The biphasic activity of autophagy and heat shock protein response in peripheral blood mononuclear cells following acute resistance exercise in resistance-trained males.

PURPOSE: Autophagy and heat shock protein (HSP) response are proteostatic systems involved in the acute and adaptive responses to exercise. These systems may upregulate sequentially following cellular stress including acute exercise, however, currently few data exist in humans. This study investigated the autophagic and HSP responses to acute intense lower body resistance exercise in peripheral blood mononuclear cells (PBMCs) with and without branched-chain amino acids (BCAA) supplementation. METHODS: Twenty resistance-trained males (22.3 ± 1.5 yr; 175.4 ± .7 cm; 86.4 ± 15.6 kg) performed a bout of intense lower body resistance exercise and markers of autophagy and HSP70 were measured immediately post- (IPE) and 2, 4, 24, 48, and 72 h post-exercise. Prior to resistance exercise, 10 subjects were randomly assigned to BCAA supplementation of 0.22 g/kg/d for 5 days pre-exercise and up to 72 h following exercise while the other 10 subjects consumed a placebo (PLCB). RESULTS: There were no difference in autophagy markers or HSP70 expression between BCAA and PLCB groups. LC3II protein expression was significantly lower 2 and 4 h post-exercise compared to pre-exercise. LC3II: I ratio was not different at any time point compared to pre-exercise. Protein expression of p62 was lower IPE, 2, and 4 h post-exercise and elevated 24 h post-exercise. HSP70 expression was elevated 48 and 72 h post-exercise. CONCLUSIONS: Autophagy and HSP70 are upregulated in PBMCs following intense resistance exercise with autophagy increasing initially post-exercise and HSP response in the latter period. Moreover, BCAA supplementation did not affect this response.

The Potential Interplay Between HIF-1α, Angiogenic, and Autophagic Signaling During Intermittent Hypoxic Exposure and Exercise.

Berkemeier QN, Deyhle MR, McCormick JJ, Escobar KA, Mermier CM. The Potential Interplay between HIF-1α, Angiogenic, and Autophagic Signaling during Intermittent Hypoxic Exposure and Exercise High Alt Med Biol. 00:000-000, 2024.-Berkemeier QN, Deyhle MR, McCormick JJ, Escobar KA, Mermier CM. The Potential Interplay between HIF-1α, Angiogenic, and Autophagic Signaling During Intermittent Hypoxic Exposure and Exercise High Alt Med Biol. 00:000-000, 2024.-Environmental hypoxia as a result of decreased barometric pressure upon ascent to high altitudes (>2,500 m) presents increased physiological demands compared with low altitudes, or normoxic environments. Competitive athletes, mountaineers, wildland firefighters, military personnel, miners, and outdoor enthusiasts commonly participate in, or are exposed to, forms of exercise or physical labor at moderate to high altitudes. However, the majority of research on intermittent hypoxic exposure is centered around hematological markers, and the skeletal muscle cellular responses to exercise in hypoxic environments remain largely unknown. Two processes that may be integral for the maintenance of cellular health in skeletal muscle include angiogenesis, or the formation of new blood vessels from preexisting vasculature and autophagy, a process that removes and recycles damaged and dysfunctional cellular material in the lysosome. The purpose of this review is to is to examine the current body of literature and highlight the potential interplay between low-oxygen-sensing pathways, angiogenesis, and autophagy during acute and prolonged intermittent hypoxic exposure in conjunction with exercise. The views expressed in this paper are those of the authors and do not reflect the official policy of the Department of Army, DOD, DOE, ORAU/ORISE or U.S. Government.

Strategies to mitigate acute kidney injury risk during physical work in hot environments.

Prolonged physical work in the heat can reduce renal function and increase the risk of acute kidney injury (AKI). This is concerning given that the latest climate change projections forecast a rise in global temperature as well as the frequency, intensity, and duration of heatwaves. This means that outdoor and indoor workers in the agriculture or construction industries will be exposed to higher heat stress in the years ahead. Several studies indicate a higher incidence of chronic kidney disease from nontraditional origins (CKDnt) in individuals exposed to high temperatures, intense physical work, and/or recurrent dehydration. It has been proposed that prolonged physical work in the heat accompanied by dehydration results in recurrent episodes of AKI that ultimately lead to permanent kidney damage and the development of CKDnt. Thus, there is a need to identify and test strategies that can alleviate AKI risk during physical work in the heat. The purpose of this review is to present strategies that might prevent and mitigate the risk of AKI induced by physical work in the heat.

Effect of heat stress on heat shock protein expression and hypertrophy-related signaling in the skeletal muscle of trained individuals.

Muscle mass is balanced between hypertrophy and atrophy by cellular processes, including activation of the protein kinase B-mechanistic target of rapamycin (Akt-mTOR) signaling cascade. Stressors apart from exercise and nutrition, such as heat stress, can stimulate the heat shock protein A (HSPA) and C (HSPC) families alongside hypertrophic signaling factors and muscle growth. The effects of heat stress on HSP expression and Akt-mTOR activation in human skeletal muscle and their magnitude of activation compared with known hypertrophic stimuli are unclear. Here, we show a single session of whole body heat stress following resistance exercise increases the expression of HSPA and activation of the Akt-mTOR cascade in skeletal muscle compared with resistance exercise in a healthy, resistance-trained population. Heat stress alone may also exert similar effects, though the responses are notably variable and require further investigation. In addition, acute heat stress in C2C12 muscle cells enhanced myotube growth and myogenic fusion, albeit to a lesser degree than growth factor-mediated hypertrophy. Though the mechanisms by which heat stress stimulates hypertrophy-related signaling and the potential mechanistic role of HSPs remain unclear, these findings provide additional evidence implicating heat stress as a novel growth stimulus when combined with resistance exercise in human skeletal muscle and alone in isolated murine muscle cells. We believe these findings will help drive further applied and mechanistic investigation into how heat stress influences muscular hypertrophy and atrophy.NEW & NOTEWORTHY We show that acute resistance exercise followed by whole body heat stress increases the expression of HSPA and increases activation of the Akt-mTOR cascade in a physically active and resistance-trained population.

Circulating markers of intestinal barrier injury and inflammation following exertion in hypobaric hypoxia.

Hypoxia induced intestinal barrier injury, microbial translocation, and local/systemic inflammation may contribute to high-altitude associated gastrointestinal complications or symptoms of acute mountain sickness (AMS). Therefore, we tested the hypothesis that six-hours of hypobaric hypoxia increases circulating markers of intestinal barrier injury and inflammation. A secondary aim was to determine if the changes in these markers were different between those with and without AMS. Thirteen participants were exposed to six hours of hypobaric hypoxia, simulating an altitude of 4572 m. Participants completed two 30-minute bouts of exercise during the early hours of hypoxic exposure to mimic typical activity required by those at high altitude. Pre- and post-exposure blood samples were assessed for circulating markers of intestinal barrier injury and inflammation. Data below are presented as mean ± standard deviation or median [interquartile range]. Intestinal fatty acid binding protein (Δ251 [103-410] pg•mL-1; p = 0.002, d = 0.32), lipopolysaccharide binding protein (Δ2 ± 2.4 µg•mL-1; p = 0.011; d = 0.48), tumor necrosis factor-α (Δ10.2 [3-42.2] pg•mL-1; p = 0.005; d = 0.25), interleukin-1ß (Δ1.5 [0-6.7] pg•mL-1 p = 0.042; d = 0.18), and interleukin-1 receptor agonist (Δ3.4 [0.4-5.2] pg•mL-1p = 0.002; d = 0.23) increased from pre- to post-hypoxia. Six of the 13 participants developed AMS; however, the pre- to post-hypoxia changes for each marker were not different between those with and without AMS (p > 0.05 for all indices). These data provide evidence that high altitude exposures can lead to intestinal barrier injury, which may be an important consideration for mountaineers, military personnel, wildland firefighters, and athletes who travel to high altitudes to perform physical work or exercise.

Could Orthostatic Stress Responses Predict Acute Mountain Sickness Susceptibility Prior to High Altitude Travel? A Pilot Study.

Bellovary, Bryanne N., Andrew D. Wells, Zachary J. Fennel, Jeremy B. Ducharme, Jonathan M. Houck, Trevor J. Mayschak, Ann L. Gibson, Scott N. Drum, and Christine M. Mermier. Could orthostatic stress responses predict acute mountain sickness susceptibility before high altitude travel? A pilot study. High Alt Med Biol. 24:19-26, 2023. Purpose: This study assessed head-up tilt (HUT) responses in relation to acute mountain sickness (AMS)-susceptibility during hypoxic exposure. Materials and Methods: Fifteen participants completed three lab visits: (1) protocol familiarization and cycle maximal oxygen consumption (VO2max) test; (2) HUT test consisting of supine rest for 20 minutes followed by 70° tilting for ≤40 minutes; and (3) 6 hours of hypobaric hypoxic exposure (4,572 m) where participants performed two 30-minute cycling bouts separated by 1 hour at a 50% VO2max workload within the first 3 hours and rested when not exercising. During HUT, systolic blood pressure (SBP), diastolic blood pressure, heart rate (HR), and variability (blood pressure variability [BPV] and HR variability [HRV]) were measured continuously. The AMS scores were determined after 6 hours of exposure. Correlations determined relationships between HUT cardiovascular responses and AMS scores. Repeated-measures analysis of variance (ANOVA) assessed differences between those with and without AMS symptoms during HUT. Results: Higher AMS scores correlated with greater change in SBP variability (r = 0.52, p = 0.048) and blunted changes in HRV (root mean square of successive differences between normal heartbeats r = 0.81, p = 0.001, percentage of adjacent normal sinus intervals that differ by more than 50 milliseconds [pNN50] r = 0.87, p < 0.001) during HUT. A pNN50 interaction (p = 0.02) suggested elevated cardiac sympathetic activity at baseline and a blunted increase in cardiac sympathetic influence throughout HUT in those with AMS (pNN50 baseline: AMS = 26.2% ± 15.3%, no AMS = 51.0% ± 13.5%; first 3 minutes into HUT: AMS = 17.2% ± 19.1%, no AMS = 17.1% ± 10.9%; end of HUT: AMS = 6.2% ± 9.1%, no AMS 11.0% ± 10.0%). Conclusions: The results suggest autonomic responses via HUT differ in AMS-susceptible individuals. Changes in HRV and BPV during HUT may be a promising predictive measurement for AMS-susceptibility, but further research is needed for confirmation.

Ibuprofen Increases Markers of Intestinal Barrier Injury But Suppresses Inflammation at Rest and After Exercise in Hypoxia.

PURPOSE: The purpose of this study was to evaluate the effects of acute ibuprofen consumption (2 × 600-mg doses) on markers of enterocyte injury, intestinal barrier dysfunction, inflammation, and symptoms of gastrointestinal (GI) distress at rest and after exercise in hypobaric hypoxia. METHODS: Using a randomized double-blind placebo-controlled crossover design, nine men (age, 28 ± 3 yr; weight, 75.4 ± 10.5 kg; height, 175 ± 7 cm; body fat, 12.9% ± 5%; V̇O 2 peak at 440 torr, 3.11 ± 0.65 L·min -1 ) completed a total of three visits including baseline testing and two experimental trials (placebo and ibuprofen) in a hypobaric chamber simulating an altitude of 4300 m. Preexercise and postexercise blood samples were assayed for intestinal fatty acid binding protein (I-FABP), ileal bile acid binding protein, soluble cluster of differentiation 14, lipopolysaccharide binding protein, monocyte chemoattractant protein-1, tumor necrosis factor α (TNF-α), interleukin-1ß, and interleukin-10. Intestinal permeability was assessed using a dual sugar absorption test (urine lactulose-to-rhamnose ratio). RESULTS: Resting I-FABP (906 ± 395 vs 1168 ± 581 pg·mL -1 ; P = 0.008) and soluble cluster of differentiation 14 (1512 ± 297 vs 1642 ± 313 ng·mL -1 ; P = 0.014) were elevated in the ibuprofen trial. Likewise, the urine lactulose-to-rhamnose ratio (0.217 vs 0.295; P = 0.047) and the preexercise to postexercise change in I-FABP (277 ± 308 vs 498 ± 479 pg·mL -1 ; P = 0.021) were greater in the ibuprofen trial. Participants also reported greater upper GI symptoms in the ibuprofen trial ( P = 0.031). However, monocyte chemoattractant protein-1 ( P = 0.007) and TNF-α ( P = 0.047) were lower throughout the ibuprofen trial compared with placebo (main effect of condition). CONCLUSIONS: These data demonstrate that acute ibuprofen ingestion aggravates markers of enterocyte injury and intestinal barrier dysfunction at rest and after exercise in hypoxia. However, ibuprofen seems to suppress circulating markers of inflammation.

The physiological, perceptual, and thermoregulatory responses to facemask use during exercise.

The use of masks in public settings and when around people has been recommended to limit the spread of Coronavirus disease 2019 (COVID-19) by major public health agencies. Several different types of masks classified as either medical- or non-medical grade are commonly used among the public. However, concerns with difficulty breathing, re-breathing exhaled carbon dioxide, a decrease in arterial oxygen saturation, and a decrease in exercise performance have been raised regarding the use of mask during exercise. We review the current knowledge related to the effect of different masks during exercise on cardiorespiratory, metabolic, thermoregulatory, and perceptual responses. As such, the current literature seems to suggest that there are minimal changes to cardiovascular, metabolic, and no changes to thermoregulatory parameters with facemask use. However, differences in ventilatory parameters have been reported with submaximal and maximal intensity exercise to volitional fatigue. Literature on perceptual responses to exercise indicate an impact on ratings of perceived exertion, dyspnea, and overall discomfort dependent on mask use as well as exercise intensity. In conclusion, data from the current literature suggests a minimal impact on physiological, perceptual, and thermoregulatory responses dependent on the type of mask used during exercise.

Body fat percentage is independently and inversely associated with serum antibody responses to SARS-CoV-2 mRNA vaccines.

Vaccination is widely considered the most effective preventative strategy to protect against severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection. An individual's exercise habits, and physical fitness have been shown to impact the immune response following vaccination using traditional vaccine platforms, but their effects are not well characterized following administration of newer vaccination technology (mRNA vaccines). We investigated these effects on the magnitude of antibody responses following SARS-CoV-2 mRNA vaccination while accounting for known covariates (age, sex, time since vaccination, and the type of vaccine administered). Adults of varying fitness levels (18-65 years; N = 50) who had received either the Moderna or Pfizer SARS-CoV-2 mRNA vaccine between 2 weeks and 6 months prior, completed health history and physical activity questionnaires, had their blood drawn, body composition, cardiorespiratory fitness, and strength assessed. Multiple linear regressions assessed the effect of percent body fat, hand grip strength, cardiorespiratory fitness, and physical activity levels on the magnitude of receptor binding domain protein (RBD) and spike protein subunit 1 (S1) and 2 (S2) while accounting for known covariates. Body fat percentage was inversely associated with the magnitude of S1 (p = 0.006, ß = - 366.56), RBD (p = 0.003, ß = - 249.30), and S2 (p = 0.106, ß = - 190.08) antibodies present in the serum following SARS-CoV-2 mRNA vaccination. Given the increasing number of infections, variants, and the known waning effects of vaccination, future mRNA vaccinations such as boosters are encouraged to sustain immunity; reducing excess body fat may improve the efficacy of these vaccinations.

The heat shock connection: skeletal muscle hypertrophy and atrophy.

Skeletal muscle is an integral tissue system that plays a crucial role in the physical function of all vertebrates and is a key target for maintaining or improving health and performance across the lifespan. Based largely on cellular and animal models, there is some evidence that various forms of heat stress with or without resistance exercise may enhance skeletal muscle growth or reduce its loss. It is not clear whether these stimuli are similarly effective in humans or meaningful compared with exercise alone across various heating methodologies. Furthermore, the magnitude by which heat stress may influence whole body thermoregulatory responses and the connection to skeletal muscle adaptation remains ambiguous. Finally, the underlying mechanisms, which may include interaction between relevant heat shock proteins and intracellular hypertrophy and atrophy related factors, remain unclear. In this narrative review, we examine the relevant literature regarding heat stress alone or in combination with resistance exercise emphasizing skeletal muscle hypertrophy and atrophy across cellular and animal models, as well as human investigations. In addition, we present working mechanistic theories for heat shock protein-mediated signaling effects regarding hypertrophy and atrophy-related signaling processes. Importantly, continued research is necessary to determine the practical effects and mechanisms of heat stress with and without resistance exercise on skeletal muscle function via growth and maintenance.

Exercise in hypobaric hypoxia increases markers of intestinal injury and symptoms of gastrointestinal distress.

NEW FINDINGS: What is the central question of this study? What is the effect of hypobaric hypoxia on markers of exercise-induced intestinal injury and symptoms of gastrointestinal (GI) distress? What is the main finding and its importance? Exercise performed at 4300 m of simulated altitude increased intestinal fatty acid binding protein (I-FABP), claudin-3 (CLDN-3) and lipopolysaccharide binding protein (LBP), which together suggest that exercise-induced intestinal injury may be aggravated by concurrent hypoxic exposure. Increases in I-FABP, LBP and CLDN-3 were correlated to exercise-induced GI symptoms, providing some evidence of a link between intestinal barrier injury and symptoms of GI distress. ABSTRACT: We sought to determine the effect of exercise in hypobaric hypoxia on markers of intestinal injury and gastrointestinal (GI) symptoms. Using a randomized and counterbalanced design, nine males completed two experimental trials: one at local altitude of 1585 m (NORM) and one at 4300 m of simulated hypobaric hypoxia (HYP). Participants performed 60 min of cycling at a workload that elicited 65% of their NORM V̇O2max${\dot V_{{{\rm{O}}_{\rm{2}}}{\rm{max}}}}$ . GI symptoms were assessed before and every 15 min during exercise. Pre- and post-exercise blood samples were assessed for intestinal fatty acid binding protein (I-FABP), claudin-3 (CLDN-3) and lipopolysaccharide binding protein (LBP). All participants reported at least one GI symptom in HYP compared to just one participant in NORM. I-FABP significantly increased from pre- to post-exercise in HYP (708 ± 191 to 1215 ± 518 pg ml-1 ; P = 0.011, d = 1.10) but not NORM (759 ± 224 to 828 ± 288 pg ml-1 ; P > 0.99, d = 0.27). CLDN-3 significantly increased from pre- to post-exercise in HYP (13.8 ± 0.9 to 15.3 ± 1.2 ng ml-1 ; P = 0.003, d = 1.19) but not NORM (13.7 ± 1.8 to 14.2 ± 1.6 ng ml-1 ; P = 0.435, d = 0.45). LBP significantly increased from pre- to post-exercise in HYP (10.8 ± 1.2 to 13.9 ± 2.8 µg ml-1 ; P = 0.006, d = 1.12) but not NORM (11.3 ± 1.1 to 11.7 ± 0.9 µg ml-1 ; P > 0.99, d = 0.32). I-FABP (d = 0.85), CLDN-3 (d = 0.95) and LBP (d = 0.69) were all significantly higher post-exercise in HYP compared to NORM (P ≤ 0.05). Overall GI discomfort was significantly correlated to ΔI-FABP (r = 0.71), ΔCLDN-3 (r = 0.70) and ΔLBP (r = 0.86). These data indicate that cycling exercise performed in hypobaric hypoxia can cause intestinal injury, which might cause some commonly reported GI symptoms.

Can linear regression confirm VO2max was attained in middle-aged and older adults?

PURPOSE: Evaluate the efficacy of a regression method for identifying a VO2 plateau to confirm the attainment of VO2max compared to a verification trial in middle-aged and older adults. METHODS: Eleven men and ten women (age 61.0 ± 8.1, VO2max 21.8-50.3 ml/kg/min, n = 21) completed an individualized ramp graded exercise test (GXT) on the cycle ergometer, and one hour later, a verification trial at 105% of their maximal work rate (WR) achieved during the GXT. A plateau in VO2 was used to confirm VO2max was attained. VO2 plateau was identified using the difference between the highest VO2 between the two trials and a linear regression analysis of the VO2-WR relationship during the GXT. McNemar's test of marginal homogeneity was used to detect differences in the proportion of paired data of individuals' attainment of VO2max criteria. RESULTS: Of the 21 participants, 15 (71.4%) met the verification criterion while 6 (28.6%) did not, compared to the regression method where 16 (76.2%) achieved the regression criterion while 5 (23.8%) did not. McNemar's test revealed no significant difference between participants' ability to achieve the regression and verification criteria (p = 0.999). CONCLUSION: The regression method is an effective strategy for confirming VO2max was attained with middle-aged and older adults on a cycle ergometer. This time-efficient regression method is comparable with the verification criterion but does not require a second maximal test, which may be advantageous for those where the verification trial may not be practical.

High-altitude exposures and intestinal barrier dysfunction.

Gastrointestinal complaints are often reported during ascents to high altitude (>2,500 m), though their etiology is not known. One potential explanation is injury to the intestinal barrier which has been implicated in the pathophysiology of several diseases. High-altitude exposures can reduce splanchnic perfusion and blood oxygen levels causing hypoxic and oxidative stress. These stressors might injure the intestinal barrier leading to consequences such as bacterial translocation and local/systemic inflammatory responses. The purpose of this mini-review is to 1) discuss the impact of high-altitude exposures on intestinal barrier dysfunction and 2) present medications and dietary supplements which may have relevant impacts on the intestinal barrier during high-altitude exposures. There is a small but growing body of evidence which shows that acute exposures to high altitudes can damage the intestinal barrier. Initial data also suggest that prolonged hypoxic exposures can compromise the intestinal barrier through alterations in immunological function, microbiota, or mucosal layers. Exertion may worsen high-altitude-related intestinal injury via additional reductions in splanchnic circulation and greater hypoxemia. Collectively these responses can result in increased intestinal permeability and bacterial translocation causing local and systemic inflammation. More research is needed to determine the impact of various medications and dietary supplements on the intestinal barrier during high-altitude exposures.

A Metabolic Profile of Peripheral Heart Action Training.

Purpose: Peripheral heart action (PHA) is a style of circuit training that alternates upper and lower body resistance exercises with minimal rest between sets. The purpose of this study was to compare the metabolic demands of PHA to traditional hypertrophy training (TRAD) and to provide between sex comparison for both types of resistance training (RT). Methods: Twenty resistance-trained individuals underwent two bouts of volume-load matched RT: PHA and TRAD. We measured oxygen uptake (VO2), heart rate (HR), blood lactate (BL) concentration, rating of perceived exertion (RPE), excess post-exercise oxygen consumption (EPOC), and duration of each session. Results: PHA elicited significantly greater %VO2max (p < .001), %HRmax (p < .001), RPE (p < .001), and EPOC (p < .001) compared to TRAD. PHA was also completed in less time (p < .001). Compared to TRAD, BL was significantly higher at mid-exercise (p < .001), post-exercise (p < .001), and 5-min post-exercise (p < .001) during PHA. There were no between-sex differences for BL at any time-point for TRAD. However, during PHA, BL was significantly higher for males at mid-exercise (p = .04), post-exercise (p = .02), and 5-min post-exercise (p = .002). No between-sex differences were detected for HR, VO2, RPE, or duration for either style of RT. Conclusions: PHA is a time-effective and metabolically demanding circuit that may lead to strength and cardiorespiratory adaptations. Males produced more BL than females during PHA, but not TRAD, suggesting that they incurred more metabolic stress during the bout of circuit training.

Predictive model specific to young adults for estimating thoracic gas volume for air-displacement plethysmography.

BACKGROUND: Thoracic gas volume either measured (mTGV) or predicted by the BodPod® (bpTGV) is used during air-displacement plethysmography to obtain a better estimate of percent body fat. Evidence suggests that bpTGV underestimates mTGV for young adults and this is especially evident for young males. AIMS: We developed, validated, and cross-validated a TGV prediction model (pTGV) for males and females 18-30 years of age to address this underestimation. MATERIALS & METHODS: Participants (N = 181; 18-30 years) that had their body composition assessed with the BodPod® were retrospectively randomly assigned to one of two independent subgroups, a validation (n = 145) or cross-validation (n = 36) sample. Ten iterations of the k-fold validation procedure were performed to assess the internal replicability of pTGV within the validation sample. External replicability of pTGV was evaluated by assessing the difference and standard error of the estimate (SEE) compared to mTGV in the cross-validation group. RESULTS: The model using height, sex and body mass yielded the highest adjusted R2 (0.627) and the lowest SEE (0.56 L): pTGV = 0.615338 × Sex (0 = Female, 1 = Male) + 0.056267 × Height (cm) - 0.011006 × Body Mass (kg) - 5.358839. R2 remained stable across 10 iterations of the k-fold procedure (average R2 = 0.64). Differences between pTGV and mTGV were not significantly different than zero for the total cross-validation sample (-0.06 ± 0.7 L; SEE = 3.0%), for males (-0.11 ± 0.7 L; SEE = 3.7%), or for females (-0.02 ± 0.7 L; SEE = 5.3%). CONCLUSION: We recommend that when it is impractical to obtain mTGV, the strong internal and external replicability of the new prediction model supports its use for males and females ages 18-30 years old during air-displacement plethysmography.

Effect of Predicted Versus Measured Thoracic Gas Volume on Body Fat Percentage in Young Adults.

The BodPod® (COSMED, Concord, CA) uses predicted (pTGV) or measured thoracic gas volume (mTGV) during estimations of percentage body fat (%BF). In young adults, there is inconsistent evidence on the variation between pTGV and mTGV, and the effect of sex as a potential covariate on this relationship is unknown. This study examined the difference between TGV assessments and its effect on %BF and potential sex differences that may impact this relationship. A retrospective analysis of BodPod® pTGV and mTGV for 95 men and 86 women ages 18-30 years was performed. Predicted TGV was lower than mTGV for men (-0.49 ± 0.7 L; p < .0001). For men, %BF derived by pTGV was lower than that by mTGV (-1.3 ± 1.8%; p < .0001). For women, no differences were found between pTGV and mTGV (-0.08 ± 0.6 L; p > .05) or %BF (-0.03 ± 0.2%; p > .05). The two-predictor model of sex and height was able to account for 57.9% of the variance in mTGV, F(2, 178) = 122.5, p < .0001. Sex corrected for the effect of height was a significant predictor of mTGV (ß = 0.483 L, p < .0001). There is bias for pTGV to underestimate mTGV in individuals with a large mTGV, which can lead to significant underestimations of %BF in young adults; this was especially evident for men in this study. Sex is an important covariate that should be considered when deciding to use pTGV. The results indicate that TGV should be measured whenever possible for both men and women ages 18-30 years.

The Potential Role of Exercise-Induced Muscle Damage in Exertional Heat Stroke.

Exertional heat stroke (EHS) is a life-threatening condition that affects mainly athletes, military personnel, firefighters, and occupational workers. EHS is frequently observed in non-compensable conditions (where the body is unable to maintain a steady thermal balance) as a result of heavy heat stress and muscle contraction associated with prolonged and strenuous physical and occupational activities, resulting in central nervous system dysfunction followed by multi-organ damage and failure. Since the pathophysiology of EHS is complex and involves multiple organs and systems, any condition that changes the interrelated systems may increase the risk for EHS. It has been suggested that exercise-induced muscle damage (EIMD) can lead to thermoregulatory impairment and systemic inflammation, which could be a potential predisposing factor for EHS. In this review article, we aim to (1) address the evidence of EIMD as a predisposing factor for EHS and (2) propose a possible mechanism of how performing muscle-damaging exercise in the heat may aggravate muscle damage and subsequent risk of EHS and acute kidney injury (AKI). Such an understanding could be meaningful to minimize the risks of EHS and AKI for individuals with muscle damage due to engaging in physical work in hot environments.

Comparison of resting metabolic rate prediction equations in college-aged adults.

Prediction equations have been considered an accurate method for estimating resting metabolic rate (RMR) across multiple populations, but their accuracy for college-aged individuals not on an athletics team remains to be determined. Sixty-two college-aged (18-30 yrs) males (n = 31) and females (n = 31) had their RMR measured (RMRm), using indirect calorimetry, and body composition assessed via air-displacement plethysmography. The World Health Organization (WHO), Mifflin-St Jeor (Mifflin), Harris-Benedict (HB), Cunningham, and Nelson equations were used to estimate RMR. No difference was observed between the Cunningham and RMRm regardless of sex (p ≥ 0.05). All other prediction equations estimated a significantly lower RMR for males (p < 0.05). The Mifflin and Nelson equations predicted an RMR that was significantly lower than RMRm for females (p < 0.05). When compared with RMRm, no difference was detected for females using the WHO, HB, or Cunningham (p ≥ 0.05). Only the Nelson equation predicted an RMR that was outside of the clinically acceptable range (±10% of RMRm) regardless of sex. The Cunningham, WHO, and HB equations can accurately predict RMR for college-aged males and females. RMR prediction equations used in this study are less accurate for those with greater RMRs. Novelty: For adults 18-30 years old that are not on an athletics team, the Cunningham equation can accurately predict RMR. The Nelson equation should not be used to predict RMR for this population. There is a systematic bias for RMR prediction equations to underestimate higher measured RMR values.

Heat acclimation during low-intensity exercise increases V̇O2max and Hsp72, but not markers of mitochondrial biogenesis and oxidative phosphorylation, in skeletal tissue.

NEW FINDINGS: What is the central question of this study? Heat acclimation increases tolerance to exercise performed in the heat and may improve maximal oxygen uptake (VO2 max) and performance in temperate environments. However, it is unknown if HA affects the expression of proteins related to mitochondrial biogenesis and oxidative capacity in skeletal muscle. What is the main finding and its importance? We showed that heat acclimation increased VO2 max in a temperate environment but did not change markers of mitochondrial biogenesis and oxidative phosphorylation in the skeletal muscle. ABSTRACT: Heat acclimation (HA) increases tolerance to exercise performed in the heat and may improve maximal oxygen uptake ( V̇O2max ) in temperate environments. However, it is unknown if HA affects the expression of proteins related to mitochondrial biogenesis and oxidative capacity in skeletal muscle. The purpose of this study was to investigate the effect of HA on skeletal muscle markers of mitochondrial biogenesis and oxidative phosphorylation in recreationally trained adults. Thirteen (7 males and 6 females) individuals underwent 10 days of HA. Participants performed two 45 min bouts of exercise (walking at 30-40% maximal velocity at 3% grade) with 10 min rest per session in a hot environment (∼42°C and 30-50% relative humidity). V̇O2max , ventilatory thresholds (VT), and protein expression of peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), mitochondrial transcription factor A (TFAM), calcium/calmodulin-dependent protein kinase (CaMK), electron transport chain (ETC) complexes I-IV, and heat shock protein 72 (Hsp72) in skeletal muscle were measured pre- and post-HA. Comparing day 1 to day 10, HA was confirmed by lower resting core temperature (Tcore ) (P = 0.026), final Tcore (P < 0.0001), mean heart rate (HR) (P = 0.002), final HR (P = 0.003), mean ratings of perceived exertion (RPE) (P = 0.026) and final RPE (P = 0.028). Pre- to post-HA V̇O2max (P = 0.045) increased but VT1 (P = 0.263) and VT2 (P = 0.239) were unchanged. Hsp72 (P = 0.007) increased, but skeletal muscle protein expression (PGC-1α, P = 0.119; TFAM, P = 0.763; CaMK, P = 0.19; ETC I, P = 0.629; ETC II, P = 0.724; ETC III, P = 0.206; ETC IV, P = 0.496) were not affected with HA. HA during low-intensity exercise increased V̇O2max in a temperate environment and Hsp72 but it did not affect markers of mitochondrial biogenesis and oxidative phosphorylation in the skeletal muscle.