Limb, sex, but not acute dietary capsaicin, modulate the near-infrared spectroscopy-vascular occlusion test estimate of muscle metabolism.

The downward slope during the near-infrared spectroscopy (NIRS)-vascular occlusion test (NIRS-VOT) is purported as a simplified estimate of metabolism. Whether or not the NIRS-VOT exhibits sex- or limb-specificity or may be acutely altered remains to be elucidated. Thus, we investigated if there is limb- or sex specificity in tissue desaturation rates (DeO2) during a NIRS-VOT, and if acute dietary capsaicin may alter this estimate of muscle metabolism. Young healthy men (n = 25, 21 ± 4 years) and women (n = 20, 20 ± 1 years) ingested either placebo or capsaicin, in a counterbalanced, single-blind, crossover design after which a simplified NIRS-VOT was conducted to determine the DeO2 (%/s), as an estimate of oxidative muscle metabolism, in both the forearm (flexors) and thigh (vastus lateralis). There was a significant limb effect with the quadriceps having a greater DeO2 than the forearm (-2.31 ± 1.34 vs. -1.78 ± 1.22%/s, p = 0.007, ηp 2 = 0.19). There was a significant effect of sex on DeO2 (p = 0.005, ηp 2 = 0.203) with men exhibiting a lesser DeO2 than women (-1.73 ± 1.03 vs. -2.36 ± 1.32%/s, respectively). This manifested in significant interactions of limb*capsaicin (p = 0.001, ηp 2 = 0.26) as well as limb*capsaicin*sex on DeO2 (p = 0.013, ηp 2 = 0.16) being observed. Capsaicin does not clearly alter O2-dependent muscle metabolism, but there was apparent limb and sex specificity, interacting with capsaicin in this NIRS-derived assessment.

Tissue-specific mitochondrial toxicity of cigarette smoke concentrate: consequence to oxidative phosphorylation.

Cigarette smoke exposure is a well-known risk factor for developing numerous chronic health conditions, including pulmonary disease and cardiometabolic disorders. However, the cellular mechanisms mediating the toxicity of cigarette smoke in extrapulmonary tissues are still poorly understood. Therefore, the purpose of this study was to characterize the acute dose-dependent toxicity of cigarette smoke on mitochondrial metabolism by determining the susceptibility and sensitivity of mitochondrial respiration from murine skeletal (gastrocnemius and soleus) and cardiac muscles, as well as the aorta to cigarette smoke concentrate (CSC). In all tissues, exposure to CSC inhibited tissue-specific respiration capacity, measured by high-resolution respirometry, according to a biphasic pattern. With a break point of 451 ± 235 µg/mL, the aorta was the least susceptible to CSC-induced mitochondrial respiration inhibition compared with the gastrocnemius (151 ± 109 µg/mL; P = 0.008, d = 2.3), soleus (211 ± 107 µg/mL; P = 0.112; d = 1.7), and heart (94 ± 51 µg/mL; P < 0.001; d = 2.6) suggesting an intrinsic resistance of the vascular smooth muscle mitochondria to cigarette smoke toxicity. In contrast, the cardiac muscle was the most susceptible and sensitive to the effects of CSC, demonstrating the greatest decline in tissue-specific respiration with increasing CSC concentration (P < 0.001, except the soleus). However, when normalized to citrate synthase activity to account for differences in mitochondrial content, cardiac fibers' sensitivity to cigarette smoke inhibition was no longer significantly different from both fast-twitch gastrocnemius and slow-twitch soleus muscle fibers, thus suggesting similar mitochondrial phenotypes. Collectively, these findings established the acute dose-dependent toxicity of cigarette smoke on oxidative phosphorylation in permeabilized tissues involved in the development of smoke-related cardiometabolic diseases.NEW & NOTEWORTHY Despite numerous investigations into the mechanisms underlying cigarette smoke-induced mitochondrial dysfunction, no studies have investigated the tissue-specific mitochondrial toxicity to cigarette smoke. We demonstrate that, while aorta is least sensitive and susceptible to cigarette smoke-induced toxicity, the degree of cigarette smoke-induced toxicity in striated muscle depends on the tissue-specific mitochondrial content. We conclude that while the mitochondrial content influences cigarette smoke-induced toxicity in striated muscles, aorta is intrinsically protected against cigarette smoke-induced mitochondrial toxicity.

Impact of high intensity interval exercise with and without heat stress on cardiovascular and aerobic performance: a pilot study.

BACKGROUND: Heat stress during aerobic exercise training may offer an additional stimulus to improve cardiovascular function and performance in a cool-temperate environment. However, there is a paucity of information on the additive effects of high-intensity interval exercise (HIIE) and acute heat stress. We aimed to determine the effects of HIIE in combination with acute heat stress on cardiovascular function and exercise performance. METHODS: Twelve active (peak O2 consumption [VO2peak]: 47 ± 8 ml·O2/min/kg) young adults were counterbalanced to six sessions of HIIE in hot (HIIE-H, 30 ± 1 °C, 50 ± 5% relative humidity [RH]) or temperate conditions (HIIE-T, 20 ± 2 °C, 15 ± 10% RH). Resting heart rate (HR), HR variability (HRV), central (cBP) and peripheral blood pressure (pBP), peripheral mean arterial pressure (pMAP), pulse wave velocity (PWV), VO2peak, and 5-km treadmill time-trial were measured pre- and post-training. RESULTS: Resting HR and HRV were not significantly different between groups. However, expressed as percent change from baseline, cSBP (HIIE-T: + 0.9 ± 3.6 and HIIE-H: -6.6 ± 3.0%, p = 0.03) and pSBP (HIIE-T: -2.0 ± 4.6 and HIIE-H: -8.4 ± 4.7%, p = 0.04) were lower in the heat group. Post-training PWV was also significantly lower in the heat group (HIIE-T: + 0.4% and HIIE-H: -6.3%, p = 0.03). Time-trial performance improved with training when data from both groups were pooled, and estimated VO2peak was not significantly different between groups (HIIE-T: 0.7% and HIIE-H: 6.0%, p = 0.10, Cohen's d = 1.4). CONCLUSIONS: The addition of acute heat stress to HIIE elicited additive adaptations in only cardiovascular function compared to HIIE alone in active young adults in temperate conditions, thus providing evidence for its effectiveness as a strategy to amplify exercise-induced cardiovascular adaptations.

We like to move it, move it: A perspective on performing passive leg movement as a non-invasive assessment of vascular function in pediatric populations.

The passive leg movement (PLM) technique is a non-invasive assessment of lower-limb vascular function. PLM is methodologically simple to perform and utilizes Doppler ultrasound to determine leg blood flow (LBF) through the common femoral artery at rest and in response to passive movement of the lower leg. LBF responses to PLM have been reported to be mostly nitric oxide (NO)-mediated when performed in young adults. Moreover, PLM-induced LBF responses, as well as the NO contribution to PLM-induced LBF responses, are reduced with age and in various diseased populations, demonstrating the clinical utility of this non-invasive test. However, no PLM studies to date have included children or adolescents. Since its conception in 2015, our laboratory has performed PLM on hundreds of individuals including a large cohort of children and adolescents. Thus, the purpose of this perspective article is threefold: 1) to uniquely discuss the feasibility of performing PLM in children and adolescents, 2) to report PLM-induced LBF values from our laboratory in 7-17-year-olds, and 3) to discuss considerations for making comparisons among pediatric populations. Based on our experiences performing PLM in children and adolescents (among various other age groups), it is our perspective that PLM can feasibly be performed in this population. Further, data from our laboratory may be used to provide context for typical PLM-induced LBF values that could be observed in children and adolescents, as well as across the lifespan.

Effects of cigarette smoke on in situ mitochondrial substrate oxidation of slow- and fast-twitch skeletal muscles.

Epidemiological and clinical evidence suggests that cigarette smoke exposure alters glucose and fatty acid metabolism, leading to greater susceptibility to metabolic disorders. However, the effects of cigarette smoke exposure on mitochondrial substrate oxidation in the skeletal muscle are still poorly understood. Accordingly, this study aimed to examine the acute effects of cigarette smoke on mitochondrial respiratory capacity, sensitivity, and concurrent utilization of palmitoylcarnitine (PC), a long-chain fatty acid, and pyruvate, a product of glycolysis, in permeabilized gastrocnemius and soleus muscle fibers exposed to an acute (1 h) dose (4 %) of cigarette smoke concentrate. Cigarette smoke decreased both mitochondrial respiratory capacity (CONTROL: 50.4 ± 11.8 pmolO2/s/mgwt and SMOKE: 22.3 ± 4.4 pmolO2/s/mgwt, p < 0.01) and sensitivity for pyruvate (CONTROL: 0.10 ± 0.04 mM and SMOKE: 0.11 ± 0.04 mM, p < 0.01) in the gastrocnemius muscle. In the soleus, only the sensitivity for pyruvate-stimulated mitochondrial respiration trended toward a decrease (CONTROL: 0.11 ± 0.04 mM and SMOKE: 0.23 ± 0.15 mM, p = 0.08). In contrast, cigarette smoke did not significantly alter palmitoylcarnitine-stimulated mitochondrial respiration in either muscle. In the control condition, pyruvate-supported respiration was inhibited by the concurrent addition of palmitoylcarnitine in the fast-twitch gastrocnemius muscle (-27.1 ± 19.7 %, p < 0.05), but not in the slow-twitch soleus (-9.2 ± 17.0 %). With cigarette smoke, the addition of palmitoylcarnitine augmented the maximal respiration rate stimulated by the concurrent addition of pyruvate in the gastrocnemius (+18.5 ± 39.3 %, p < 0.05). However, cigarette smoke still significantly impaired mitochondrial respiratory capacity with combined substrates compared to control (p < 0.05). Our findings underscore that cigarette smoke directly impairs mitochondrial respiration of carbohydrate-derived substrates and is a primary mechanism underlying cigarette smoke-induced muscle dysfunction, which leads to a vicious cycle involving excess glucose conversion into fatty acids and lipotoxicity.

Physiologic strain of SCBA confidence course training compared to circuit training and live-fire training.

Firefighting is a dangerous occupation and even training carries substantial risks. Self-contained breathing apparatus confidence courses (SCBACC) are a common type of training. PURPOSE: Compare the physiological strain of SCBACC to live-fire training (LFT) and circuit training (CT) among academy cadets. METHODS: Cadets wore physiologic status monitors to assess heart rate (HR) and estimated core temperature (ECT) during CT, LFT, and SCBACC of similar duration (33-38 min). RESULTS: Data from 52 cadet firefighters (28 ±â€¯4 yrs old) were analyzed. ECT (38.6 ±â€¯0.4 vs 39.3 ±â€¯0.7 vs. 39.3 ±â€¯0.6ᵒC), peak HR (182.6 ±â€¯9.1 vs. 192.7 ±â€¯9.5 vs 195.9 ±â€¯9.6 bpm), and age-predicted maximal HR (APMHR%; 94.6 ±â€¯4.6 vs 99.9 ±â€¯4.9 vs. 101.5 ±â€¯4.8%) were significantly (p < 0.05) lower for CT than SCBACC and LFT, respectively. CONCLUSIONS: SCBACC produced physiological strain greater than CT and similar to LFT. SCBACC resulted in sustained HR at 100% of age-predicted maximal values, a peak ECT of 39.3 °C, and should be considered as physiologically stressful as LFT.