Cited by 63Coffee research and impactsHeart Rate Variability and Autonomic ControlCardiovascular and exercise physiology

Caffeine delays autonomic recovery following acute exercise

Bunsawat, Kanokwan, White, Daniel W, Kappus, Rebecca M, Baynard, Tracy·2015·European Journal of Preventive Cardiology

Abstract

BACKGROUND: Impaired autonomic recovery of heart rate (HR) following exercise is associated with an increased risk of sudden death. Caffeine, a potent stimulator of catecholamine release, has been shown to augment blood pressure (BP) and sympathetic nerve activity; however, whether caffeine alters autonomic function after a bout of exercise bout remains unclear. METHODS: In a randomized, crossover study, 18 healthy individuals (26 ± 1 years; 23.9 ± 0.8 kg·m(-2)) ingested caffeine (400 mg) or placebo pills, followed by a maximal treadmill test to exhaustion. Autonomic function and ventricular depolarization/repolarization were determined using heart rate variability (HRV) and corrected QT interval (QTc), respectively, at baseline, 5, 15, and 30 minutes post-exercise. RESULTS: Maximal HR (HRmax) was greater with caffeine (192 ± 2 vs. 190 ± 2 beat·min(-1), p < 0.05). During recovery, HR, mean arterial pressure (MAP), and diastolic blood pressure (DBP) remained elevated with caffeine (p < 0.05). Natural log transformation of low-to-high frequency ratio (LnLF/LnHF) of HRV was increased compared with baseline at all time points in both trials (p < 0.05), with less of an increase during 5 and 15 minutes post-exercise in the caffeine trial (p < 0.05). QTc increased from baseline at all time points in both trials, with greater increases in the caffeine trial (p < 0.05). CONCLUSIONS: Caffeine ingestion disrupts post-exercise autonomic recovery because of increased sympathetic nerve activity. The prolonged sympathetic recovery time could subsequently hinder baroreflex function during recovery and disrupt the stability of autonomic function, potentiating a pro-arrhythmogenic state in young adults.

Integrity signals

Registry

Crossref · 10.1177/2047487314554867

Cites

41 of 41 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

12 of 38 cited sources checked · 2 supported · 0 flagged · accuracy not yet measured

  • Findingown data

    The increase in LnLF/LnHF was less in the caffeine trial than in the placebo trial at 5 and 15 minutes post-exercise.

    “Natural log transformation of low-to-high frequency ratio (LnLF/LnHF) of HRV was increased compared with baseline at all time points in both trials (p < 0.05), with less of an increase during 5 and 15 minutes post-exercise in the caffeine trial (p < 0.05).”
    • Also stated in: § Results · plain
      “LnLF/LnHF increased from baseline at all time points in both trials, with greater increases during 5 and 15 minutes post-exercise in the placebo trial (p < 0.05).”
    Quote in the paperSubstantial claim
  • Findingown data

    No arrhythmia was detected in the ECG recordings in this study.

    “In the present study, we did not detect any arrhythmia in the ECG recordings, possibly because the dosage was not high enough to produce arrhythmias, as seen in several case studies of caffeine overdose.19”
    Quote in the paperNot a substantial claim
  • Findingown data

    QTc increases were greater in the caffeine trial than in the placebo trial.

    “QTc increased from baseline at all time points in both trials, with greater increases in the caffeine trial (p < 0.05).”
    • Also stated in: § Results · plain
      “QTc increased from baseline at all time points in both trials, with greater increases in the caffeine trial (p < 0.05).”
    Quote in the paperNot a substantial claim
  • Findingown data

    Mean arterial pressure increased from baseline in the caffeine trial at all recovery time points.

    “Compared with baseline, MAP and DBP increased in the caffeine trial at all recovery time points (p < 0.05, Figure 1).”
    Quote in the paperNot a substantial claim
  • Findingown data

    QTc increased from baseline at all post-exercise time points in both trials.

    “QTc increased from baseline at all time points in both trials, with greater increases in the caffeine trial (p < 0.05).”
    • Also stated in: § Results · plain
      “QTc increased from baseline at all time points in both trials, with greater increases in the caffeine trial (p < 0.05).”
    Quote in the paperNot a substantial claim
  • Classified as probably not a substantial claim. 32
  • May combine two claims. 18
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Caffeine elevates blood pressure.

    “elevated blood pressure (BP), 14,15”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [14] 14. Sondermeijer HP, van Marle AG, Kamen P and Krum H. Acute effects of caffeine on heart rate variability. Am J Cardiol 2002; 90: 906-907. source
    • cites [15] 15. Waring WS, Goudsmit J, Marwick J, et al. Acute caffeine intake influences central more than peripheral blood pressure in young adults. Am J Hypertens 2003; 16: 919-924. source
  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Caffeine has previously been shown to prolong time to exhaustion and increase oxygen consumption during endurance exercise.

    “Caffeine has previously been shown to prolong time to exhaustion and increase oxygen consumption during endurance exercise.29,30”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [29] 29. Toner MM, Kirkendall DT, Delio DJ, et al. Metabolic and cardiovascular responses to exercise with caffeine. Ergonomics 1982; 25: 1175-1183. source

      In the Results and Conclusions (page not provided), the paper reports increased maximal oxygen consumption after caffeine. It also explicitly says exercise time to exhaustion was unchanged, so it does not support the claimed prolongation. (LLM, conf=0.91)

      Experimental — accuracy not yet measured
    • cites [30] 30. Fisher SM, McMurray RG, Berry M, et al. Influence of caffeine on exercise performance in habitual caffeine users. Int J Sports Med 1986; 7: 276-280. source
  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Prolongation of the QT interval can disrupt the electrophysiological environment, leading to ventricular instability and the risk of cardiac arrhythmias/cardiac death.

    “In addition, prolongation of the QT interval can disrupt the electrophysiolocal environment, leading to ventricular instability and the risk of cardiac arrhythmias/cardiac death.10”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [10] 10. Straus SM, Kors JA, De Bruin ML, et al. Prolonged QTc interval and risk of sudden cardiac death in a population of older adults. J Am Coll Cardiol 2006; 47: 362-367. source

      The paper’s background states that QT prolongation has been associated with ventricular arrhythmias that may trigger ventricular fibrillation and sudden cardiac death. Its Discussion also reports an increased risk of sudden cardiac death with prolonged QTc. It does not establish that QT prolongation disrupts the electrophysiological environment or causes ventricular instability; page numbers were unavailable in our copy. (LLM, conf=0.85)

      Experimental — accuracy not yet measured
  • Classified as probably not a substantial claim.

    Premisecitation

    LnLF reflects the actions of the sympathetic nervous system through baroreflex-mediated changes in heart rate.

    “LnLF is said to reflect the actions of the sympathetic nerve system through baroreflex-mediated changes in HR, 36,37”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites [36] 36. Goldstein DS, Bentho O, Park MY and Sharabi Y. Low- frequency power of heart rate variability is not a measure of cardiac sympathetic tone but may be a measure of modulation of cardiac autonomic outflows by barore- flexes. Exp Physiol 2011; 96: 1255-1261. source

      In “LF Power is Related to Baroreflex Function” (page unavailable), the paper reports that log LF power correlates with baroreflex-cardiovagal gain, supporting the baroreflex part of the claim. It also says log LF power does not correlate with cardiac sympathetic outflow and that it cannot separate baroreflex modulation of sympathetic from parasympathetic outflow. The source therefore does not support presenting LnLF specifically as a reflection of sympathetic nervous system activity. (LLM, conf=0.88)

      Experimental — accuracy not yet measured
    • cites [37] 37. Moak JP, Goldstein DS, Eldadah BA, et al. Supine low- frequency power of heart rate variability reflects barore- flex function, not cardiac sympathetic innervation. Heart Rhythm 2009; 4: 1523-1529. source

      The Discussion says LF power predominantly reflects baroreflex-mediated changes in both cardiovagal and sympathetic noradrenergic outflows. The claim captures the baroreflex-mediated sympathetic component, but presents it as though LF reflects sympathetic activity alone; the paper emphasizes that LF power is not an index of cardiac sympathetic innervation. The study's measurements were made with subjects supine. (LLM, conf=0.86)

      Experimental — accuracy not yet measured
  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    Post-exercise recovery is a critical phase for sudden cardiovascular events, predominantly in the 30 minutes immediately following vigorous exercise, attributable to increased sympathetic and decreased parasympathetic nerve activity.

    “In particular, post-exercise recovery is a critical phase for sudden cardiovascular events, predominantly in the 30 minutes immediately following vigorous exercise, 5 which is attributable to increased sympathetic and decreased parasympathetic nerve activity.6”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites [5] 5. Neves VR, Kiviniemi AM, Hautala AJ, et al. Heart Rate Dynamics after Exercise in Cardiac Patients with and with- out Type 2 Diabetes. Front Physiol 2011; 2: 57. source

      The Introduction reports increased risk of sudden cardiac death in the 30 minutes after vigorous exercise. But the Discussion’s “Post-exercise HR dynamics” section describes prolonged sympathetic activity alongside rapid restoration of vagal activity, not decreased parasympathetic activity as the explanation for recovery-phase events. It also presents the autonomic explanation as a possibility, rather than an established cause. (LLM, conf=0.88)

      Experimental — accuracy not yet measured
    • cites [6] 6. Vanoli E, De Ferrari GM, Stramba-Badiale M, et al. Vagal stimulation and prevention of sudden death in con- scious dogs with a healed myocardial infarction. Circ Res 1991; 68: 1471-1481. source

      The Electrophysiological Effects section describes vagal activity as protective against arrhythmias in the presence of elevated sympathetic activity, supporting the proposed autonomic mechanism in general. But this study concerns dogs undergoing exercise and induced myocardial ischemia; it does not establish that a sympathetic–parasympathetic imbalance causes events during post-exercise recovery. The 30-minute timing is attached to a different citation in the citing sentence. (LLM, conf=0.83)

      Experimental — accuracy not yet measured
  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Low heart rate variability predicts cardiovascular mortality with vulnerability to sudden cardiac arrest and cardiac arrhythmias after acute myocardial infarction.

    “Low HRV, attributed to depressed parasympathetic modulation, has been shown to predict cardiovascular mortality with vulnerability to sudden cardiac arrest and cardiac arrhythmias after acute myocardial infarction.5”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [5] 5. Neves VR, Kiviniemi AM, Hautala AJ, et al. Heart Rate Dynamics after Exercise in Cardiac Patients with and with- out Type 2 Diabetes. Front Physiol 2011; 2: 57. source

      The References list a study associating decreased heart rate variability with increased mortality after acute myocardial infarction. The Introduction separately discusses sudden cardiac death after vigorous exercise and the prognostic value of delayed heart-rate recovery, but does not link low HRV to sudden cardiac arrest or arrhythmias after infarction, or attribute low HRV to depressed parasympathetic modulation. No page numbers are provided in our copy. (LLM, conf=0.72)

      Experimental — accuracy not yet measured
  • Classified as probably not a substantial claim.

    Premisecitation

    The influence of caffeine on post-exercise autonomic recovery remains unclear.

    “The effects of caffeine on autonomic function have been studied at rest and during exercise; 14,35 however, the influence of caffeine on post-exercise autonomic recovery remains unclear.”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [14] 14. Sondermeijer HP, van Marle AG, Kamen P and Krum H. Acute effects of caffeine on heart rate variability. Am J Cardiol 2002; 90: 906-907. source
    • cites [35] 35. Richardson T, Rozkovec A, Thomas P, et al. Influence of caffeine on heart rate variability in patients with long- standing type 1 diabetes. Diabetes Care 2004; 27: 1127-1131. source
  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    The first minute of heart rate recovery is largely attributable to parasympathetic reactivation, whereas further HR reduction depends on the gradual decrease in sympathetic nerve activity.

    “The first minute of HR recovery is largely attributable to parasympathetic reactivation, whereas further HR reduction depends on the gradual decrease in sympathetic nerve activity.25,26”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [25] 25. Perini R, Orizio C, Comande A, et al. Plasma norepin- ephrine and heart rate dynamics during recovery from submaximal exercise in man. Eur J Appl Physiol 1989; 58: 879-883. source
    • cites [26] 26. Fisher JP. Autonomic control of the heart during exercise in humans: role of skeletal muscle afferents. Exp Physiol 2014; 99: 300-305. source

      The 'Muscle metaboreceptors and cardiac autonomic control' section (page not specified) proposes that parasympathetic activity reactivates when exercise stops and can lower heart rate despite sympathetic influence. It does not establish that this accounts for the first minute of recovery or that later heart-rate reduction depends on a gradual decline in sympathetic nerve activity. (LLM, conf=0.86)

      Experimental — accuracy not yet measured
  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    Changes in autonomic tone can directly influence the QT interval, prolongation of which disrupts the electrophysiological environment.

    “Furthermore, changes in autonomic tone can directly influence the QT interval, prolongation of which disrupts the electrophysiolocal environment.10”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [10] 10. Straus SM, Kors JA, De Bruin ML, et al. Prolonged QTc interval and risk of sudden cardiac death in a population of older adults. J Am Coll Cardiol 2006; 47: 362-367. source

      The introductory passage (page not provided) says QT prolongation has been associated with ventricular arrhythmias that may trigger sudden cardiac death, supporting a connection to electrical disturbances. It does not say that changes in autonomic tone directly influence the QT interval or establish that prolongation disrupts the electrophysiological environment. (LLM, conf=0.78)

      Experimental — accuracy not yet measured
  • Classified as probably not a substantial claim.

    Premisecitation

    Heart rate variability and heart rate recovery are non-invasive methods that provide information regarding cardiac sympathetic and parasympathetic modulations of heart rate during and after exercise.

    “Heart rate variability (HRV) and heart rate recovery (HRR) are non-invasive methods that provide information regarding the cardiac sympathetic and parasympathetic modulations of HR during and after exercise.8,9”
    Quote in the paperSubstantial claim1 of 2 sources checked
    • cites [8] 8. Nissinen SI, Makikallio TH, Seppanen T, et al. Heart rate recovery after exercise as a predictor of mortality among survivors of acute myocardial infarction. Am J Cardiol 2003; 91: 711-714. source
    • cites [9] 9. Cahalin LP, Arena R, Labate V, et al. Predictors of abnormal heart rate recovery in patients with heart fail- ure reduced and preserved ejection fraction. Eur J Prev Cardiol 2013; 21: 906-914. source

      The Introduction and Discussion (page numbers not provided) say that heart rate recovery after exercise reflects parasympathetic reactivation and sympathetic deactivation. The paper does not make the corresponding claim about heart rate variability; it appears only in the title of a cited reference. Thus the source supports the HRR portion, but not the statement about both methods. (LLM, conf=0.87)

      Experimental — accuracy not yet measured
  • May combine two claims.

    Findingown data

    The lower LnLF/LnHF ratio in the caffeine trial was caused by a reduced LnLF without a change in LnHF.

    “The lower LnLF/LnHF ratio in the caffeine trial was caused by a reduced LnLF without a change in LnHF.”
    Quote in the paperSubstantial claim
  • May combine two claims.

    Findingown data

    There were no trial differences in resting HR, HR-1, %HRR-1, %HRR-2, RERmax, and RPEmax.

    “with no trial differences found in resting HR, HR-1, %HRR-1, %HRR-2, RER max and RPE max .”
    Quote in the paperNot a substantial claim
  • May combine two claims.

    Interpretationreasoning

    An increased HR and BP and a longer QTc interval with caffeine ingestion suggest a prolonged sympathetic recovery time, which could subsequently attenuate baroreflex function recovery.

    “An increased HR and BP and a longer QTc interval with caffeine ingestion, suggesting a prolonged sympathetic recovery time, could subsequently attenuate baroreflex function recovery, which is consistent with the higher HR and BP during post-exercise recovery with caffeine.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Caffeine inhibits baroreflex function.

    “inhibited baroreflex function, 16”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [16] 16. Mosqueda-Garcia R, Tseng CJ, Biaggioni I, et al. Effects of caffeine on baroreflex activity in humans. Clin Pharmacol Ther 1990; 48: 568-574. source
  • Probably not a substantial claim: may not pass S4 (based). May combine two claims.

    Interpretationreasoning

    Prolonged sympathetic recovery time could subsequently hinder baroreflex function during recovery and disrupt the stability of autonomic function, potentiating a pro-arrhythmogenic state in young adults.

    “The prolonged sympathetic recovery time could subsequently hinder baroreflex function during recovery and disrupt the stability of autonomic function, potentiating a pro-arrhythmogenic state in young adults.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Interpretationreasoning

    The higher HRmax with caffeine may be explained by the increased work capacity caused by caffeine.

    “The higher HR max may be explained by the increased work capacity caused by caffeine.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Caffeine prolongs the QT interval.

    “prolonged QT interval, 17”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [17] 17. Shah SA, Lacey CS, Bergendahl T, et al. QTc interval prolongation with high dose energy drink consumption in a healthy volunteer. Int J Cardiol 2014; 172: e336-e337. source
  • May combine two claims.

    Interpretationcitation

    Caffeine prolonged the recovery of HR and BP following exercise, suggesting a caffeine-induced increase in sympathetic nerve activity which perturbed cardiovascular homeostasis.

    “Although caffeine enhanced work capacity in healthy adults, it prolonged the recovery of HR and BP following exercise, suggesting a caffeine-induced increase in sympathetic nerve activity, 12 which perturbed cardiovascular homeostasis.34”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [12] 12. Corti R, Binggeli C, Sudano I, et al. Coffee acutely increases sympathetic nerve activity and blood pressure independently of caffeine content: role of habitual versus nonhabitual drinking. Circulation 2002; 106: 2935-2940. source
    • cites [34] 34. Esler M. The autonomic nervous system and cardiac arrhythmias. Clin Auton Res 1992; 2: 133-135. source
  • May combine two claims.

    Interpretationreasoning

    Caffeine could disrupt the stability in autonomic function particularly following exercise termination, which could predispose young and healthy adults to a pro-arrhythmogenic state.

    “This is clinically important because caffeine could disrupt the stability in autonomic function particularly following exercise termination, which could predispose young and healthy adults to a pro-arrhythmogenic state.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    Respiration was paced with a metronome at 12 breaths per minute.

    “Respiration was paced with a metronome at 12 breath-sÁmin À1 .”
    Quote in the paperNot a substantial claim
  • Classified as probably not a substantial claim.

    Study design and conductcitation

    HRV data were collected 5 minutes post-exercise to allow for steady heart rates.

    “HRV data were collected 5 minutes post-exercise to allow for steady HRs. 25”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [25] 25. Perini R, Orizio C, Comande A, et al. Plasma norepin- ephrine and heart rate dynamics during recovery from submaximal exercise in man. Eur J Appl Physiol 1989; 58: 879-883. source
  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Complete autonomic recovery may take longer after relatively greater exercise bouts, depending on intensity, duration, and fitness, hence greater risk of sudden cardiovascular events.

    “Complete autonomic recovery may take even longer after relatively greater exercise bouts, depending on the intensity, duration, and fitness of the individual, hence greater risk of sudden cardiovascular events.7”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [7] 7. Seiler S, Haugen O and Kuffel E. Autonomic recovery after exercise in trained athletes: intensity and duration effects. Med Sci Sports Exerc 2007; 39: 1366-1373. source
  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    Delayed heart rate recovery after exercise is associated with autonomic dysfunction and increased mortality, in which parasympathetic reactivation is impaired.

    “Delayed HRR after exercise is associated with autonomic dysfunction and increased mortality, in which parasympathetic reactivation is impaired.8”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [8] 8. Nissinen SI, Makikallio TH, Seppanen T, et al. Heart rate recovery after exercise as a predictor of mortality among survivors of acute myocardial infarction. Am J Cardiol 2003; 91: 711-714. source
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductreasoning

    HRV following caffeine ingestion prior to exercise was not examined.

    “HRV following caffeine ingestion prior to exercise was not examined; the focus of the study was recovery and resting effects of caffeine ingestion have been previously described.”
    Quote in the paperNot a substantial claim
  • Classified as probably not a substantial claim.

    Study design and conductreasoning

    Female participants were tested during the first 7 days of their menstrual cycle to control for the effects of sex hormones on HRV.

    “Female participants were tested during the first 7 days of their menstrual cycle to control for the effects of sex hormones on HRV.”
    Quote in the paperSubstantial claim
  • Classified as probably not a substantial claim. May combine two claims.

    Study design and conductnone given

    ECG data were automatically peak detected and visually inspected for accuracy and the occurrence of ectopic beats.

    “The ECG data were automatically peak detected, visually inspected for accuracy and the occurrence of ectopic beats, and subsequently used to generate a tachogram of the R-R interval time event series.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Study design and conductcitation

    HRV is an indirect method of assessing autonomic function but is widely used in clinical research.

    “Finally, we used HRV to assess autonomic function, which is an indirect method; however, this method has been widely used in clinical research and is, in humans, the best method of estimating sympathetic and parasympathetic interactions.39”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [39] 39. TaskForce. Heart rate variability: standards of measure- ment, physiological interpretation and clinical use. Task Force of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. Circulation 1996; 93: 1043-1065. source
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductnone given

    The study was approved by the institutional review board at the University of Illinois at Chicago.

    “The study was approved by the institutional review board at the University of Illinois at Chicago.”
    Quote in the paperNot a substantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductown data

    The authors did not measure sympathetic nerve activity.

    “We did not measure sympathetic nerve activity, and although its increase is speculative in the present study, caffeine has previously been shown to increase sympathetic nerve activity.12”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [12] 12. Corti R, Binggeli C, Sudano I, et al. Coffee acutely increases sympathetic nerve activity and blood pressure independently of caffeine content: role of habitual versus nonhabitual drinking. Circulation 2002; 106: 2935-2940. source
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Caffeine consumption transiently increases the risk of acute cardiovascular events.

    “Caffeine consumption also transiently increases the risk of acute cardiovascular events, 18”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [18] 18. Baylin A, Hernandez-Diaz S, Kabagambe EK, et al. Transient exposure to coffee as a trigger of a first non- fatal myocardial infarction. Epidemiology 2006; 17: 506-511. source
  • Classified as probably not a substantial claim.

    Study design and conductnone given

    Participants abstained from caffeinated and alcoholic beverages, food, and strenuous exercise for at least 12 hours before each testing session.

    “All participants abstained from caffeinated and alcoholic beverages, food, and strenuous exercise for at least 12 hours before each testing session, separated by at least 48 hours.”
    Quote in the paperSubstantial claim
  • Classified as probably not a substantial claim. May combine two claims.

    Study design and conductown data

    The study was a randomized, double-blind, crossover trial.

    “Eighteen young and healthy volunteers (10 males and 8 females; age 26 Æ 1 years; BMI 23.9 Æ 0.8 kgÁm À2 ; waist circumference 78.4 Æ 2.1 cm) participated in this randomized, double-blind, crossover study.”
    Quote in the paperSubstantial claim
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    A higher dosage of caffeine is associated with sudden cardiac death.

    “given that a higher dosage is associated with sudden cardiac death.38”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [38] 38. Lown B. Sudden cardiac death: the major challenge con- fronting contemporary cardiology. Am J Cardiol 1979; 43: 313-328. source
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    The caffeine-induced elevated blood pressure has been suggested to be partly mediated by increased peripheral resistance.

    “The caffeine-induced elevated BP has been suggested to be partly mediated by increased peripheral resistance, 32”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [32] 32. Sung BH, Lovallo WR, Pincomb GA and Wilson MF. Effects of caffeine on blood pressure response during exercise in normotensive healthy young men. Am J Cardiol 1990; 65: 909-913. source
  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    During exercise recovery, heart rate decreases in a mono-exponential manner, dependent on exercise intensity.

    “During exercise recovery, HR decreases in a mono-exponential manner, dependent on exercise intensity.25”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [25] 25. Perini R, Orizio C, Comande A, et al. Plasma norepin- ephrine and heart rate dynamics during recovery from submaximal exercise in man. Eur J Appl Physiol 1989; 58: 879-883. source
  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductown data

    The authors did not directly measure catecholamine or caffeine concentrations in the blood.

    “We did not directly measure catecholamine or caffeine concentrations in the blood, but these effects have been shown in a previous study.32”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [32] 32. Sung BH, Lovallo WR, Pincomb GA and Wilson MF. Effects of caffeine on blood pressure response during exercise in normotensive healthy young men. Am J Cardiol 1990; 65: 909-913. source
  • Classified as probably not a substantial claim.

    Study design and conductreasoning

    All testing sessions were conducted at the same time of day to reduce diurnal variations.

    “All testing sessions were conducted at the same time of day (between 07:00 and 10:00 h) to reduce diurnal variations.”
    Quote in the paperSubstantial claim
37 of 37
  • The authors state this as an assumption.

    No previous study has examined the prolonged effects of caffeine on autonomic recovery following acute dynamic exercise.

    “To the best of our knowledge, this is the first study to examine the prolonged effects of caffeine on autonomic recovery following acute dynamic exercise.”
  • The authors state this as an assumption.

    The observed autonomic and hemodynamic effects of caffeine in this study are due to increased sympathetic nerve activity.

    “We did not measure sympathetic nerve activity, and although its increase is speculative in the present study, caffeine has previously been shown to increase sympathetic nerve activity.12”
2 of 2

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Caffeine alone interferes with post-exercise autonomic recovery via increased sympathetic activity.

    “Caffeine alone has also been shown to interfere with post-exercise autonomic recovery via increased sympathetic activity [ 25 ]”

    From Acute effects of commercial energy drink consumption on exercise performance and cardiovascular safety: a randomized, double-blind, placebo-controlled, crossover trial (2024) · cites this paper as [25]

    The Abstract reports disrupted post-exercise autonomic recovery with caffeine and attributes it to increased sympathetic nerve activity. The Limitations section qualifies that mechanism: sympathetic nerve activity was not measured, and its increase in this study is speculative. Thus the recovery effect is supported, but the claim presents the proposed mechanism as demonstrated. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • Earlier research suggests a decrease in heart rate variability linked to caffeine dose.

    “The findings suggest a decrease in HRV linked to dose [ 19 ], time [ 20 , 21 ], and form of ingestion (such as drinks, gum, and capsules) [ 11 , 21 , 22 ].”

    From Impact of Caffeine Intake Strategies on Heart Rate Variability during Post-Exercise Recovery: A Systematic Review and Meta-Analysis (2024) · cites this paper as [19]

    The Experimental design section reports a single 400 mg caffeine dose versus placebo, and the post-exercise recovery discussion reports a lower increase in an HRV measure with caffeine. The paper therefore supports an effect of caffeine on HRV after exercise, but it does not compare caffeine doses or establish a dose-linked decrease. Page numbers are unavailable in our copy. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • Based on the studies by Gonzaga et al. and Bunsawat et al., the impact of CAF on post-exercise recovery after treadmill endurance exercises is particularly pronounced.

    “Based on the studies by Gonzaga et al. [ 18 ] and Bunsawat et al. [ 19 ], the impact of CAF on post-exercise recovery after treadmill endurance exercises is particularly pronounced.”

    From Impact of Caffeine Intake Strategies on Heart Rate Variability during Post-Exercise Recovery: A Systematic Review and Meta-Analysis (2024) · cites this paper as [19]

    The Experimental design describes a maximal treadmill test, and the Results report higher heart rate and greater QTc increases during recovery with caffeine. This supports an effect on post-exercise recovery, but the paper does not compare exercise types or establish that the effect is particularly pronounced after treadmill endurance exercise. (LLM, conf=0.82)

    Experimental — accuracy not yet measured
  • The safety of CAF intake, as evaluated through HRV parameters, may be significantly affected when intake is less than 60 minutes prior to exercise.

    “The safety of CAF intake, as evaluated through HRV parameters, may be significantly affected when intake is less than 60 minutes prior to exercise.”

    From Impact of Caffeine Intake Strategies on Heart Rate Variability during Post-Exercise Recovery: A Systematic Review and Meta-Analysis (2024) · cites this paper as [19]

    The Experimental design section reports caffeine ingestion 45 minutes before exercise, and the post-exercise recovery section reports a significant difference in HRV measures between caffeine and placebo. The Conclusions say caffeine could disrupt autonomic stability after exercise, but the study tested only the 45-minute interval in young, healthy volunteers; it does not establish an effect for intake at any time less than 60 minutes before exercise or directly measure safety. (LLM, conf=0.85)

    Experimental — accuracy not yet measured
  • Higher doses may impose a greater cardiometabolic burden, indicated by acute elevations in blood pressure, impaired flow-mediated dilation, and delayed post-exercise autonomic recovery.

    “Moreover, acute elevations in blood pressure, impaired flow-mediated dilation, and delayed post-exercise autonomic recovery indicate that higher doses may impose a greater cardiometabolic burden [62].”

    From Pre-Exercise Caffeine as a Modulator of Exercise-Induced Acute Cardiometabolic Responses: A Narrative Review (2026) · cites this paper as [62]

    The Abstract and the section on post-exercise hemodynamics report elevated blood pressure and prolonged heart-rate and autonomic recovery after 400 mg of caffeine versus placebo. The paper does not report flow-mediated dilation or compare caffeine doses, so it does not establish that higher doses produce a greater burden across all three indicators. (LLM, conf=0.90)

    Experimental — accuracy not yet measured

Cites

Flagged first, then by citations

Research works printed but not linked: 2

  1. Bazett HC, 1920, Heart, 7, 353
  2. Ivy JL, 1979, Med Sci Sports Exerc, 11, 6

Cited by

Sorted by citations

Authors
Bunsawat, K., White, D. W., Kappus, R. M., & Baynard, T.
Affiliations
University of Illinois Chicago (US)
Corresponding author
Bunsawat, Kanokwan
Venue
European Journal of Preventive Cardiology
Published
2014-10-08
Volume
22
Issue
11
Pages
1473-1479
ISSN
  • 2047-4873 (ISSN-L)
  • 2047-4881
OpenAlex
W2130872823
Cited by
61
References
40
Citations by year
2026: 1 · 2025: 4 · 2024: 7 · 2023: 2 · 2022: 8 · 2021: 7 · 2020: 4 · 2019: 6 · 2018: 8 · 2017: 8 · 2016: 4 · 2015: 2
FWCI
3.39
Type
journal article
Language
en
Open access
closed
Locations
  • European Journal of Preventive Cardiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Pharmacology › Coffee research and impacts
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
  • Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
Keywords
caffeine, autonomic recovery, post-exercise recovery, heart rate variability, QTc interval, sympathetic activity, baroreflex, sudden cardiac death risk, catecholamines, exercise-induced arrhythmia, blood pressure
MeSH terms
Adult, Autonomic Nervous System, Caffeine, Chicago, Double-Blind Method, Female, Heart, Heart Rate, Humans, Male, Time Factors, Exercise, Baroreflex, Cross-Over Studies, Recovery of Function, Arterial Pressure, Healthy Volunteers

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-10-11.

Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-11.

Cited sources are checked by gpt-6-sol.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

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