Contribution of the Autonomic Nervous System to Recovery in Firefighters

Participants

A total of 37 male career active-duty firefighters (age = 39 ± 9 years, height = 178.8 ± 5.4 cm, mass = 87.9 ± 11.2 kg, body mass index = 27.7 ± 3.9 kg/m²) from the same department volunteered for this study. Participants were cleared for full active-duty service; free of cardiopulmonary, metabolic, renal, and musculoskeletal conditions; and not taking medications that could influence HR. All participants gave written informed consent, and the study was approved by the Institutional Review Board of the University of Wisconsin–Milwaukee.

Procedures

All participants completed 2 testing sessions. The submaximal test was completed at a fire station, and the maximal test was completed in the Human Performance and Sport Physiology Laboratory at the University of Wisconsin–Milwaukee. Testing sessions were separated by at least 24 hours but no longer than 96 hours. Participants wore exercise clothing during both testing sessions. To ensure consistency, all data were collected by the same researcher (R.J.F.).

Heart-Rate Recovery Measures

The HR (in bpm) and R-R interval (in milliseconds) data were collected using the Polar V800 watch and H7 monitor (250-Hz sampling rate; Polar Electro, Kempele, Finland), which has demonstrated acceptable criterion validity in reference to electrocardiography when collecting HR and R-R interval data during resting and activity states.^21,22 Data were transferred from the watch to a desktop computer via software (Polar Electro) for subsequent analysis.

Percentage Maximal HR Data

Resting HR (HR_Rest) was averaged during a 5-minute pretest period. The HR immediately after cessation of exercise was identified (HR₀), and all remaining HRR measures were averaged as 30-second epochs (eg, HR₃₀, HR₆₀, and HR₉₀) for a total of 21 HRR measures during the 10-minute recovery period. The HR data were normalized to each participant's age-predicted HR maximum and expressed as a percentage of maximal HR (%MHR).

To describe the HRR profiles of each participant, we fitted the 21 HRR measures within both the submaximal and maximal protocols of each participant to a monoexponential curve¹³ (Figure 1) using the nlinfit function in MATLAB (version R2018a; The MathWorks, Inc, Natick, MA): \(\def\upalpha{\unicode[Times]{x3B1}}\)\(\def\upbeta{\unicode[Times]{x3B2}}\)\(\def\upgamma{\unicode[Times]{x3B3}}\)\(\def\updelta{\unicode[Times]{x3B4}}\)\(\def\upvarepsilon{\unicode[Times]{x3B5}}\)\(\def\upzeta{\unicode[Times]{x3B6}}\)\(\def\upeta{\unicode[Times]{x3B7}}\)\(\def\uptheta{\unicode[Times]{x3B8}}\)\(\def\upiota{\unicode[Times]{x3B9}}\)\(\def\upkappa{\unicode[Times]{x3BA}}\)\(\def\uplambda{\unicode[Times]{x3BB}}\)\(\def\upmu{\unicode[Times]{x3BC}}\)\(\def\upnu{\unicode[Times]{x3BD}}\)\(\def\upxi{\unicode[Times]{x3BE}}\)\(\def\upomicron{\unicode[Times]{x3BF}}\)\(\def\uppi{\unicode[Times]{x3C0}}\)\(\def\uprho{\unicode[Times]{x3C1}}\)\(\def\upsigma{\unicode[Times]{x3C3}}\)\(\def\uptau{\unicode[Times]{x3C4}}\)\(\def\upupsilon{\unicode[Times]{x3C5}}\)\(\def\upphi{\unicode[Times]{x3C6}}\)\(\def\upchi{\unicode[Times]{x3C7}}\)\(\def\uppsy{\unicode[Times]{x3C8}}\)\(\def\upomega{\unicode[Times]{x3C9}}\)\(\def\bialpha{\boldsymbol{\alpha}}\)\(\def\bibeta{\boldsymbol{\beta}}\)\(\def\bigamma{\boldsymbol{\gamma}}\)\(\def\bidelta{\boldsymbol{\delta}}\)\(\def\bivarepsilon{\boldsymbol{\varepsilon}}\)\(\def\bizeta{\boldsymbol{\zeta}}\)\(\def\bieta{\boldsymbol{\eta}}\)\(\def\bitheta{\boldsymbol{\theta}}\)\(\def\biiota{\boldsymbol{\iota}}\)\(\def\bikappa{\boldsymbol{\kappa}}\)\(\def\bilambda{\boldsymbol{\lambda}}\)\(\def\bimu{\boldsymbol{\mu}}\)\(\def\binu{\boldsymbol{\nu}}\)\(\def\bixi{\boldsymbol{\xi}}\)\(\def\biomicron{\boldsymbol{\micron}}\)\(\def\bipi{\boldsymbol{\pi}}\)\(\def\birho{\boldsymbol{\rho}}\)\(\def\bisigma{\boldsymbol{\sigma}}\)\(\def\bitau{\boldsymbol{\tau}}\)\(\def\biupsilon{\boldsymbol{\upsilon}}\)\(\def\biphi{\boldsymbol{\phi}}\)\(\def\bichi{\boldsymbol{\chi}}\)\(\def\bipsy{\boldsymbol{\psy}}\)\(\def\biomega{\boldsymbol{\omega}}\)\(\def\bupalpha{\bf{\alpha}}\)\(\def\bupbeta{\bf{\beta}}\)\(\def\bupgamma{\bf{\gamma}}\)\(\def\bupdelta{\bf{\delta}}\)\(\def\bupvarepsilon{\bf{\varepsilon}}\)\(\def\bupzeta{\bf{\zeta}}\)\(\def\bupeta{\bf{\eta}}\)\(\def\buptheta{\bf{\theta}}\)\(\def\bupiota{\bf{\iota}}\)\(\def\bupkappa{\bf{\kappa}}\)\(\def\buplambda{\bf{\lambda}}\)\(\def\bupmu{\bf{\mu}}\)\(\def\bupnu{\bf{\nu}}\)\(\def\bupxi{\bf{\xi}}\)\(\def\bupomicron{\bf{\micron}}\)\(\def\buppi{\bf{\pi}}\)\(\def\buprho{\bf{\rho}}\)\(\def\bupsigma{\bf{\sigma}}\)\(\def\buptau{\bf{\tau}}\)\(\def\bupupsilon{\bf{\upsilon}}\)\(\def\bupphi{\bf{\phi}}\)\(\def\bupchi{\bf{\chi}}\)\(\def\buppsy{\bf{\psy}}\)\(\def\bupomega{\bf{\omega}}\)\(\def\bGamma{\bf{\Gamma}}\)\(\def\bDelta{\bf{\Delta}}\)\(\def\bTheta{\bf{\Theta}}\)\(\def\bLambda{\bf{\Lambda}}\)\(\def\bXi{\bf{\Xi}}\)\(\def\bPi{\bf{\Pi}}\)\(\def\bSigma{\bf{\Sigma}}\)\(\def\bPhi{\bf{\Phi}}\)\(\def\bPsi{\bf{\Psi}}\)\(\def\bOmega{\bf{\Omega}}\)\begin{equation}{\it HR} = {\it HR}_\infty + {\it HR}_{amp}\left( {{e^{{{ - t} \over {HR{R_\tau }}}}}} \right){\rm {,}}\end{equation}where HR_∞ is the asymptotic value of HR, HR_amp is the difference between HR₀ and HR_∞, t is time (in seconds), and HRR_τ is the decay constant.

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Statistical Analysis

To descriptively examine the ability of HR to recover after submaximal and maximal protocols, we calculated the mean %MHR and 95% confidence intervals (CIs) at each HRR measure and subsequently compared them with the mean percentage of maximal heart rate [%MHR_Rest]. Any 95% CIs for the mean %MHR data that did not overlap with the mean %MHR_Rest 95% CIs were considered different and meaningfully different from rest.

Parametric repeated-measures analyses of covariance were used to identify differences among the mean HR_∞, HR_amp, and HRR_τ parameters associated with each protocol (submaximal and maximal). Given the potential influence of obesity on vagal tone,²⁶ body mass index was used as a covariate in the model. We calculated partial η² (η²_p) effect sizes to determine the effect of the exercise protocol on these HRR parameters.

To descriptively examine the ability of HRV to recover after submaximal and maximal protocols, we computed the mean lnRMSSD and 95% CIs at each HRR measure and subsequently compared them with the mean lnRMSSD_Rest data. Any 95% CIs of the mean lnRMSSD data that did not overlap with the mean lnRMSSD_Rest 95% CIs were considered different and, thus, meaningfully different from rest.

Finally, given that La⁻ data demonstrated a nonnormal distribution (W = 0.901, P < .001), 2 Friedman tests and a post hoc follow-up Wilcoxon signed rank test were used to examine differences in La⁻ concentration at La⁻₀ and La⁻₆₀₀ compared with La⁻_Rest in the submaximal and maximal protocols.

All statistical analyses were performed using SPSS (version 25; IBM Corp, Armonk, NY). The α level was set at .05 for all parametric repeated-measures analyses of covariance and all nonparametric Friedman and Wilcoxon signed rank tests. We interpreted η²_p effect sizes using the following criteria: η²_p < 0.06 (small), 0.06 ≤ η²_p < 0.14 (medium), or η²_p ≥ 0.14 (large).²⁷

Heart-Rate Recovery and Heart-Rate Variability After Submaximal Exercise

The HR₀ during the submaximal protocol (140.0 ± 14.5 bpm) was consistent with that reported by researchers in previous studies of submaximal exercise in a similar population.^8,16,28,29 The submaximal HRR profiles demonstrated a rapid initial decrease in HR, followed by no change in %MHR after approximately 150 seconds (Figure 2A). After 10 minutes of recovery, the %MHR₆₀₀ was still greater than %MHR at rest by 23%. The HRV results indicated that lnRMSSD decreased from lnRMSSD₃₀ to lnRMSSD₆₀ but then increased from lnRMSSD₉₀ to lnRMSSD₁₈₀ such that it was not different than lnRMSSD_Rest (Figure 3A). However, lnRMSSD once again decreased from lnRMSSD₂₁₀ through lnRMSSD₆₀₀, with each time point being different than lnRMSSD_Rest. Collectively, these findings indicate that recovery from the submaximal test was initially a product of PSNS reactivation, but after 210 seconds, the incomplete recovery was likely due to the lack of complete SNS withdrawal.^9,12

Researchers^12,16 have reported fast and slow phases of HRR. The initial decline in HR was a function of PSNS reactivation and the later and slower changes in HR were a function of SNS withdrawal. In addition, elevated La⁻ during recovery has been suggested to prompt an extended slow phase.^9,12,28 The La⁻₀ response in this study (5.6 ± 1.9 mmol/L) differed from that of Gladwell et al⁸ (2.9 ± 0.5 mmol/L), perhaps because of differences in exercise (step test versus supine cycle ergometer) or duration (3 versus 20 minutes) or both. Nonetheless, our step test resulted in moderately elevated La⁻ levels that were greater at La⁻₆₀₀ (4.3 ± 2.3 mmol/L) than at La⁻_Rest (2.1 ± 1.3 mmol/L), reflecting that complete SNS withdrawal may not have been possible, as supported by the lnRMSSD results, and, thus, explaining why HR_∞ was greater than %MHR_Rest after 10 minutes of recovery.

The pattern of lnRMSSD during recovery may also provide insight into the ANS imbalance at the end of recovery. Researchers^12,30 have postulated that HRR and HRV represent independent aspects of the PSNS contribution to recovery: HRR represents vagal (ie, PSNS) tone and HRV represents vagal (ie, PSNS) modulation. Specifically, the initial decrease in HR is a product of vagal tone, but the lack of change in lnRMSSD is a function of vagal modulation.^16,29 In our study, the decrease in HR and initial increase in lnRMSSD after the submaximal test demonstrated the onset of vagal tone, but the subsequent decrease in lnRMSSD showed that vagal modulation was unable to overcome the lack of SNS withdrawal, leading to incomplete ANS recovery, as exhibited by suppressed lnRMSSD and elevated HR_∞.

Heart-Rate Recovery and Heart-Rate Variability After Maximal Exercise

In this study, the immediate HR after maximal exercise (181.5 ± 10.8 bpm) was consistent with previous reports^16,20,24 of maximal exercise in a similar population. Although the HRR after maximal exercise displayed a greater overall change in HR than that with submaximal exercise, the elevated HR_∞ indicated that the HR from 180 seconds to the end of the 10-minute recovery was at a higher level than the submaximal response (101.6 ± 12.0 bpm versus 77.8 ± 12.4 bpm; Table 1). Furthermore, unlike after submaximal exercise (Figure 3A), the posttest HRV (lnRMSSD₀) after maximal exercise remained suppressed and different from lnRMSSD_Rest through the entire recovery period (Figure 3B). It is possible that our findings indicated a lack of PSNS reactivation, perhaps associated with elevated La⁻ levels.

As observed in the submaximal recovery results, the reduction in HR in the presence of depressed HRV may signify that HRR and HRV represent independent measures of cardiac ANS function.^12,16 As such, after maximal-intensity exercise, vagal tone recovery (ie, HRR) occurs without vagal modulation recovery (ie, HRV) and could explain the impaired HRV throughout the 10 minutes of recovery seen in this study and others^12,16,24 despite the reduction in HR. It is possible that, after exercise, the removal of central nervous system command reduces the SNS stimulation to the heart, which is no longer needed because the task has ended. Therefore, the re-established vagal tone (HRR) reduces HR without vagal modulation (HRV) and SNS withdrawal, suppressing lnRMSSD during the entire recovery period.

Suppressed vagal reactivation has been previously associated with an increase in metabolite accumulation, such as La⁻.^8,12,28 In our investigation, La⁻₀ (13.3 ± 2.3 mmol/L) and La⁻₆₀₀ (11.7 ± 2.3 mmol/L) were both greater than La⁻_Rest (2.0 ± 1.2 mmol/L), and La⁻₀ was similar to that after fire-suppression tasks (13.0 ± 3.0 mmol/L).³¹ The elevated La⁻ may support a greater SNS influence on regulation of HR during recovery and interfere with a full transition to PSNS regulation of HR,¹² with a particularly strong influence on the slow phase of HRR.^9,23 The suppressed lnRMSSD during recovery that we identified suggests that the PSNS may not have reactivated during the 10-minute window. Furthermore, the HRR profiles revealed differences in the HR_∞ for submaximal (77.8 ± 12.4 bpm) and maximal (101.6 ± 12.0 bpm) exercise. Freeman et al⁶ proposed that an absence of PSNS tone, without the influence of a pathologic condition, results in an HR_Rest between 100 and 110 bpm. Therefore, the collective interpretation of the decreased HR that is still >100 bpm in the presence of suppressed lnRMSSD and elevated La⁻ implies that the influence of the SNS is greater than the ability of the PSNS to re-engage in HR modulation.

Practical Applications for Athletic Trainers

As more athletic trainers are employed in the fire service and working with occupational athletes,³² their expertise will increasingly be needed to help refine postfire-recovery protocols both at the scene and after return to the firehouse. The current National Fire Protection Association³³ recommendations for recovery at an incident scene indicate that a minimum of 10 minutes of recovery, if practical, should be provided after exiting a fire for the first time and a minimum of 20 minutes should be provided after a second self-contained breathing apparatus cylinder is used. Based on the current results, regardless of exercise intensity, 10 minutes of seated recovery may not be adequate to reduce the long-term ANS risk factors for later cardiac injury. It is unclear how the ANS would respond to a repeated submaximal or maximal test, and future researchers should determine if repeated exposure to fire-suppression activities has a compound effect on ANS recovery. This information will help investigators develop best practices for facilitating ANS recovery and reduce ANS factors linked to a cardiac event after a fire call.

Related to recovery protocol development is the information used to make decisions about recovery status. Although current practices (eg, vital signs) in emergency scene management remain relevant, technological advancements allow for immediate access to information such as HRR and HRV. Our results demonstrated that, although measuring HRR is noninvasive, this information does not represent the complete story of recovery, and therefore, mismanagement of recovery may occur. For example, our maximal-exercise test showed that all participants recovered approximately 33.8 bpm during the first minute, which was within the suggested HRR values after maximal exercise.⁷ However, the HRV results indicated the participants were not fully recovered from an ANS perspective. This could be a concern during actual fire-service calls in which a firefighter performs multiple bouts of fire suppression while at a location and, thus, may further exacerbate an already impaired PSNS modulation. This may not have an immediate effect, but it could become an important component of the SCD incidences that occur after a firefighter returns from a fire service call and has an ANS profile that does not favor PSNS regulation at rest. Future authors should identify methods that allow athletic trainers access to such information as part of managing recovery in firefighters and explore the need for implementing recovery protocols after return to the firehouse.

Finally, our results provide insight to support the development of recovery strategies to mitigate the risk for cardiac injury after a call. The current data are consistent with the existing literature, indicating that the greater the intensity, the greater the impairment of PSNS reactivation.²⁹ From a practical perspective, the firefighter's recovery may be specific to the type of service call. Kaikkonen et al³⁴ reported that HRV was lower after fire and rescue calls than after medical calls, which implies that firefighters may be under more SNS influences after fire calls. By acknowledging that different service calls result in different responses, recovery protocols can be adapted to match the type of call.

Limitations

The design constraints of the study did not allow us to include a control group; therefore, the results are relevant only to the firefighter population. Also, our tools did not permit examination of respiration rate and direct assessment of the SNS. However, the tools represent methods likely to be used in the field by athletic trainers or other health care professionals. The 10-minute seated recovery period was chosen to be comparable with previous studies and is consistent with the minimum recommendations of the National Fire Protection Association. It is possible that ANS recovery would have been observed during a longer recovery period. We used a controlled laboratory approach to maximize the opportunity to understand how HRR and HRV might respond in this population. Nonetheless, researchers should examine these measures in response to actual fire-suppression activity. Lastly, all participants were male career structural firefighters, and their responses may not represent the responses of female, volunteer, or wildland firefighters.