Implementing BFR during Cycling II

Following the previous post that introduced the concept of BFR to improve endurance-related fitness parameters, we will examine in detail a session that will illustrate practical implementation. After some trial and error, I decided to use a series of 2-minute inflations, followed by 2 minutes of deflation, but no rest (except while the cuffs were inflating) at a power approximately at the LT1. What this translates to is an initial stopping of pedaling while the cuffs inflate, cycle for 2 minutes, hitting the deflate button in the Saga app, and continuing cycling for 2 minutes then repeating. Since my legs were pretty well shot after the 2 minute cuff interval, the power during the deflation was lower than the LT1. I simply strived for an "active" recovery and resumption of blood flow into and out of the leg. As an aside, I would not recommend keeping the cuffs inflated during the "rest" to minimize the chance of thrombosis.

In this session, I used the Moxy as the NIRS device and the Faros 180 ECG at a 1000 Hz sample rate. 

The following plot of power (with HR and muscle O2 sat) shows this graphically:

 

• The interval numbers are in red, power is black, HR is blue, and muscle O₂ sat is red.
• As with the last post data, there is a rapid O₂ desaturation, accompanied by the HR rise.
• HR peaks during the BFR intervals were above 160 bpm, corresponding to the severe intensity domain.
• The times when power reaches zero correspond to the cuff inflation (do not pedal when they pump). 

Though we see that muscle O₂ dropped, is that a "good" response or not? After all, perhaps with higher pressure it could have fallen further. To better judge how profound the O₂ desaturation was, I performed a Wingate 30s later in the session (after some moderate intensity recovery):

 

The Wingate O₂ nadir was 26%, compared with the BFR nadirs of about 22%, certainly demonstrating the achievement of near maximal hypoxia for that leg muscle/sensor configuration. Sure, a higher cuff pressure may have yielded even lower O₂ values; however, it would not be feasible due to pain. Although this is not a mandatory step, knowing that your BFR O₂ nadir is close to the maximal seen during SIT is reassuring that the BFR pressure x time x cycling power is appropriate.

What about HRV and DFA a1?

 

• As expected from the preliminary observations in my last post, there is rapid DFA a1 decline into the uncorrelated to anticorrelated range. 
• For those unclear what this range of DFA a1 signifies, here is an excerpt from one of our recent publications: 

Physiology of DFA a1 based thresholds

Although multiple studies have shown agreement between the RCP or second lactate threshold with the HRVT2, variation still exists on an individual basis. This intrinsic variability may in part be due to the differences between a marker of ANS balance and measures derived from metabolic responses such as V̇O₂ and V̇CO₂. HRV specifically arises from the opposing influences of the stimulatory sympathetic and inhibitory parasympathetic branches of the ANS on the sinoatrial node, resulting in fractal correlation behavior of the cardiac beat sequence (Goldberger 1991, 1996; White and Raven 2014; Michael et al. 2017). This behavior is postulated to be an attempt by the cardiovascular system to best adapt to a rapidly changing environment (Goldberger 1991; Fossion et al. 2018). For example, various functional advantages may exist behind the changes seen in correlation patterns as exercise intensity changes (Goldberger 1996; Goldberger et al. 2002; Fossion et al. 2018). At intensities in the low to moderate range, where future physiological needs may be variable, cardiac plasticity and flexibility are preferred (DFA a1 is correlated, 0.75 ≤ n ≤ 1.5) but these same processes become more rigid (DFA a1 is uncorrelated/anticorrelated, ≤ 0.5), in the heavy to severe domain. Anticorrelated behavior refers to a pattern viewed as an immediate self-correction mechanism associated with the potential failure of homeostatic regulation and as an ultimate protective response that can only be maintained for short time spans (Seely and Macklem 2004; Muñoz 2018; Fossion et al. 2018). Therefore, although the random beat pattern (DFA = 0.5) that occurs close to the heavy-severe boundary transition may be widespread across populations, some intrinsic variability regarding the exact metabolic rate at which this takes place could be expected. This contrasts with metabolic measures such as VCO₂, V̇O₂ or lactate responses which specifically characterize the RCP or maximal lactate steady state (Meyer et al. 2005; Faude et al. 2009; Keir et al. 2022). However, despite some intraindividual variation in HRVT2 to RCP agreement, repeatability of these thresholds are still seen in both well-trained athletes over a 4-month period of testing (Fleitas-Paniagua et al. 2024b) and by non-athletic participants (Sempere-Ruiz et al. 2024) implying that this is a stable, “personal” physiologic marker.

In short, at each interval repeat, a rapid DFA a1 decline is heralding an autonomic perturbation pattern seen at the highest intensity domain, despite cycling power only at LT1 for 2 minutes.

 

Lactate responses:

Although we saw evidence that major HR elevation, O₂ desaturation, and DFA a1 decline all occur with the BFR session, what about an index of blood chemistry itself? As a piece of background info, the Kilgas study did look at lactate after BFR at either 60 or 80% AOP:

 

But we don't know at what point of the multiset session lactate began to rise.

Yet another study looked at lactate, but also after the "set" of multiple repeats:

 

Therefore, I had two questions to answer: 1) What was the La at the end of the set? and 2) how quickly does the La "ramp up". The second is important as it pertains to the "time under high La" which will stimulate La transport mechanisms and metabolism/breakdown machinery. 

Lactate measured by the Nova Lactate Plus (with a fresh bottle of strips). The values after 2 and 3 sets were done on a different day (with a 1 minute break in the protocol to test) than the post 7 set value, which was not interrupted.

• Baseline                                1.5 mmol/L 
• After 2 x 2x2 minutes           4.0 mmol/L
• After 5 x 2x2 minutes           4.7 mmol/L
• After 7 x 2x2 minutes           6.5 mmol/L 

• These results are encouraging, with end La certainly in the severe intensity domain range. Earlier values also represent levels, at least in the realm near the LT2.
• The entire time spent doing the 2 x 2 sets was close to 30 minutes. That is an impressive lactate elevation timespan (and does not count the further time of decay metabolism). 
• Therefore, La responses support both the HR, O2 desaturation and DFA a1 changes that occurred. 

Some takeaway points:

• It appears that practical BFR can be accomplished with consumer grade equipemnt.
• Although this was only my third training session, there is enough objective data to indicate sufficient physiologic disruption to (hopefully) enhance fitness (peak power, thresholds, VO2 max, durability) over time. I emphasize this as encouragement for those out there trying to implement this type of program in a rapid fashion that should not take much time.
• As mentioned, using a percent of the AOP is not realistic for the general user. Accurate measurement requires a Doppler, and even with that available, blood pressure varies on a day to day basis and is position/activity dependent. A more rational approach is to start with a ballpark estimate and use the objective metrics noted above (HR, muscle O2, and DFA a1), along with pain as a guide.
• Training Gear Recommendations: Polar H10 with Fatmaxxer and a Moxy O2 sensor. Yes, if you have a lactate meter that is complimentary, and I certainly would not turn down Kubios Scientific HRV with a high sample rate ECG. Although I am a proponent of using DFA a1, for this indication, watching the muscle O₂ drop in real time is a very compelling reason to use the Moxy. I do like the Saga cuffs, but with the caveat not to trust the AOP.
• Hopefully I have given readers a framework to follow.
• My plan is to continue incorporating BFR sessions once or twice a week and reevaluate performance metrics in about 6 weeks. I will report back.....

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