What can we take from it?

Although I found this paper quite challenging to read, I really enjoyed it and learnt a lot from it. The researchers recruited the participants well because they ensured that they did not have a bone fracture in the previous 12 months, no injury and did not have a condition or take any medication known to affect bone metabolism. They also took into account fasting vitamin D concentration, which is important because low serum vitamin D levels have been associated with low bone density.

I really liked the use of figures and tables in the paper. I think it was good to have a figure outlining the overall study design, which helped with the understanding of the protocol. The table with the subject characteristics was helpful and there was a good use of charts to graphically display the results.

A small point of interest in the study design is that the researchers relied on the participants correctly adhering to the diet that the researchers prescribed. There could have been variation in the timing of the consumption of food, however the researchers ensured that the participants verbally confirmed their adherence.

Overall, I think this was a good study with an appropriate design for the question being asked. Craig Sale, who is one of the authors of the paper, said in conclusion: “There is only a small and transient influence of intensity on the bone metabolic response to one hour of exercise. Most likely, from this and subsequent studies from our group, the effect of exercise duration on bone is more critical.” Further research in this area is being carried out by Craig and his research partners.

Craig has answered some questions about his research that were tweeted by followers on Twitter. It is a great opportunity to find out more about the research and I would highly recommend having a read through his answers.

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Q&As with Craig Sale, Reader in Applied Physiology at Nottingham Trent University

For journal club we looked at the following paper:

Scott JP, Sale C, Greeves JP, et al. The role of exercise intensity in the bone metabolic response to an acute bout of weight-bearing exercise. J Appl Physiol 2011; 110 (2): 423-32

I was lucky enough to ask one of the authors, Craig Sale, some questions about his research. Craig is a Reader in Applied Physiology at Nottingham Trent University and one of his research areas of interest is bone health and metabolism.Thanks to those of you who tweeted your questions. I hope you find this interesting and it gives you a better insight into Craig’s research.

Q: Why did you decide to carry out this research?

A: To answer a possible question over the influences on the bone metabolic response to exercise that had arisen from two previous studies from our group.  Two obvious potential influences were exercise duration and intensity and we wanted to examine the latter here.

Q: How did you recruit the participants?

A: Primarily through posters, email and word of mouth.

Q: Why did you choose the study design of three 8-day experimental conditions, separated by a minimum of 1 week?

A: Some of the bone markers are sensitive to exercise and feeding, so for this reason we wanted a control period prior to the exercise trial itself, hence the 3 d lead in period.  In order to get the most relevant information on the bone metabolic response to exercise, the days following the exercise are most critical.  In this study we chose to examine a 4 d follow-up period for this reason, which was based upon our previous study.  You need at least a 1 week separation between trials as bone markers can remain elevated over this period.

Q: How did you randomise the participants into the experimental conditions?

A: There were 6 possible combinations of 3 conditions so the first 6 subjects were randomly assigned to one of the 6 combinations then the 6 combinations were ‘re-set’ and the last 4 subjects were assigned on this basis.

Q: How did you ensure that the participants adhered to the diet that you prescribed?

A: This study was conducted with free-living participants and so it is hard to directly confirm adherence to the dietary control.  However, subjects verbally confirmed their adherence to the dietary control on each occasion.

Q: Your findings showed that daily calcium intake of the participants exceeded the recommended daily intake of 700mg a day and there was large variation in calcium intake, do you think this could have affected your results?

A: The habitual dietary intake of the subjects was variable, but this was reduced somewhat by the dietary control imposed during the experimental trials.  Some variability would have remained but the effects of this on the bone metabolic responses to exercise is not likely to be large in this within subjects design.

Q: What populations do you intend your findings to be beneficial for?

A: These findings, particularly when combined with the evidence from other well-controlled exercise studies, would be of benefit for any athletic individual.

Q: How much, in your opinion, are the changes in bone turnover due to mechanical muscle tension placed on the bone?

A: As far as a specific quantification is concerned, this is obviously impossible to answer directly.  However, it is clear that muscle contractions, occurring concomitant with the direct impact loading of the bone, produced during exercise can generate further osteogenic loading. As such, the effects of muscle contraction in this sense are likely to contribute significantly to changes in bone with exercise and particularly training.

Q: What would you like people to take away from your research and how do you hope to develop your findings?

A: That there is only a small and transient influence of intensity on the bone metabolic response to one hour of exercise.  Most likely, from this and subsequent studies from our group, the effect of exercise duration on bone is more critical.  This makes sense from a mechanical loading perspective and it would be of interest to examine the influence of changes in “mechanical” intensity rather than cardiovascular exercise intensity. We now have several studies continuing on the effects of exercise and diet/nutrition on bone metabolism as well as studies examining the influence of exercise training on bone structure and geometry.

Thank you to Craig for taking the time to answer the questions about his research and sharing his knowledge.

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Comparisons of post-exercise chocolate milk and a commercial recovery beverage following cycling training on recovery and performance

We looked at the following paper for week 3 journal club:

Pritchett KL, Pritchett RC, Green JM et al. Comparisons of post-exercise chocolate milk and a commercial recovery beverage following cycling training on recovery and performance. JEP online 2011; 16(6): 29-39.

What was the aim of the paper?

The researchers wanted to compare the effects of chocolate milk to a commercial carbohydrate (CHO)/protein (PRO) drink after exercise. They hypothesised that because of similar CHO:PRO ratio of chocolate milk to the commercial drink, drinking chocolate milk for one week would be as effective in reducing markers of muscle damage (creatine kinase) and soreness compared to the commercial drink. They also believed that chocolate milk would be just as effective in enhancing time to exhaustion at 85% of VO2 max. The research was carried out by researchers at Central Washington University, The University of Alabama and The University of North Alabama.

What did the study involve?

This was a counterbalanced repeated-measures crossover design study. 10 recreationally trained cyclists completed two trials, each lasting one week, with a week between each trial. The first treatment period consisted of the participants receiving either a commercial drink (Endurox R4) or chocolate milk (Mayfeild, lowfat chocolate milk) based on the ACSM recommendation of 1g CHO/kg body weight immediately after exercise and 2 hours after. Participants self-reported training information and rating of perceived exertion (RPE). At the end of the week the participants completed a trial on the cycle erg at 85% of VO2 max until exhaustion. The researchers measured creatine kinase (CK) at baseline, before the test and around 24 hours after the last day of the trial. Heart rate was recorded every minute during the test and muscle soreness on one day of the treatment (the researchers did not state when) using an analogue scale. One week following the intervention, the participants repeated the second intervention period with the other drink. Food and training were monitored during the two periods to ensure that they were similar between the two.

What were the main results?

There were no significant differences between the two drinks for calorie, protein and carbohydrate, but there was a signficant difference in fat (chocolate milk 4.6gm and commercial drink 2.7gm). All participants preferred the taste of the chocolate milk. There were no significant differences in macronutrient intake, muscle soreness, RPE, CK and training between the two trials.

What can we take from it?

Although this study was an easy read, I agree with Matt that it did not really add anything to what we already know about the effects of drinks on recovery. The main point was that they did not use a control trial, which would have been easy to implement, with the athletes carrying out their usual diet and exercise. This would have allowed us to understand more about the effects of a commercial drink/chocolate drink on recovery. The authors do highlight in their discussion that a control trial was not used because it is well established that a post-exercise meal provides more benefit than nothing at all, but I think it would have helped to highlight this.

The repeated-measures crossover design of the study helped to eliminate any bias, so the researchers and participants were unaware of what they were drinking. Although it would have been quite easy to distinguish between the taste and consistency of the two drinks. I would have liked for the authors to explain how they randomised the participants. I was pleased to see that they had included a power calculation in the methods, which had indicated that they needed only six participants, but they used 10 to ensure sufficient statistical power.

There were large differences in daily dietary intake between the subjects for each trial, as indicated by the large standard deviations. This could have influenced the results. A final point that I have with the methods is that the results relied on the participants self-reporting their training programmes and diet during the two trials. They could have under or over-reported, which would have introduced bias.

The following points from the journal club comments are really interesting and sum up the research really well.

  • It’s common for athletes of all levels across a wide range of sports to use chocolate shakes over the more common (and expensive) over-the-counter recovery powders and shakes. 
  • As the diets were matched and isocalorific over the two interventions, the results were fairly predictable.
  • The recovery nutrition could possibly have been met by the subject habitual diet in-between each training session, and neither drink having an impact on recovery.
  • I would have liked to see why the specific recovery beverage was chosen and how it compares to its competitors (i.e. energy, protein, carb, fat, like in table 2)

Overall, the research looked at a very popular recovery beverage (chocolate milk) but it would be good to see more research in this area.

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