Background: Previous studies of the Elevation Training Mask (ETM) describe comparisons between groups using the ETM and controls for effects on aerobic performance. However, comparisons have not been made to intermittent hypoxic training (IHT). Further, how the ETM impacts exercise economy is unknown. Therefore, we sought to determine the effects of training with the ETM compared to IHT on aerobic performance and cycling economy. Methods: Thirty participants were randomized into an ETM, IHT, or control group (n = 10 each). Pre-and post-testing occurred using a ramp VO2max test on a cycle ergometer allowing submaximal power output (PO) measures of economy. Economy was measured using POs of 100, 125, and 150W. High-intensity cycling interval training (HIIT) occurred 2x/week for 30 min/session for six weeks. Sessions were 20 min of HIIT (30s at 100% peak power output (PPO) of pre VO2max, 90s active recovery at 25W, 10 bouts) with a 5-minute warm-up and cool-down. Repeated measures ANOVA was used for statistical analyses. RESULTS: All participants improved VO2max, PPO, and PO at ventilatory threshold 2 pre-to post-training (p < 0.05). Interactions between groups showed that the RER for the IHT group increased at 100W and 125W, and decreased at RERmax pre-to post-training while the ETM group showed the opposite response (p < 0.05). Conclusion: The ETM and IHT groups performed similarly to the control at maximal and submaximal effort following six weeks of training. The IHT group, but not the ETM group, experienced an increased glycolytic energy shift during submaximal exercise.

Heat acclimation (HA) increases tolerance to exercise performed in the heat and may improve maximal oxygen uptake (V O 2 max) 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). V O 2 max , ventilatory thresholds (VT), and protein expression of peroxisome proliferatoractivated 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 (T core) (P = 0.026), final T core (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-HAV O 2 max (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,

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 trueV̇normalO2max${\dot V_{{{\rm{O}}_{\rm{2}}}{\rm{max}}}}$. 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.

Implementing permissive dehydration (DEH) during short-term heat acclimation (HA) may accelerate adaptations to the heat. However, HA with DEH may augment risk for acute kidney injury (AKI). This study investigated the effect of HA with permissive DEH on time-trial performance and markers of AKI. Fourteen moderately trained men (age and VO2max = 25 ± 0.5 yr and 51.6 ± 1.8 mL.kg−1.min−1) were randomly assigned to DEH or euhydration (EUH). Time-trial performance and VO2max were assessed in a temperate environment before and after 7 d of HA. Heat acclimation consisted of 90 min of cycling in an environmental chamber (40 °C, 35% RH). Neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) were assessed pre- and post-exercise on day 1 and day 7 of HA. Following HA, VO2max did not change in either group (p = 0.099); however, time-trial performance significantly improved (3%, p < 0.01) with no difference between groups (p = 0.485). Compared to pre-exercise, NGAL was not significantly different following day 1 and 7 of HA (p = 0.113) with no difference between groups (p = 0.667). There was a significant increase in KIM-1 following day 1 and 7 of HA (p = 0.002) with no difference between groups (p = 0.307). Heat acclimation paired with permissive DEH does not amplify improvements in VO2max or time-trial performance in a temperate environment versus EUH and does not increase markers of AKI.

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 in comparison to 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 mini-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. Additionally, 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.