Prolonged treadmill running in normobaric hypoxia causes gastrointestinal barrier permeability and elevates circulating levels of pro- and anti-inflammatory cytokines

Hill, Garrett W; Gillum, Trevor; Lee, Benjamin; Romano, P; Schall, Zach J; Hamilton, Ally M; Kuennen, Matthew R.

doi:10.1139/apnm-2019-0378

Cited by 26 publications

(31 citation statements)

References 57 publications

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“…* P ≤ 0.05. n = 9. Similar to our findings, Lee and Thake (2017) and Hill et al (2020) reported increases in I-FABP following exercise in hypoxic (13.5%…”

Section: Discussionsupporting

confidence: 93%

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

McKenna

Fennel

Berkemeier

et al. 2022

Experimental Physiology

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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.

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“…* P ≤ 0.05. n = 9. Similar to our findings, Lee and Thake (2017) and Hill et al (2020) reported increases in I-FABP following exercise in hypoxic (13.5%…”

Section: Discussionsupporting

confidence: 93%

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

McKenna

Fennel

Berkemeier

et al. 2022

Experimental Physiology

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“…Finally, we were not able to set another trial using the same absolute exercise intensity between hypoxia and normoxia. In the previous study, endurance exercise under hypoxia caused greater IL-6 elevation compared with exercise at the same absolute exercise intensity (i.e., same running velocity) under normoxia (Hill et al, 2020). Therefore, muscle damage and inflammatory responses after endurance training hypoxia may be augmented when the same absolute exercise intensity is selected under normoxia.…”

Section: Discussionmentioning

confidence: 85%

“…Some of the previous studies demonstrated the effect of a single session of exercise under hypoxia on muscle damage and inflammatory response (Sumi et al, 2018;Britto et al, 2020;Hill et al, 2020). In our previous study, we compared the acute responses of muscle damage and inflammation following a single session of endurance exercise between hypoxia and normoxia.…”

Section: Introductionmentioning

confidence: 97%

Impact of Three Consecutive Days of Endurance Training Under Hypoxia on Muscle Damage and Inflammatory Responses

Sumi

Yamaguchi

Goto

2021

Front. Sports Act. Living

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Purpose: The purpose of this study was to determine the effect of 3 consecutive days of endurance training under hypoxia on muscle damage, inflammation, and performance responses.Methods: Nine active healthy males completed two trials in different periods, consisting of either 3 consecutive days of endurance training under hypoxia [fraction of inspired oxygen (Fio2): 14.5%, HYP] or normoxia (Fio2: 20.9%, NOR). They performed daily 90-min sessions of endurance training consisting of high-intensity endurance interval pedaling [10 × 4-min pedaling at 80% of maximal oxygen uptake (V˙o2max) with 2 min of active rest at 30% of V˙o2max] followed by 30-min continuous pedaling at 60% of V˙o2max during 3 consecutive days (days 1–3). Venous blood sample, muscular performance of lower limb, and score of subjective feelings were determined every morning (days 1–4) to evaluate muscle damage and inflammation. On day 4, subjects performed an incremental exercise test (IET) to evaluate the performance response.Results: Pedaling workload during daily endurance training was significantly lower in the HYP trial (interval exercise: 166 ± 4 W) than in the NOR trial (194 ± 8 W; P < 0.0001). Serum creatine kinase (CK) and high-sensitivity C-reactive protein (hsCRP) concentrations did not significantly change during days 1–4 in either trial. Maximal voluntary contraction (MVC) of knee extension (P < 0.0001) and drop jump (DJ) index (P = 0.004) were significantly decreased with training in both trials, with no significant difference between trials. The muscle soreness and fatigue scores significantly increased in both trials (P < 0.0001). However, the HYP trial showed a significantly lower score of fatigue on day 4 compared with the NOR trial (P = 0.004). Maximal aerobic power output during IET on day 4 did not significantly differ between trials.Conclusion: Three consecutive days of endurance training under hypoxia induced comparable levels of muscle damage, inflammation, and performance responses compared with the same training under normoxia.

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“…Where measured, I-FABP responses quickly recover within 1-2 h of exercise termination, irrespective of the intensity/duration of the protocol [124,140]. Like DSAT results, I-FABP responses are elevated in otherwise matched exercise interventions comparing: hypoxic (F i O 2 = 0.14) versus normoxic environments [137,143]; permissive dehydration versus rehydration [144]; and post NSAID ingestion [123]. In comparison, since initial investigation [86], no studies have monitored the magnitude and time-course of I-BABP responses following exercise.…”

Section: Severity Of Gi Barrier Integrity Loss Following Exertional-hmentioning

confidence: 90%

The Gastrointestinal Exertional Heat Stroke Paradigm: Pathophysiology, Assessment, Severity, Aetiology and Nutritional Countermeasures

Ogden

Child

Fallowfield³

et al. 2020

Nutrients

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Exertional heat stroke (EHS) is a life-threatening medical condition involving thermoregulatory failure and is the most severe condition along a continuum of heat-related illnesses. Current EHS policy guidance principally advocates a thermoregulatory management approach, despite growing recognition that gastrointestinal (GI) microbial translocation contributes to disease pathophysiology. Contemporary research has focused to understand the relevance of GI barrier integrity and strategies to maintain it during periods of exertional-heat stress. GI barrier integrity can be assessed non-invasively using a variety of in vivo techniques, including active inert mixed-weight molecular probe recovery tests and passive biomarkers indicative of GI structural integrity loss or microbial translocation. Strenuous exercise is strongly characterised to disrupt GI barrier integrity, and aspects of this response correlate with the corresponding magnitude of thermal strain. The aetiology of GI barrier integrity loss following exertional-heat stress is poorly understood, though may directly relate to localised hyperthermia, splanchnic hypoperfusion-mediated ischemic injury, and neuroendocrine-immune alterations. Nutritional countermeasures to maintain GI barrier integrity following exertional-heat stress provide a promising approach to mitigate EHS. The focus of this review is to evaluate: (1) the GI paradigm of exertional heat stroke; (2) techniques to assess GI barrier integrity; (3) typical GI barrier integrity responses to exertional-heat stress; (4) the aetiology of GI barrier integrity loss following exertional-heat stress; and (5) nutritional countermeasures to maintain GI barrier integrity in response to exertional-heat stress.

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Prolonged treadmill running in normobaric hypoxia causes gastrointestinal barrier permeability and elevates circulating levels of pro- and anti-inflammatory cytokines

Cited by 26 publications

References 57 publications

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

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

Impact of Three Consecutive Days of Endurance Training Under Hypoxia on Muscle Damage and Inflammatory Responses

The Gastrointestinal Exertional Heat Stroke Paradigm: Pathophysiology, Assessment, Severity, Aetiology and Nutritional Countermeasures

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