CrossFit™, a popular high-intensity training modality, has been the subject of scrutiny, with concerns of elevated risk of injury and health. Despite these concerns empirical evidence regarding physiologic stresses including acute oxidative stress is lacking. Therefore, the purpose of this investigation was to examine the acute redox response to a CrossFit™ bout. Furthermore, these findings were compared to a high-intensity treadmill bout as a point of reference. Ten males 26.4 ± 2.7 yrs having three or more months of CrossFit™ experience participated in the present study. Blood plasma was collected at four time points: Pre-exercise (PRE), immediately-post-exercise (IPE), 1 hr-post (1-HP) and 2 hr-post (2-HP), to examine oxidative damage and antioxidant capacity. Regarding plasma oxidative damage, CrossFit™ and Treadmill elicited a time-dependent increase of lipid peroxides 1-HP (CrossFit™=+143%,Treadmill=+115%) and 2-HP (CrossFit™=+256%,Treadmill+167%). Protein Carbonyls were increased IPE in CF only (+5%), while a time-dependent decrease occurred 1-HP (CrossFit™=−16%,Treadmill=−8%) and 2-HP (CF=−16%,TM=−1%) compared to IPE. Regarding antioxidant capacity, Ferric Reducing Antioxidant Power also demonstrated a time-dependent increase within CrossFit™ and Treadmill: IPE (CrossFit™=+25%,Treadmill=+17%), 1-HP (CrossFit™=+26%,Treadmill=+4.8%), 2-HP (CrossFit™=+20%,Treadmill=+12%). Total Enzymatic Antioxidant Capacity showed a time-dependent decrease in IPE (CrossFit™= −10%,Treadmill=−12%), 1-HP (CrossFit™= −12%,Treadmill=−6%), 2-HP (CrossFit™= −7%,Treadmill=−11%). No trial-dependent differences were observed in any biomarker of oxidative stress. The CrossFit™ bout elicited an acute blood oxidative stress response comparable to a traditional bout of high-intensity treadmill running. Results also confirm that exercise intensity and the time course of exercise recovery influence oxidative responses.

The aim of this study was to compare postexercise autonomic nervous system (ANS) recovery between a high-intensity training protocol (HITP) and high-intensity treadmill running (TM) in 10 physically fit males. For each trial, ANS activity was measured through the heart rate variability markers of log-transformed square root of the successive R-R differences (lnRMSSD) and high frequency power (lnHF). These markers were analyzed in 5-minute segments at 5-10 minutes of the pre-exercise period (PRE) and during the postexercise period at 15-20 minutes (POST15-20min), 20-25 minutes (POST20-25min), 25-30 minutes (POST25-30min), and 1 hour (POST60min). Plasma epinephrine (E) and norepinephrine (NE) were also examined at PRE, immediately post exercise (IPE), 1-hour post (1HP), and 2-hour post (2HP). The results of this study demonstrate a significant overall time-dependent decreases in lnRMSSD and lnHF (p = 0.003 and 0.001, respectively) in both trials. Trial-dependent differences were also observed in postexercise lnRMSSD and lnHF measures, HITP being significantly lower than TM (p = 0.002 and 0.000, respectively). lnRMSSD at POST60min-HITP remained significantly lower compared to PRE (p ≤ 0.05). lnHF returned to baseline in HIPT and TM (p = 0.081 and 0.065, respectively). A time-dependent increase in E and NE was observed in both trials at time point IPE when compared to PRE (p ≤ 0.05). E at 1HP and 2HP returned to near resting levels (p = 0.62, p = 0.26), whereas NE remained slightly elevated in both groups (p = 0.003, p = 0.021). A trial-dependent increase was observed with the HITP eliciting a greater E response (p = 0.025) and NE response (p = 0.03). The HITP causes a greater disruption of the ANS than intensity-matched TM exercise.

Exercise is a potent stimulus against cardiac ischemia reperfusion (IR) injury, although the protective mechanisms are not completely understood. The study purpose was to examine whether the mitochondrial or sarcolemmal ATP-sensitive potassium channel (mito K_ATPor sarc K_ATP, respectively) mediates exercise-induced cardioprotection against post-IR cell death and apoptosis. Eighty-six, 4-mo-old male Sprague Dawley rats were randomly assigned to treadmill exercise (Ex; 30 m/min, 3 days, 60 min, ∼70 maximal oxygen uptake) and sedentary (Sed) treatments. Rats were exposed to regional cardiac ischemia (50 min) and reperfusion (120 min) or Sham (170 min; no ligation) surgeries. Exercise subgroups received placebo (saline), 5-hydroxydecanoate (5HD; 10 mg/kg ip), or HMR1098 (10 mg/kg ip) to inhibit mito K_ATPor sarc K_ATPchannel. Comprehensive outcome assessments included post-IR ECG arrhythmias, cardiac tissue necrosis, redox perturbations, and autophagy biomarkers. No arrhythmia differences existed between exercised and sedentary hearts following extended-duration IR ( P < 0.05). The sarc K_ATPchannel was confirmed essential ( P = 0.002) for prevention of antinecrotic tissue death with exercise (percent infarct, Sed = 42%; Ex = 20%; Ex5HD = 16%; ExHMR = 42%), although neither the mito K_ATP( P = 0.177) nor sarc K_ATP( P = 0.274) channel provided post-IR protection against apoptosis (terminal deoxynucleotidyl transferase deoxy UTP-mediated nick-end labeling-positive nuclei/mm², Sham = 1.8 ± 0.5; Sed = 19.4 ± 6.7; Ex = 7.5 ± 4.6; Ex5HD = 14.0 ± 3.9; ExHMR = 11.1 ± 1.8). Exercise preconditioning also appears to preserve basal autophagy levels, as assessed by Beclin 1 ( P ≤ 0.001), microtubule-associated protein-1 light-chain 3B ratios ( P = 0.020), and P62 ( P ≤ 0.001), in the hours immediately following IR. Further research is needed to better understand these findings and corresponding redox changes in exercised hearts.

The evaluation of Autonomic Nervous System (ANS) recovery following exercise provides insight into the transient stress placed on the cardiovascular system. High-Intensity Functional Training (HIFT) is a form of intense exercise that is prescribed in various modalities and durations; however, little is known about the influence of HIFT duration on ANS recovery. Ten apparently healthy males (28.1 ± 5.4 yrs) performed two HIFT sessions (<5-minute and 15-minute) in a crossover fashion. ANS activity was measured using plasma Epinephrine (E) and Norepineprine (NE); Heart Rate Variability markers of the log transformed Root Mean Square of Successive Differences (lnRMSSD) and High-Frequency power (lnHF). No trial dependent differences were observed in lnRMSSD (p = 0.822), lnHF (p = 0.886), E (p = 0.078), or NE (p = 0.194). A significant main time effect was observed in both trials with a depression in lnRMSSD and lnHF following the trials (p < 0.05) and recovering by 2-hours post (p = 0.141, p > 0.999) respectively. A trial dependent increase in E and NE occurred immediately post (p < 0.05) and recovered by 1-hour post (p > 0.999, p > 0.999) respectively. The HIFT bouts examined within this study demonstrated similar transient strain of the ANS.

Previous research findings indicate that environmental temperature can influence exercise-induced oxidative-stress responses, although the response to variable temperatures is unknown. The purpose of this study was to investigate the effect of warm, cold, and “neutral,” or room, environmental temperatures on the blood oxidative stress associated with exercise and recovery. Participants (N = 12, age 27 ± 5 yr, VO_2max = 56.7 ± 5.8 ml · kg^-1 · min^-1, maximal cycle power output = 300 ± 39 W) completed 3 exercise sessions consisting of a 1-hr ride at 60% W_max, at 40% relative humidity in warm (33 °C), cold (7 °C), and room-temperature environments (20 °C) in a randomized crossover fashion. Rectal core temperature was monitored continually as participants remained in the respective trial temperature throughout a 3-hr recovery. Blood was collected preexercise and immediately, 1 hr, and 3 hr postexercise and analyzed for oxidative-stress markers including ferric-reducing ability of plasma (FRAP), Trolox-equivalent antioxidant capacity (TEAC), lipid hydroperoxides, and protein carbonyls. Core temperature was significantly elevated by all exercise trials, but recovery core temperatures reflected the given environment. FRAP (p < .001), TEAC (p < .001), and lipid hydroperoxides (p < .001) were elevated after warm exercise while protein carbonyls were not altered (p > .05). These findings indicate that moderate-intensity exercise and associated recovery in a warm environment elicits a blood oxidative-stress response not observed at comparable exercise performed at lower temperatures.