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.

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.

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.

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.

Repeated sprint exercise in hypoxia stimulates HIF-1-dependent gene expression in skeletal muscle.

PURPOSE: Our aim was to determine the effect of repeated sprint exercise in hypoxia on HIF-1 and HIF-1-regulated genes involved in glycolysis, mitochondrial turnover and oxygen transport. We also determined whether genes upregulated by exercise in hypoxia were dependent on the activation of HIF-1 in an in vitro model of exercise in hypoxia. METHODS: Eight endurance athletes performed bouts of repeated sprint exercise in control and hypoxic conditions. Skeletal muscle was sampled pre, post and 3 h post-exercise. HIF-1α protein and HIF1A, PDK1, GLUT4, VEGFA, BNIP3, PINK1 and PGC1A mRNA were measured. C2C12 myotubes were exposed to hypoxia and muscle contraction following treatment with a HIF-1α inhibitor to determine whether hypoxia-sensitive gene expression was dependent on HIF-1α. RESULTS: Sprint exercise in hypoxia increased HIF-1α protein expression immediately post-exercise [fold change (FC) = 3.5 ± 2.0]. Gene expression of PDK1 (FC = 2.1 ± 1.2), BNIP3 (FC = 2.4 ± 1.4) and VEGFA (FC = 2.7 ± 1.7) increased 3 h post-exercise in hypoxia but not control. PGC1A mRNA increased 3 h post-exercise in control (FC = 5.16) and hypoxia (FC = 5.7 ± 4.1) but there was no difference between the trials. Results from the in vitro experiment showed that hypoxia plus contraction also increased PDK1, BNIP3, and VEGFA gene expression. These responses were inhibited when HIF-1 protein activity was suppressed. CONCLUSION: Repeated sprint exercise in hypoxia upregulates some genes involved in glycolytic metabolism, mitochondrial turnover, and oxygen transport. HIF-1α is necessary for the expression of these genes in skeletal muscle cells.

The effect of prolonged interval and continuous exercise in the heat on circulatory markers of intestinal barrier integrity.

PURPOSE: The purpose of this study was to determine the effect of prolonged high-intensity interval (INT) and moderate-intensity continuous (CONT) treadmill exercise in the heat on markers of enterocyte injury and bacterial endotoxin translocation. METHODS: Nine males completed 2 h of work-matched exercise in the heat (40 °C and 15% RH) as either INT (2 min at 80% VO2max and 3 min at 30% VO2max) or CONT (~ 50% of VO2max). Blood samples collected pre- and post-exercise were assayed for intestinal fatty acid-binding protein (I-FABP), claudin-3 (CLDN-3), and lipopolysaccharide-binding protein (LBP). RESULTS: I-FABP was significantly increased from pre- to post-exercise in CONT (913.96 ± 625.13 to 1477.26 ± 760.99 pg•mL-1; p = 0.014, d = 0.766) and INT (714.59 ± 470.27 to 1547.93 ± 760.99 pg•mL-1; p = 0.001, d = 1.160). Pre- to post-exercise changes in I-FABP were not different between CONT and INT (p = 0.088, d = 0.414). LBP was significantly increased from pre- to post-exercise in INT (15.94 ± 2.90 to 17.35 ± 3.26 µg•mL-1; p = 0.028, d = 0.459) but not CONT (18.11 ± 5.35 to 16.93 ± 5.39 µg•mL-1; p = 0.070, d = 0.226), and pre- to post-exercise changes in LBP were higher in the INT compared to CONT (p < 0.001, d = 1.160). No significant changes were detected from pre- to post-exercise for CLDN-3 in CONT (14.90 ± 2.21 to 15.30 ± 3.07 µg•mL-1) or INT (15.55 ± 1.63 to 16.41 ± 2.11 µg•mL-1) (p > 0.05). CONCLUSIONS: We conclude that prolonged exercise in the heat induces enterocyte injury, but interval (or intermittent) exercise may cause greater bacterial endotoxin translocation which may increase the risk for local and systemic inflammation.

The effect of interval and continuous work on markers of acute kidney injury in a hot environment.

PURPOSE: To examine the effect of high-intensity interval work (HIIW) and moderate-intensity continuous work (MICW) on markers of acute kidney injury (AKI) and kidney function in a hot environment. METHODS: Nine males completed 2 h of work (2 × 60 min with 10 min passive rest) in a hot environment (40 °C and 15% relative humidity) as either HIIW [2 min at 80% peak oxygen consumption (VO2peak) and 3 min at 30% VO2peak] or MICW (matched for total work of HIIW). Blood and urine samples were collected immediately before (Pre), after (Post), 1 h (1 h Post), and 24 h after (24 h Post) the trials. Urine flow rate (UFR), creatinine clearance, insulin-like growth factor binding protein 7 (IGFBP7), urinary neutrophil gelatinase-associated lipocalin (uNGAL), and urinary kidney injury marker 1 (uKIM-1) were measured to assess kidney function and injury. RESULTS: Log IGFBP7 (p < 0.01), log uNGAL (p < 0.01), and log uKIM-1 (p = 0.01) all displayed a main effect for time after both HIIW and MICW. IGFBP7 (p = 0.01) and uKIM-1 (p < 0.01), corrected for Uosm, were higher after HIIW compared to MICW at Post, while IGFBP7 was also higher 1 h Post after HIIW compared to MICW (p = 0.02). UFR significantly decreasing from Pre to Post (p < 0.01) and 1 h Post (p < 0.01), but no main effect for condition (p = 0.53). CONCLUSION: Both HIIW and MICW in a hot environment caused an increase in biomarkers of kidney injury (IGFBP7, KIM-1, and NGAL), but HIIW may have a greater impact on biomarkers related to AKI.

The effect of repetition tempo on cardiovascular and metabolic stress when time under tension is matched during lower body exercise.

PURPOSE: To investigate the effect of repetition tempo on cardiovascular and metabolic stress when time under tension (TUT) and effort are matched during sessions of lower body resistance training (RT). METHODS: In a repeated-measures, cross-over design, 11 recreationally trained females (n = 5) and males (n = 6) performed 5 sets of belt squats under the following conditions: slow-repetition tempo (SLOW; 10 reps with 4-s eccentric and 2-s concentric) and traditional-repetition tempo (TRAD; 20 reps with 2-s eccentric and 1-s concentric). TUT (60 s) was matched between conditions and external load was adjusted so that lifters were close to concentric muscular failure at the end of each set. External load, total volume load (TVL), impulse (IMP), blood lactate, ratings of perceived exertion (RPE), HR, and muscle oxygenation were measured. RESULTS: Data indicated that TVL (p < 0.001), blood lactate (p = 0.017), RPE (p = 0.015), and HR (p < 0.001) were significantly greater during TRAD while external load (p = 0.030) and IMP (p = 0.002) were significantly greater during SLOW. Whether it was expressed as minimal values or change scores, muscle oxygenation was not different between protocols. CONCLUSION: When TUT is matched, TVL, cardiovascular stress, metabolic stress, and perceived exertion are greater when faster repetition tempos are used. In contrast, IMP and external load are greater when slower repetition tempos are used.

The combined effects of exercise-induced muscle damage and heat stress on acute kidney stress and heat strain during subsequent endurance exercise.

PURPOSE: The purpose of the study was to investigate the combined effect of downhill running and heat stress on muscle damage, as well as on heat strain and kidney stress during subsequent running in the heat. METHODS: In a randomized cross-over study, ten non-heat-acclimated, physically active males completed downhill running in temperate (EIMD in Temp) and hot (EIMD in Hot) conditions followed by an exercise-heat stress (HS) test after 3-h seated rest. Blood and urine samples were collected immediately pre- and post-EIMD and HS, and 24 h post-EIMD (post-24 h). Core temperature and thermal sensation were measured to evaluate heat strain. Serum creatine kinase (CK), maximal voluntary isometric contraction of the quadriceps (MVC) and perceived muscle soreness were measured to evaluate muscle damage. Urinary neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) levels were measured to indicate acute kidney stress. RESULTS: CK, MVC and perceived soreness were not different between conditions at any timepoints. In the EIMD in Hot condition, urinary NGAL was significantly elevated from pre- to post-HS (pre-HS: 6.56 {1.53-12.24} ng/min, post-HS: 13.72 {7.67-21.46} ng/min, p = 0.034). Such elevation of NGAL or KIM-1 was not found in the EIMD in Temp condition. CONCLUSIONS: As compared with downhill running in a temperate environment, downhill running in a hot environment does not appear to aggravate muscle damage. However, elevated NGAL levels following EIMD in a hot environment suggest such exercise may increase risk of mild acute kidney injury during subsequent endurance exercise in the heat.

Moderate-intensity continuous training and high-intensity interval training improve cognition, and BDNF levels of middle-aged overweight men.

The prevalence of overweight and obesity is increasing worldwide, which has been associated with poor cognitive outcomes. Participating in regular physical exercise may also improve cognition, and levels of brain-derived neurotrophic factor (BDNF), but the optimal exercise prescription remains to be elucidated. The purpose of the present study is to compare the effects of moderate intensity continuous training (MICT) and high intensity interval training (HIIT) on cognition, and serum BDNF levels in middle-aged and overweight men. Twenty-five sedentary, overweight men participated in the 8-week training intervention. Subjects were randomized into MICT (n = 12) or HIIT (n = 13) and performed exercise sessions 3x/week for 8-weeks. Cognitive function, and serum BDNF levels were assessed pre- and post-intervention. Statistical analysis was carried out using the Graph Pad Prism 7.0, and the level of significance was set at 5%. Significant improvements were observed in cognitive test scores, and BDNF levels in MICT and HIIT groups (p < 0.05). There were no significant differences in cognitive function between MICT and HIIT. The present study implicates that 8 weeks of MICT or HIIT may be a very useful non-pharmacological treatment option to improve cognitive function, and BDNF levels in middle-aged overweight men.

Aerobic Adaptations to Resistance Training: The Role of Time under Tension.

Generally, skeletal muscle adaptations to exercise are perceived through a dichotomous lens where the metabolic stress imposed by aerobic training leads to increased mitochondrial adaptations while the mechanical tension from resistance training leads to myofibrillar adaptations. However, there is emerging evidence for cross over between modalities where aerobic training stimulates traditional adaptations to resistance training (e.g., hypertrophy) and resistance training stimulates traditional adaptations to aerobic training (e.g., mitochondrial biogenesis). The latter is the focus of the current review in which we propose high-volume resistance training (i.e., high time under tension) leads to aerobic adaptations such as angiogenesis, mitochondrial biogenesis, and increased oxidative capacity. As time under tension increases, skeletal muscle energy turnover, metabolic stress, and ischemia also increase, which act as signals to activate the peroxisome proliferator-activated receptor gamma coactivator 1-alpha, which is the master regulator of mitochondrial biogenesis. For practical application, the acute stress and chronic adaptations to three specific forms of high-time under tension are also discussed: Slow-tempo, low-intensity resistance training, and drop-set resistance training. These modalities of high-time under tension lead to hallmark adaptations to resistance training such as muscle endurance, hypertrophy, and strength, but little is known about their effect on traditional aerobic training adaptations.

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.

HIIT is superior than MICT on cardiometabolic health during training and detraining.

PURPOSE: This study investigated the cardiometabolic health of overweight/obese untrained individuals in response to 8 weeks of HIIT and MICT using a field approach, and to 4 weeks of training cessation (TC). METHODS: Twenty-two subjects performed 8 weeks of moderate intensity continuous training (MICT-n = 11) or high-intensity interval training (HIIT-n = 11) (outdoor running), followed by 4 weeks of TC. Cardiorespiratory fitness, body composition, arterial blood pressure, glucose metabolism and blood lipids were measured pre-training (PRE), post-training (POST) and TC. RESULTS: HIIT improved eight indicators of cardiometabolic health ([Formula: see text], BMI, body fat, visceral fat, systolic blood pressure, total cholesterol, fasting glucose and triglycerides-p < 0.05) while MICT only three ([Formula: see text], BMI, and visceral fat-p < 0.05). After 4 weeks of TC, four positive adaptations from HIIT were negatively affected ( [Formula: see text], visceral fat, systolic blood pressure and total cholesterol-p < 0.05) and three in the MICT group ([Formula: see text], BMI and visceral fat, p < 0.05). CONCLUSION: Eight weeks of HIIT performed in a real-world setting promoted a greater number of positive adaptations in cardiometabolic health of individuals with overweight/obese compared to MICT. Most of the positive effects of the HIIT protocol were also found to be longer lasting and maintained after the suspension of high-intensity interval running for 4 weeks. Conversely, all positive effects of MICT protocols were reversed after TC.

Thermoregulatory and metabolic responses to a half-marathon run in hot, humid conditions.

This study describes the thermoregulatory and metabolic responses during a simulated half-marathon (21 km) run performed outdoors in a hot, humid environment. Ten male runners were recruited for the study, The run was carried out individually under solar radiation on a predetermined path in the following environmental conditions (ambient temperature: 27.96 ± 1.70 °C, globe temperature: 28.52 ± 2.51 °C, relative humidity: 76.88 ± 7.49%, wet bulb globe temperature: 25.80 ± 1.18 °C). Core temperature, skin temperature, head temperature, heat storage, heart rate, expired gases, rating of perceived exertion, and speed were measured or calculated before the start, every 3 km, and immediately following the run. Comparisons were made for each dependent variable using one-way repeated measures analysis of variance tests, and a Bonferroni test. Average run time and pace were 101:00 ± 9:52 min and 4:48 ± 00:16 min km-1, respectively. Participants significantly reduced their running speed, oxygen consumption, and heat storage at 9 km (p < 0.05). While core temperature was significantly increased at 6 km (p < 0.05) before plateauing for the remainder of the run. The key finding was that most of the runners reduced their pace when a Tcore of 39 °C was reached which occurred between 6 and 9 km of the run, yet runners were able to increase their speed demonstrating an "end-spurt" near the end of the run.

Metabolic effects of two high-intensity circuit training protocols: Does sequence matter?

BACKGROUND/OBJECTIVE: The integration of high-intensity interval training (HIIT) and circuit weight training (CWT) is seamless and practical for meeting recommended exercise guidelines. The purpose of this study was to determine the ideal combination of HIIT and CWT to elicit desired acute cardiorespiratory and metabolic responses in variables such as energy expenditure (EE), oxygen consumption (VO2), heart rate (HR), blood lactate (BLa-), excess post-exercise oxygen consumption (EPOC), rating of perceived exertion (RPE), and enjoyment. METHODS: Fourteen trained males (25.7 ±â€¯4.4 yr) completed two exercise protocols matched for volume and recovery periods. On one day, participants performed six HIIT bouts prior to three rounds of a nine exercise CWT protocol (HIC). The second day (separated by ≥ 72 h) consisted of three rounds of three mini-circuits (three exercises per circuit) integrated with three HIIT bouts between the first and second and second and third mini-circuits (TRI). VO2, HR, and EE were monitored throughout both protocols. EPOC for a 20-min duration, [BLa-] (five time points), RPE, and enjoyment were measured post-exercise. RESULTS: Energy expenditure was significantly higher during the HIC compared to the TRI protocol (p = .012), as well as EPOC (p = .034). [BLa-] was significantly greater immediate-, 5min-, 10min- and 20min-post-exercise following HIC as compared to TRI. Mean values for HIC and TRI were similar (p > .05) for HR and RPE. CONCLUSION: Performing HIIT prior to CWT elicits a higher metabolic perturbation compared to the TRI protocol. Although a significant EE difference was detected between the two trials, the practical difference (∼20 kcal) between protocols indicates both protocols are similarly effective for caloric expenditure, metabolic and cardiorespiratory response.

High-intensity interval training reduces monocyte activation in obese adults.

Alterations in the distribution and activation of monocyte subsets are frequently observed in individuals with obesity and their participation in the pathological complications of obesity is proposed. High-intensity interval training (HIIT) can be a time-efficient alternative to counteract the inflammatory outcomes of obesity, but so far, its effects on monocytes in obesity has not been fully explored. In this study, we investigated whether 8 weeks of HIIT can modify the distribution and activation of the three monocyte subsets (classical, intermediate and non-classical monocytes) in individuals with obesity. Our data show that individuals with obesity have a higher percentage of non-classical monocytes compared to control, lean individuals, and consequently an imbalance among the CD16+ monocyte subsets. Also, the expression of HLA-DR by intermediate monocytes is higher in insulin-resistant obese individuals, which indicates monocyte activation in obesity. After 8 weeks of HIIT, the percentage of non-classical monocytes was reduced in individuals with obesity, restoring the balance among the CD16+ monocytes. Also, the expression of HLA-DR by intermediate monocytes in insulin-resistant obese subjects was lower after HIIT. Both findings indicate that monocyte activation in individuals with obesity was reduced by HIIT. These modifications were observed in the absence of changes in weight and body composition, although they were accompanied by the improvement in the metabolic status (reduced insulin levels). Our findings indicate that HIIT can be considered a time-efficient strategy to manage obesity-related monocyte alterations and strengthen the immunomodulatory potential of HIIT.

Late Neutrophil Priming Following a Single Session of High-intensity Interval Exercise.

This study evaluated the effect of an acute high-intensity interval exercise (HIIE) session on the function of human neutrophils. Twelve sedentary men performed a HIIE session (8 bouts of 60 s at 90% of peak power, intercalated with 75 s of active recovery at 30 W). Neutrophils were collected before, 30 min and 24 h after the exercise session for the evaluation of phagocytic capacity, expression of phagocytic receptors, reactive oxygen species generation, and redox status. 24 h after the HIIE session, an increase was observed in both neutrophil phagocytic capacity and yeast-induced generation of reactive oxygen species, which indicates neutrophil priming in response to an acute HIIE session. Neutrophils also presented an increase in superoxide dismutase activity 24 h after the exercise. Improvement in neutrophil function was accompanied by increased serum levels of IL-8 and increased concentration of plasma lactate dehydrogenase. Our findings show a late activating effect of one HIIE session on neutrophils. We propose that priming of neutrophils by HIIE may play a role in skeletal muscle inflammation after exercise.

Telemedicine-Based Health Coaching Is Effective for Inducing Weight Loss and Improving Metabolic Markers.

BACKGROUND: To assess the efficacy of health coaching (HC) delivered through videoconferencing (VC) to favorably change physical activity (PA), weight, and metabolic markers in adults with high body mass index (BMI). MATERIALS AND METHODS: Thirty adults (BMI ≥30 kg/m2) were randomly assigned to one of three groups: VC, in-person (IP), or control group (CG). Participants received wireless watches and weight scales to sync with their personal smartphones; recorded data were wirelessly uploaded to a secure database. Participants assigned to VC and IP received individualized HC by a multidisciplinary team (registered dietitian, exercise physiologist, and medical doctor) based on data uploaded over the 12-week intervention. Steps/day and weight loss were analyzed through analyses of covariance. RESULTS: Within- and between-group changes in weight (kg), glucose, insulin, hemoglobin A1c (HbA1c), and Homeostasis Model Assessment estimate of insulin resistance (HOMA-IR) were analyzed through analyses of variance. Weight loss was greater (p < 0.05) for VC (8.23 ± 4.5 kg; 7.7%) than IP (3.2 ± 2.6 kg; 3.4%) and CG (2.9 ± 3.9 kg; 3.3%), respectively. Steps/day were significantly higher in VC than IP at week 4 and VC was significantly higher than the CG at weeks 6, 8, 9, and 11 (p ≤ 0.05). No within- or between-group differences were found for glucose, insulin, or HbA1C. HOMA-IR decreased for VC only (p ≤ 0.05). CONCLUSIONS: Our innovative, multidisciplinary, telemedicine HC delivered through VC led to more favorable changes in weight loss, PA (steps/day), and HOMA-IR than IP or no HC. VC may be an economical approach to improve health and promote behavior change in obese adults. CLINICAL TRIAL REGISTRATION NUMBER: ClinicalTrials.gov identifier NCT03278951.

Infrared photobiomodulation (PBM) therapy improves glucose metabolism and intracellular insulin pathway in adipose tissue of high-fat fed mice.

Obesity represents a continuously growing global epidemic and is associated with the development of type 2 diabetes mellitus. The etiology of type 2 diabetes is related to the resistance of insulin-sensitive tissues to its action leading to impaired blood glucose regulation. Photobiomodulation (PBM) therapy might be a non-pharmacological, non-invasive strategy to improve insulin resistance. It has been reported that PBM therapy in combination with physical exercise reduces insulin resistance. Therefore, the aim of this study was to investigate the effects of PBM therapy on insulin resistance in obese mice. Male Swiss albino mice received low-fat control diet (n = 16, LFC) or high-fat diet (n = 18, HFD) for 12 weeks. From 9th to 12th week, the mice received PBM therapy (LASER) or Sham (light off) treatment and were allocated into four groups: LFC Sham (n = 8), LFC PBM (n = 8), HFD Sham (n = 9), and HFD PBM (n = 9). The PBM therapy was applied in five locations: to the left and right quadriceps muscle, upper limbs and center of the abdomen, during 40 s at each point, once a day, 5 days a week, for 4 weeks (780 nm, 250 mW/cm2, 10 J/cm2, 0.4 J per site; 2 J total dose per day). Insulin signaling pathway was evaluated in the epididymal adipose tissue. PBM therapy improved glucose tolerance and phosphorylation of Akt (Ser473) and reversed the HFD-induced reduction of GLUT4 content and phosphorylation of AS160 (Ser588). Also, PBM therapy reversed the increased area of epididymal and mesenteric adipocytes. The results showed that chronic PBM therapy improved parameters related to obesity and insulin resistance in HFD-induced obesity in mice.