Higher Muscle Tissue Oxygenation When Exposed to Hypobaric Hypoxia Than Normobaric Hypoxia

There has been recent debate on the potential difference in physiological response between exposure to simulated altitude (normobaric hypoxia) and terrestrial altitude (hypobaric hypoxia). Purpose: To determine the difference in the physiological response to normobaric and hypobaric hypoxia during exercise. Methods: Eight recreationally active subjects (27 ± 5 y old, 73.1 ± 7.4 kg body weight, 170.6 ± 6.7 cm height, and 19.3 ± 9.2 % body fat) completed incremental cycling exercise to volitional fatigue in three separate environments: normobaric normoxia (NN; 350 m), normobaric hypoxia (NH; simulated 3094 m), and hypobaric hypoxia (HH; 3094 m). Heart rate, blood oxygen saturation, and muscle tissue oxygenation were measured at rest and continuously throughout the exercise trials. Results: Blood oxygen saturation (SpO2) was ~10% higher in NN compared to the two hypoxic conditions (p \u3c 0.001) at rest and all exercise stages, with no difference between NH and HH (p \u3e 0.05). Heart rate was higher at rest in HH (98 ± 13 bpm) compared to NN (83 ± 15 bpm, p = 0.011) and NH (84 ± 14 bpm, p = 0.001) which persisted until 165 watts at which point no difference was observed (p \u3e 0.05). Muscle tissue oxygenation was 17% higher in HH compared to NN and 19% higher than NH throughout exposure (p \u3c 0.05). Conclusion: This data indicates that the hypoxic stress resulting from normobaric and hypobaric hypoxia are not the sameand that hypobaric hypoxia may not result in hypoxia at the level of the tissue

Acute High Intensity Anaerobic Training and Rhabdomyolysis Risk

International Journal of Exercise Science 8(1) : 65-74, 2015. The current popularity of high intensity anaerobic training has caused concerns over the safety and prevalence of conditions such as rhabdomyolysis; thus it is important to understand the possible risks of participating in this type of activity. The purpose of this study was to determine the magnitude of muscle damage associated with a single high intensity anaerobic training session, and the relationship of this response to markers of fitness. Fifteen recreationally trained male participants (age 22.9 ± 4.3 y, mass 87.3 ± 15.6 kg, body fat 16.8 ± 6.4%, VO2 peak 50.1 ± 7.2 ml · kg-1 · min-1 ) completed a single anaerobic training session consisting of high intensity plyometrics and calisthenics. Prior to the exercise session, participants completed a maximal aerobic capacity test, body composition analysis, and a military physical fitness test (1 min push-ups, 54 ± 14; 1 min sit-ups, 45 ± 11; 1.5 mile run, 12:17 ± 0.067 min). Serum creatine kinase (CK) was measured prior to and 48 h following the exercise session. CK at 48 h (126.3 ± 68.9 U· L-1) did not reach the limits indicating rhabdomyolysis (~881-1479 U/L) but was elevated above resting (CK resting 90.5 ± 53.4). VO2 peak (L · m-1) had a positive correlation with CK levels (r = .51; p \u3c 0.05) but body mass or any other indicator of fitness did not correlate. An increase in serum CK levels occurred, but did not reach levels of rhabdomyolysis, suggesting that a single high intensity exercise session is safe for healthy individuals who exercise regularly

Effects of passive and active leg movements to interrupt sitting in mild hypercapnia on cardiovascular function in healthy adults

Prolonged sitting in a mild hypercapnic environment impairs peripheral vascular function. The effects of sitting interruptions using passive or active skeletal muscle contractions are still unclear. Therefore, we sought to examine the vascular effects of brief periods (2 min every half hour) of passive and active lower limb movement to interrupt prolonged sitting with mild hypercapnia in adults. Fourteen healthy adults (24 ± 2 yr) participated in three experimental visits sitting for 2.5 h in a mild hypercapnic environment (CO2 = 1,500 ppm): control (CON, no limb movement), passive lower limb movement (PASS), and active lower limb movement (ACT) during sitting. At all visits, brachial and popliteal artery flow-mediated dilation (FMD), microvascular function, plasmatic levels of nitrate/nitrite and endothelin-1, and heart rate variability were assessed before and after sitting. Brachial and popliteal artery FMDs were reduced in CON and PASS (P \u3c 0.05) but were preserved (P \u3e 0.05) in ACT. Microvascular function was blunted in CON (P \u3c 0.05) but was preserved in PASS and ACT (P \u3e 0.05). In addition, total plasma nitrate/nitrite was preserved in ACT (P \u3e 0.05) but was reduced in CON and PASS (P \u3c 0.05), and endothelin-1 levels were decreased in ACT (P \u3c 0.05). Both passive and active movement induced a greater ratio between the low-frequency and high-frequency bands for heart rate variability (P \u3c 0.05). For the first time, to our knowledge, we found that brief periods of passive leg movement can preserve microvascular function, but that an intervention that elicits larger increases in shear rate, such as low-intensity exercise, is required to fully protect both macrovascular and microvascular function and circulating vasoactive substance balance

Irisin and Fibronectin Type III Domain-Containing 5 Responses to Exercise in Different Environmental Conditions

International Journal of Exercise Science 10(5): 666-680, 2017. Fibronectin type III domain-containing 5 (FNDC5) is a skeletal muscle membrane-bound precursor to the myokine irisin. Irisin is involved in stimulating adipose tissue to become more metabolically active in order to produce heat. The purpose of this study was to determine the effects of exercise in a hot (33 °C), cold (7 °C), and room temperature (RT, 20 °C) environment on the skeletal muscle gene expression of FNDC5 and the plasma concentrations of irisin. Twelve recreationally trained males completed three separate, 1 h cycling bouts at 60% of Wmax in a hot, cold, and RT environment followed by three hours of recovery at room temperature. Blood samples were taken from the antecubital vein and muscle biopsies were taken from the vastus lateralis pre-, post-, and 3 h post-exercise. Plasma concentrations of irisin did not change from pre- (9.23 ± 2.68 pg·mL-1) to post-exercise (9.6 ± 0.2 pg·mL-1, p = 0.068), but did decrease from post-exercise to 3 h post-exercise (8.9 ± 0.5 pg·mL-1, p = 0.047) regardless of temperature. However, when plasma volume shifts were considered, no differences were found in irisin (p = 0.086). There were no significant differences between trials for irisin plasma concentrations (p \u3e 0.05). No significant differences in FNDC5 were observed between the hot, cold, or RT or pre-, post-, or 3 h post-exercise time points (p \u3e 0.05). These data indicate that the temperature in which exercise takes place does not influence FNDC5 transcription or circulating irisin in a human model

Morphine activates neuroinflammation in a manner parallel to endotoxin

Opioids create a neuroinflammatory response within the CNS, compromising opioid-induced analgesia and contributing to various unwanted actions. How this occurs is unknown but has been assumed to be via classic opioid receptors. Herein, we provide direct evidence that morphine creates neuroinflammation via the activation of an innate immune receptor and not via classic opioid receptors. We demonstrate that morphine binds to an accessory protein of Toll-like receptor 4 (TLR4), myeloid differentiation protein 2 (MD-2), thereby inducing TLR4 oligomerization and triggering proinflammation. Small-molecule inhibitors, RNA interference, and genetic knockout validate the TLR4/MD-2 complex as a feasible target for beneficially modifying morphine actions. Disrupting TLR4/MD-2 protein–protein association potentiated morphine analgesia in vivo and abolished morphine-induced proinflammation in vitro, the latter demonstrating that morphine-induced proinflammation only depends on TLR4, despite the presence of opioid receptors. These results provide an exciting, nonconventional avenue to improving the clinical efficacy of opioids.Xiaohui Wang, Lisa C. Loram, Khara Ramos, Armando J. de Jesus, Jacob Thomas, Kui Cheng, Anireddy Reddy, Andrew A. Somogyi, Mark R. Hutchinson, Linda R. Watkins and Hang Yi

Exercise-Induced Interleukin-6 and Metabolic Responses in Hot, Temperate, and Cold Conditions

The purpose of this study was to determine the effects of exercise in hot, cold, and temperate environments on plasma interleukin-6 (IL-6). Eleven recreationally trained males (age = 25 ± 4 years, height = 178 ± 5 cm, weight = 79.4 ± 13.5 kg, body fat = 14.7 ± 3.6%, VO2 peak = 54.6 ± 11.5 ml kg-1 min-1) performed a 1 hr cycling bout in hot (33 °C), cold (7 °C), and temperate (20 °C) environments at 60% of Wmax followed by 3 hr of supine recovery in temperate conditions. Expired gases were measured every 15 min during exercise and once every hour during recovery. Heart rate was continuously measured throughout the trials. Blood samples were obtained from the antecubital vein pre-exercise, immediately post-exercise, and 3 hr post-exercise. Blood samples were analyzed for plasma concentrations of IL-6 using a commercial ELISA kit. Plasma IL-6 concentrations were significantly higher immediately post-exercise (14.8 ± 1.6 pg ml-1, p = 0.008) and 3 hr post-exercise (14.8 ± 0.9 pg ml-1, p = 0.018) compared to pre-exercise (11.4 ± 2.4 pg ml-1), across all trials. There were no differences in plasma IL-6 concentrations (p = 0.207) between temperature conditions.Oxygen consumption and heart rate were higher and respiratory exchange ratio was lower in the hot compared to other conditions (p \u3c 0.05). These data indicate that the temperature in which exercise occurs does not affect acute plasma IL-6 response despite differences in metabolic state