Reduced parasympathetic reactivation during recovery from exercise in(ME)/(CFS), 2015, J. Van Oosterwijck et al (also 2021)

Sly Saint · Nov 1, 2020

Not a new study.

Reduced parasympathetic reactivation during recovery from exercise in myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS)

2015
https://www.physiotherapyjournal.com/article/S0031-9406(15)02014-3/abstract

Background: Although involvement of autonomic dysfunction in ME/CFS has been proposed, conflicting evidence has made it difficult to draw firm conclusion regarding autonomic nervous system activity at rest in ME/CFS patients. Furthermore, little attempts have been made to study autonomic nervous activation in response to physical exercise, which is remarkable as severe exercise intolerance is one of the core features of ME/CFS.
Purpose: To examine whether autonomic nervous activation at rest, during an exercise stressor, and during recovery from exercise is impaired in patients with ME/CFS.
Methods: Twenty ME/CFS patients and 20 healthy, sedentary controls participated in a case–control study. Different autonomous variables, including cardiac (blood pressure (BP), heart rate (HR), and heart rate variability measures in time (RMSSD) and frequency (LF/HF) domains), respiratory and electrodermal responses were assessed using electrophysiological measures. All assessments were performed during 10 minute periods preceding (=at rest) and following (=recovery) an acute bout of exercise (=submaximal bicycle exercise test). In addition, cardiorespiratory assessments were performed continuously during exercise testing.
Results: CFS/ME patients showed similar resting HR, BP, RMSSD, electrodermal function and respiratory rate as controls. Although LF and HF in the ME/CFS patients were lower (p = .038, p = .024 resp) than in controls, the LF/HR ratio was similar (p = .314), indicating decreased sympathetic and parasympathetic activation in ME/CFS at rest while maintaining the sympatho/vagal balance.
Exercise capacity and performance parameters were similar between the ME/CFS and controls (p > .05), as were HR and BP responses during exercise. Although the LF/HF ratio increased in both groups, reflecting sympathetic dominance and parasympathetic inhibition during exercise, in ME/CFS the increase was not large enough to reach significance (p = .059) as was the case in the controls (p = .001) demonstrating that although similar sympathetic and parasympathetic modulation takes place during exercise in ME/CFS as in healthy people, the magnitude of this modulation is impaired in ME/CFS.
After the exercise mean HR declined (p < .001) in both groups, but a differential response was seen regarding full recovery. HR during recovery did not significant differ from HR at rest (p = .578) in controls, indicating HR quickly recovered to the original baseline levels following exercise. However in the ME/CFS group a significantly higher HR was observed during recovery compared to rest (p = .031), and the 10 min recovery was insufficient for the HR to return to baseline levels (p = .037).
Conclusion(s): At rest, parameters in the time-domain represented normal autonomic function in ME/CFS, while frequency-domain parameters indicated the possible presence of diminished (para)sympathetic activation. Although a similar (para)sympathetic modulation took place during exercise in ME/CFS as in healthy people, the magnitude of this modulation was impaired in those with ME/CFS. Reduced parasympathetic reactivation during recovery from exercise was observed in ME/CFS for the first time.
Implications: Delayed HR recovery and/or a reduced HR recovery as seen in ME/CFS have been associated with poor disease prognosis, high risk for adverse cardiac events, morbidity and sudden death in other pathologies, which implies that future studies should examine whether this is also the case in ME/CFS and how to safely improve HR recovery in this population.
Keywords: Autonomic nervous system; Heart rate; Aerobic exercise
Funding acknowledgements: This study was funded by the Ramsay Research Fund of the ME Association (United Kingdom).
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@PhysiosforME you might be interested in these authors research (see also Polli).

Snow Leopard · Nov 1, 2020

Heart rate (beat to beat) variation is quite nonspecific and doesn't necessarily suggest any abnormal pathology at all.

In particular, the restoration of regular HRV in healthy people occurs more rapidly in those with higher levels of fitness. As the above study did not control for fitness, the effect may simply be an artifact of lower fitness. The abstract is also from a conference, rather than a proper peer-reviewed manuscript, so key details of the methodology and results are missing (like a visualisation of change over time).

The abstract of the following review makes some clear points:
Cardiac parasympathetic reactivation following exercise: implications for training prescription
https://pubmed.ncbi.nlm.nih.gov/23912805/
doi:10.1007/s40279-013-0083-4

As a marker of cardiovascular recovery, cardiac parasympathetic reactivation following a training session is highly individualized. It appears to parallel the acute/intermediate recovery of the thermoregulatory and vascular systems, as described by the supercompensation theory. The physiological mechanisms underlying cardiac parasympathetic reactivation are not completely understood. However, changes in cardiac autonomic activity may provide a proxy measure of the changes in autonomic input into organs and (by default) the blood flow requirements to restore homeostasis. Metaboreflex stimulation (e.g. muscle and blood acidosis) is likely a key determinant of parasympathetic reactivation in the short term (0-90 min post-exercise), whereas baroreflex stimulation (e.g. exercise-induced changes in plasma volume) probably mediates parasympathetic reactivation in the intermediate term (1-48 h post-exercise). Cardiac parasympathetic reactivation does not appear to coincide with the recovery of all physiological systems (e.g. energy stores or the neuromuscular system). However, this may reflect the limited data currently available on parasympathetic reactivation following strength/resistance-based exercise of variable intensity. In this review, we quantitatively analyse post-exercise cardiac parasympathetic reactivation in athletes and healthy individuals following aerobic exercise, with respect to exercise intensity and duration, and fitness/training status. Our results demonstrate that the time required for complete cardiac autonomic recovery after a single aerobic-based training session is up to 24 h following low-intensity exercise, 24-48 h following threshold-intensity exercise and at least 48 h following high-intensity exercise. Based on limited data, exercise duration is unlikely to be the greatest determinant of cardiac parasympathetic reactivation. Cardiac autonomic recovery occurs more rapidly in individuals with greater aerobic fitness.
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With regards to metaboreflex stimluation, they state:

However, it is important to note that the apparent dose–response relationship of blood acidosis [31, 41] might be limited over time. Once the metaboreflex is activated at high levels and cardiac parasympathetic activity has been almost abolished, further increases in stress metabolite concentrations might not further affect post-exercise parasympathetic reactivation. This ‘ceiling effect’ represents a limitation of HRV as a proxy measure of overall recovery (particularly following high-intensity exercise) because the longer the exercise duration, the greater the depletion of muscle glycogen stores and neuromuscular fatigue
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The described baroreflex stimulation requires post-exercise hypervolmemia, but I'm not convinced this is a factor in ME/CFS. The increased difficulty in achieving similar VO2Peak on a second CPET after 24 hours seems to also contradict this.

There is also suggestion that delayed "parasympathetic reactivation" is due to centrally acting chemo/metaboloreflex:

Effect of Acute Hypoxia on Post-Exercise Parasympathetic Reactivation in Healthy Men
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3429061/

Following submaximal running exercise, post-exercise parasympathetic reactivation was impaired in normobaric hypoxia (FiO2 = 15.4%) compared with normoxia. However, the effect of hypoxia on post-exercise cardiac ANS function was not apparent when the exercise was supramaximal. This suggests that metaboreflex and central chemoreflex activation via blood metabolite accumulation (i.e., which induce a low blood pH) is likely the stronger determinant of parasympathetic activity restoration following exercise.
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Sly Saint · Sep 30, 2021

not sure if this has been republished or what

Reduced Parasympathetic Reactivation during Recovery from Exercise in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Received: 30 June 2021 / Revised: 21 September 2021 / Accepted: 22 September 2021 / Published: 30 September 2021

https://www.mdpi.com/2077-0383/10/19/4527

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Reduced parasympathetic reactivation during recovery from exercise in(ME)/(CFS), 2015, J. Van Oosterwijck et al (also 2021)

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