No abstract

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 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.

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(ATP) or 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(ATP) or sarc K(ATP) channel. 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(ATP) channel 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/mm(2), 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.

Findings indicate that high-altitude trekking is associated with increased blood oxidative stress.