Exposures to Elevated Core Temperatures during Football Training: The Impact on Autonomic Nervous System Recovery and Function.

Exercising with elevated core temperatures may negatively affect autonomic nervous system (ANS) function. Additionally, longer training duration under higher core temperatures may augment these negative effects. This study evaluated the relationship between exercise training duration and 24 h ANS recovery and function at ≥37 °C, ≥38 °C and ≥39 °C core temperature thresholds in a sample of male Division I (D1) collegiate American football athletes. Fifty athletes were followed over their 25-week season. Using armband monitors (Warfighter MonitorTM, Tiger Tech Solutions, Inc., Miami, FL, USA), core temperature (°C) and 24 h post-exercise baseline heart rate (HR), HR recovery and heart rate variability (HRV) were measured. For HRV, two time-domain indices were measured: the root mean square of the standard deviation of the NN interval (rMSSD) and the standard deviation of the NN interval (SDNN). Linear regression models were performed to evaluate the associations between exercise training duration and ANS recovery (baseline HR and HRV) and function (HR recovery) at ≥37 °C, ≥38 °C and ≥39 °C core temperature thresholds. On average, the athletes were 21.3 (± 1.4) years old, weighed 103.0 (±20.2) kg and had a body fat percentage of 15.4% (±7.8%, 3.0% to 36.0%). The duration of training sessions was, on average, 161.1 (±40.6) min and they ranged from 90.1 to 339.6 min. Statistically significant associations between training duration and 24 h ANS recovery and function were observed at both the ≥38.0 °C (baseline HR: ß = 0.10 ± 0.02, R2 = 0.26, p < 0.0000; HR recovery: ß = -0.06 ± 0.02, R2 = 0.21, p = 0.0002; rMSSD: ß = -0.11 ± 0.02, R2 = 0.24, p < 0.0000; and SDNN: ß = -0.16 ± 0.04, R2 = 0.22, p < 0.0000) and ≥39.0 °C thresholds (ß = 0.39 ± 0.05, R2 = 0.62, p < 0.0000; HR recovery: ß = -0.26 ± 0.04, R2 = 0.52, p < 0.0000; rMSSD: ß = -0.37 ± 0.05, R2 = 0.58, p < 0.0000; and SDNN: ß = -0.67 ± 0.09, R2 = 0.59, p < 0.0000). With increasing core temperatures, increases in slope steepness and strengths of the associations were observed, indicating accelerated ANS deterioration. These findings demonstrate that exercise training under elevated core temperatures (≥38 °C) may negatively influence ANS recovery and function 24 h post exercise and progressively worsen.

Internal or External Training Load Metrics: Which Is Best for Tracking Autonomic Nervous System Recovery and Function in Collegiate American Football?

Sport coaches increasingly rely on external load metrics for designing effective training programs. However, their accuracy in estimating internal load is inconsistent, and their ability to predict autonomic nervous system (ANS) deterioration is unknown. This study aimed to evaluate the relationships between internal and external training load metrics and ANS recovery and function in college football players. Football athletes were recruited from a D1 college in the southeastern US and prospectively followed for 27 weeks. Internal load was estimated via exercise cardiac load (ECL; average training heartrate (HR) × session duration) and measured with an armband monitor equipped with electrocardiographic capabilities (Warfighter MonitorTM (WFM), Tiger Tech Solutions, Miami, FL, USA). External load was estimated via the summation and rate of acceleration and decelerations as measured by a triaxial accelerometer using the WFM and an accelerometer-based (ACCEL) device (Catapult Player Load, Catapult Sports, Melbourne, Australia) worn on the mid-upper back. Baseline HR, HR variability (HRV) and HR recovery served as the indicators for ANS recovery and function, respectively. For HRV, two, time-domain metrics were measured: the standard deviation of the NN interval (SDNN) and root mean square of the standard deviation of the NN interval (rMSSD). Linear regression models evaluated the associations between ECL, ACCEL, and the indicators of ANS recovery and function acutely (24 h) and cumulatively (one- and two-week). Athletes (n = 71) were male and, on average, 21.3 ± 1.4 years of age. Acute ECL elicited stronger associations for 24 h baseline HR (R2 0.19 vs. 0.03), HR recovery (R2 0.38 vs. 0.07), SDNN (R2 0.19 vs. 0.02) and rMSSD (R2 0.19 vs. 0.02) compared to ACCEL. Similar results were found for one-week: 24 h baseline HR (R2 0.48 vs. 0.05), HR recovery (R2 0.55 vs. 0.05), SDNN (R2 0.47 vs. 0.05) and rMSSD (R2 0.47 vs. 0.05) and two-week cumulative exposures: 24 h baseline HR (R2 0.52 vs. 0.003), HR recovery (R2 0.57 vs. 0.05), SDNN (R2 0.52 vs. 0.003) and rMSSD (R2 0.52 vs. 0.002). Lastly, the ACCEL devices weakly correlated with ECL (rho = 0.47 and 0.43, p < 0.005). Our findings demonstrate that ACCEL poorly predicted ANS deterioration and underestimated internal training load. ACCEL devices may "miss" the finite window for preventing ANS deterioration by potentially misestimating training loads acutely and cumulatively.