bims-exemet Biomed News
on Exercise metabolism
Issue of 2021‒02‒14
sixteen papers selected by
Javier Botella Ruiz
Victoria University

  1. J Physiol. 2021 Feb 10.
    Brooks GA, Arevalo JA, Osmond AD, Leija RG, Curl CC, Tovar AP.
      After a Century, it's time to turn the page on understanding of lactate metabolism and appreciate that lactate shuttling is an important component of intermediary metabolism in vivo. Cell-Cell and intracellular Lactate Shuttles fulfill purposes of energy substrate production and distribution as well as cell signaling under fully aerobic conditions. Recognition of lactate shuttling came first in studies of physical exercise where the roles of driver (producer) and recipient (consumer) cells and tissues were obvious. Moreover, the presence of lactate shuttling as part of postprandial glucose disposal and satiety signaling has been recognized. Mitochondrial respiration creates the physiological sink for lactate disposal in vivo. Repeated lactate exposure from regular exercise results in adaptive processes such as mitochondrial biogenesis and other healthful circulatory and neurological characteristic such as improved physical work capacity, metabolic flexibility, learning, and memory. The importance of lactate and lactate shuttling in healthful living is further emphasized when lactate signaling and shuttling are dysregulated as occur in particular illnesses and injuries. Like a Phoenix, lactate has risen to major importance in 21st Century Biology. This article is protected by copyright. All rights reserved.
    Keywords:  exercise; fiber type; gene adaptation; gluconeogenesis; glycogenolysis; indirect pathway; lactate shuttle; lactate signaling; microbiome; muscle; postabsorptive metabolism; postprandial metabolism; satiety
  2. Eur J Appl Physiol. 2021 Feb 10.
    Ramos C, Cheng AJ, Kamandulis S, Subocius A, Brazaitis M, Venckunas T, Chaillou T.
      PURPOSE: Carbohydrate (CHO) restriction could be a potent metabolic regulator of endurance exercise-induced muscle adaptations. Here, we determined whether post-exercise CHO restriction following strenuous exercise combining continuous cycling exercise (CCE) and sprint interval exercise could affect the gene expression related to mitochondrial biogenesis and oxidative metabolism in human skeletal muscle.METHODS: In a randomized cross-over design, 8 recreationally active males performed two cycling exercise sessions separated by 4 weeks. Each session consisted of 60-min CCE and six 30-s all-out sprints, which was followed by ingestion of either a CHO or placebo beverage in the post-exercise recovery period. Muscle glycogen concentration and the mRNA levels of several genes related to mitochondrial biogenesis and oxidative metabolism were determined before, immediately after, and at 3 h after exercise.
    RESULTS: Compared to pre-exercise, strenuous cycling led to a severe muscle glycogen depletion (> 90%) and induced a large increase in PGC1A and PDK4 mRNA levels (~ 20-fold and ~ 10-fold, respectively) during the acute recovery period in both trials. The abundance of the other transcripts was not changed or was only moderately increased during this period. CHO restriction during the 3-h post-exercise period blunted muscle glycogen resynthesis but did not increase the mRNA levels of genes associated with muscle adaptation to endurance exercise, as compared with abundant post-exercise CHO consumption.
    CONCLUSION: CHO restriction after a glycogen-depleting and metabolically-demanding cycling session is not effective for increasing the acute mRNA levels of genes involved in mitochondrial biogenesis and oxidative metabolism in human skeletal muscle.
    Keywords:  Endurance exercise; Muscle glycogen; Oxidative metabolism; PGC1A; Sprint interval exercise; Train-low
  3. NPJ Microgravity. 2020 Aug 18. 6(1): 21
    English KL, Downs M, Goetchius E, Buxton R, Ryder JW, Ploutz-Snyder R, Guilliams M, Scott JM, Ploutz-Snyder LL.
      Historically, International Space Station (ISS) exercise countermeasures have not fully protected astronauts' musculoskeletal and cardiorespiratory fitness. Although these losses have been reduced on more recent missions, decreasing the time required to perform in-flight exercise would permit reallocation of that time to other tasks. To evaluate the effectiveness of a new training prescription, ISS crewmembers performed either the high intensity/lower volume integrated Sprint resistance (3 d wk-1) and aerobic (interval and continuous workouts, each 3 d wk-1 in alternating fashion) exercise program (n = 9: 8M/1F, 48 ± 7 y, 178 ± 5 cm, 77.7 ± 12.0 kg) or the standard ISS countermeasure consisting of daily resistance and aerobic exercise (n = 17: 14M/3F, 46 ± 6 y, 176 ± 6 cm, 80.6 ± 10.5 kg) during long-duration spaceflight. Bone mineral density (dual energy X-ray absorptiometry (DXA)), muscle strength (isokinetic dynamometry), muscle function (cone agility test), and cardiorespiratory fitness (VO2peak) were assessed pre- and postflight. Mixed-effects modeling was used to analyze dependent measures with alpha set at P < 0.05. After spaceflight, femoral neck bone mineral density (-1.7%), knee extensor peak torque (-5.8%), cone agility test time (+7.4%), and VO2peak (-6.1%) were decreased in both groups (simple main effects of time, all P < 0.05) with a few group × time interaction effects detected for which Sprint experienced either attenuated or no loss compared to control. Although physiologic outcomes were not appreciably different between the two exercise programs, to conserve time and optimally prepare crewmembers for the performance of physically demanding mission tasks, high intensity/lower volume training should be an indispensable component of spaceflight exercise countermeasure prescriptions.
  4. Acta Physiol (Oxf). 2021 Feb 11. e13625
    Jacobs RA, Lundby C.
      AIM: This study sought to provide a statistically robust reference for measures of mitochondrial function from standardized high-resolution respirometry with permeabilized human skeletal muscle (ex vivo), compare analogous values obtained via indirect calorimetry, arterial-venous O2 differences, and 31 P magnetic resonance spectroscopy (in vivo), and attempt to resolve differences across complementary methodologies as necessary.METHODS: Data derived from 831 study participants across research published throughout March 2009 to November 2019 was amassed to examine the biological relevance of ex vivo assessments under standard conditions, i.e. physiological temperatures of 37 °C and respiratory chamber oxygen concentrations of ~250-500 μM.
    RESULTS: Standard ex vivo-derived measures are lower (Z ≥ 3.01, p ≤ 0.0258) en masse than corresponding in vivo-derived values. Correcting respiratory values to account for mitochondrial temperatures 10 °C higher than skeletal muscle temperatures at maximal exercise (~ 50 °C): i.) transforms data to resemble (Z ≤ 0.8, p > 0.9999) analogous yet context-specific in vivo measures, e.g. data collected during maximal 1-leg knee extension exercise; and ii.) supports the position that maximal skeletal muscle respiratory rates exceed (Z ≥ 13.2, p < 0.0001) those achieved during maximal whole-body exercise, e.g. maximal cycling efforts.
    CONCLUSION: This study outlines and demonstrates necessary considerations when actualizing the biological relevance of human skeletal muscle respiratory control, metabolic flexibility, and bioenergetics from standard ex vivo-derived assessments using permeabilized human muscle. These findings detail how cross-procedural comparisons of human skeletal muscle mitochondrial function may be collectively scrutinized in their relationship to human health and lifespan.
    Keywords:  carbohydrate oxidation rates; fatty acid oxidation rates; human bioenergetics; metabolic flexibility; skeletal muscle mitochondria; skeletal muscle temperature
  5. Front Nutr. 2020 ;7 619216
    Jacob KJ, Sonjak V, Spendiff S, Hepple RT, Chevalier S, Perez A, Morais JA.
      Background: Frailty is a clinical condition associated with loss of muscle mass and strength (sarcopenia). Mitochondria are centrally implicated in frailty and sarcopenia. Leucine (Leu) can alter mitochondrial content in myocytes, while resistance training (RT) is the strongest stimulus to counteract sarcopenia and may enhance mitochondrial biogenesis. Objective: We determined the effects of Leu supplementation and RT on mitochondrial content and function in pre/frail elderly women in a randomized double-blinded placebo-controlled study. Methods: Nineteen pre/frail elderly women (77.5 ± 1.3 y, BMI: 25.1 ± 0.9 kg/m2), based on the Frailty Phenotype, underwent 3-months of RT 3×/week with protein-optimized diet and were randomized to 7.5 g/d of Leu supplementation or placebo alanine (Ala). Pre/post-intervention mitochondrial respiration, reactive oxygen species (ROS) production, calcium retention capacity (CRC), time to permeability transition pore (mPTP) opening, mitochondrial voltage-dependent anion channel (VDAC) protein content, leg press 1-repetition maximum (1RM), and 6-min walk test (6MWT) were measured. Results: No time, supplementation, or interaction effects were observed for respiration, ROS, time to mPTP opening, and CRC. VDAC levels significantly increased in the Leu group post-intervention (p = 0.012). Both groups significantly increased leg press 1RM and 6MWT, with no effect of supplementation. Discussion: Leu supplementation with 3 months of RT increased mitochondrial content. Future studies should investigate if there is an increase in mitochondrial turnover or a shift in quality control (mitophagy) in leucine supplemented pre/frail elderly women who undergo 12 weeks of RT. Clinical Trial Registration:, identifier: NCT01922167.
    Keywords:  frailty; leucine; mitochondria; muscle atrophy; resistance training
  6. J Physiol. 2021 Feb 12.
    Bartlett MF, Fitzgerald LF, Kent JA.
      NEW FINDINGS: The oxygen cost of high-intensity exercise at power outputs above an individual's lactate threshold (LT) is greater than would be predicted by the linear oxygen consumption-power relationship observed below the LT. However, whether these augmentations are caused by an increased ATP cost of force generation (ATPCOST ) or an increased oxygen cost of ATP synthesis is unclear. We used 31 P-MRS to measure changes in cytosolic [ADP] (intramyocellular marker of oxidative metabolism), oxidative ATP synthesis (ATPOX ), and ATPCOST during a 6-stage, stepwise knee extension protocol. ATPCOST was unchanged across stages. The relationship between [ADP] and muscle power output was augmented at workloads above the pH threshold (pHT ; proxy for LT), whereas increases in ATPOX were attenuated. These results suggest the greater oxygen cost of contractions at workloads beyond the pHT is not caused by mechanisms that increase ATPCOST , but rather mechanisms that alter intrinsic mitochondrial function or capacity.ABSTRACT: Increases in skeletal muscle metabolism and oxygen consumption are linearly related to muscle power output for workloads below the lactate threshold (LT), but are augmented (i.e., greater rate of increase relative to workload) thereafter. Presently, it is unclear whether these metabolic augmentations are caused by increases in the ATP cost of force generation (ATPCOST ) or changes in the efficiency of mitochondrial oxygen consumption and oxidative ATP synthesis (ATPOX ). To partition these two hypotheses in vivo, we used 31 P-MRS to calculate slopes relating step-changes in muscle work to concurrent changes in cytosolic phosphates and ATPOX before and after the pH threshold (pHT ; used here as a proxy for LT) within the vastus lateralis muscle of eight young adults during a stepwise knee extension test. Changes in muscle phosphates and ATPOX were linearly related to workload above and below the pHT . However, slopes above the pHT were greater for muscle phosphates (p<0.05) and lower for ATPOX (p<0.05) than were the slopes observed below the pHT . The maximal capacity for ATPOX (Vmax ) and ADP-specific ATPOX also declined beyond the pHT (p<0.05), whereas ATPCOST was unchanged (p = 0.10). These results oppose the hypothesis that high-intensity contractions increase ATPCOST and suggest that greater oxidative metabolism at workloads beyond the pHT is caused by mechanisms that affect intrinsic mitochondrial function or capacity, such as alterations in substrate selection or electron entry into the electron transport chain, temperature-mediated changes in mitochondrial permeability to protons, or stimulation of mitochondrial uncoupling by reactive oxygen species generation. This article is protected by copyright. All rights reserved.
    Keywords:  ATP cost; VO2 slow component; bioenergetics; metabolism; mitochondria; muscle; muscle fatigue; oxidative phosphorylation; uncoupling
  7. Diabetes. 2021 Feb 09. pii: db200790. [Epub ahead of print]
    Nigro P, Middelbeek RJW, Alves CRR, Rovira-Llopis S, Ramachandran K, Rowland LA, Møller AB, Takahashi H, Alves-Wagner AB, Vamvini M, Makarewicz NS, Albertson BG, Hirshman MF, Goodyear LJ.
      Recent studies demonstrate that adaptations to white adipose tissue are important components of the beneficial effects of exercise training on metabolic health. Exercise training favorably alters the phenotype of subcutaneous inguinal white adipose tissue (iWAT) in male mice including decreasing fat mass, improving mitochondrial function, inducing beiging and stimulating the secretion of adipokines. Here, we find that despite performing more voluntary wheel running compared to males, these adaptations do not occur in the iWAT of female mice. Consistent with sex-specific adaptations, we report that mRNA expression of androgen receptor co-activators are upregulated in iWAT from trained male mice, and that testosterone treatment of primary adipocytes derived from the iWAT of male, but not female mice, phenocopies exercise-induced metabolic adaptations. Sex-specificity also occurs in the secretome profile, as we identify Cysteine Rich Secretory Protein 1(Crisp1) as a novel adipokine that is only secreted from male iWAT in response to exercise. Crisp1 expression is upregulated by testosterone and functions to increase glucose and fatty acid uptake. Our finding that adaptations to iWAT with exercise training are dramatically greater in male mice has potential clinical implications for understanding the different metabolic response to exercise training in males and females, and demonstrates the importance of investigating both sexes in studies of adipose tissue biology.
  8. Exp Physiol. 2021 Feb 09.
    Ryan BJ, Foug KL, Gioscia-Ryan RA, Varshney P, Ludzki AC, Ahn C, Schleh MW, Gillen JB, Chenevert TL, Horowitz JF.
      NEW FINDINGS: What is the central question of this study? Does exercise training modify tissue iron storage in adults with obesity? What is the main finding and its importance? Twelve weeks of moderate-intensity exercise or high-intensity interval training lowered whole-body iron stores, decreased the abundance of the key iron storage protein in skeletal muscle (ferritin), and tended to lower hepatic iron content. These findings show that exercise training can reduce tissue iron storage in adults with obesity and may have important implications for obese individuals with dysregulated iron homeostasis.ABSTRACT: The regulation of iron storage is critical to human health, as both excess and deficient iron storage have adverse consequences. Recent studies suggest altered iron storage in adults with obesity, with increased iron accumulation in their liver and skeletal muscle. Exercise training increases iron use for processes such as red blood cell production and can lower whole-body iron stores in humans. However, the effects of exercise training on liver and muscle iron stores in adults with obesity have not been assessed. The aim of this study was to determine the effects of 12 weeks of exercise training on whole-body iron stores, liver iron content, and the abundance of ferritin (the key iron storage protein) in skeletal muscle in adults with obesity. Twenty-two inactive adults (11 women, 11 men; age: 31±6 years, BMI: 33±3 kg/m2 ) completed 12 weeks (4 sessions/week) of either moderate-intensity continuous training (MICT; 45 minutes at 70%HRmax; n = 11) or high-intensity interval training (HIIT; 10 × 1-minute at 90%HRmax, 1-minute active recovery; n = 11). Whole-body iron stores were lower after training, as indicated by decreased plasma concentrations of ferritin (p = 3E-5 ) and hepcidin (p = 0.02) without any change in C-reactive protein. Hepatic R2*, an index of liver iron content, was 6% lower after training (p = 0.06). Training reduced the skeletal muscle abundance of ferritin by 10% (p = 0.03), suggesting lower muscle iron storage. Interestingly, these adaptations were similar in MICT and HIIT. Our findings indicate that exercise training decreased iron storage in adults with obesity, which may have important implications for obese individuals with dysregulated iron homeostasis. This article is protected by copyright. All rights reserved.
    Keywords:  exercise training adaptations; iron homeostasis; iron storage
  9. J Physiol. 2021 Feb 10.
    Scalzo RL, Schauer IE, Rafferty D, Knaub LA, Kvaratskhelia N, Johnson TK, Pott GB, Abushamat LA, Whipple MO, Huebschmann AG, Cree-Green M, Reusch JEB, Regensteiner JG.
      KEY POINTS: People with type 2 diabetes (T2D) have impaired skeletal muscle oxidative flux due to limited oxygen delivery. In the current study, this impairment in oxidative flux in people with T2D was abrogated with a single-leg exercise training protocol. Additionally, single-leg exercise training increased skeletal muscle CD31 content, calf blood flow, and state 4 mitochondrial respiration in all participants.ABSTRACT: Cardiorespiratory fitness is impaired in type 2 diabetes (T2D) conferring significant cardiovascular risk in this population; interventions are needed. Previously, we reported that a T2D-associated decrement in skeletal muscle oxidative flux is ameliorated with acute use of supplemental oxygen, suggesting that skeletal muscle oxygenation is rate limiting to in vivo mitochondrial oxidative flux during exercise in T2D. We hypothesized that single-leg exercise training (SLET) would improve the T2D-specific impairment in in vivo mitochondrial oxidative flux during exercise. Adults with (n = 19) and without T2D (n = 22) with similar body mass indexes and levels of physical activity participated in two weeks of SLET. Following SLET, in vivo oxidative flux measured by 31 P-MRS increased in participants with T2D, but not people without T2D, measured by the increase in initial phosphocreatine synthesis (P = 0.0455 for the group x exercise interaction) and maximum rate of oxidative ATP synthesis (P = 0.0286 for the interaction). Additionally, oxidative phosphorylation increased in all participants with SLET (P = 0.0209). After SLET, there was no effect of supplemental oxygen on any of the in vivo oxidative flux measurements in either group (P>0.02), consistent with resolution of the T2D-associated oxygen limitation previously observed at baseline in subjects with T2D. State 4 mitochondrial respiration also improved in muscle fibers ex vivo. Skeletal muscle vasculature content and calf blood flow increased in all participants with SLET (P<0.0040); oxygen extraction in the calf increased only in T2D (P = 0.0461). SLET resolves the T2D-associated impairment of skeletal muscle in vivo mitochondrial oxidative flux potentially through improved effective blood flow/oxygen delivery. This article is protected by copyright. All rights reserved.
    Keywords:  blood flow; diabetes; exercise; skeletal muscle
  10. Int J Environ Res Public Health. 2021 Feb 09. pii: 1645. [Epub ahead of print]18(4):
    Liu X, Xue X, Tian J, Qin X, Zhou S, Chen A, Han Y.
      The objectives of this study were to compare the antidepressant effects between endurance and resistance exercise for optimizing interventions and examine the metabolomic changes in different types of skeletal muscles in response to the exercise, using a rat model of chronic unpredictable mild stress (CUMS)-induced depression. There were 32 male Sprague-Dawley rats randomly divided into a control group (C) and 3 experimental groups: CUMS control (D), endurance exercise (E), and resistance exercise (R). Group E underwent 30 min treadmill running, and group R performed 8 rounds of ladder climbing, 5 sessions per week for 4 weeks. Body weight, sucrose preference, and open field tests were performed pre and post the intervention period for changes in depressant symptoms, and the gastrocnemius and soleus muscles were sampled after the intervention for metabolomic analysis using the 1H-NMR technique. The results showed that both types of exercise effectively improved the depression-like symptoms, and the endurance exercise appeared to have a better effect. The levels of 10 metabolites from the gastrocnemius and 13 metabolites from the soleus of group D were found to be significantly different from that of group C, and both types of exercise had a callback effect on these metabolites, indicating that a number of metabolic pathways were involved in the depression and responded to the exercise interventions.
    Keywords:  1H-NMR; depression; exercise; metabolomics; skeletal muscle
  11. Am J Physiol Endocrinol Metab. 2021 Feb 08.
    Kumagai H, Coelho AR, Wan J, Mehta H, Yen K, Huang A, Zempo H, Fuku N, Maeda S, Oliveira PJ, Cohen P, Kim SJ.
      Obesity and type 2 diabetes are metabolic diseases, often associated with sarcopenia and muscle dysfunction. MOTS-c, a mitochondrial-derived peptide, acts as a systemic hormone and has been implicated in metabolic homeostasis. Although MOTS-c improves insulin sensitivity in skeletal muscle, whether MOTS-c impacts muscle atrophy is not known. Myostatin is a negative regulator of skeletal muscle mass and also one of the possible mediators of insulin resistance-induced skeletal muscle wasting. Interestingly, we found that plasma MOTS-c levels are inversely correlated with myostatin levels in human subjects. We further demonstrated that MOTS-c prevents palmitic acid-induced atrophy in differentiated C2C12 myotubes, while MOTS-c administration decreased myostatin levels in plasma in diet-induced obese mice. By elevating AKT phosphorylation, MOTS-c inhibits the activity of an upstream transcription factor for myostatin and other muscle wasting genes, FOXO1. MOTS-c increases mTORC2 and inhibits PTEN activity, which modulates AKT phosphorylation. Further upstream, MOTS-c increases CK2 activity, which leads to PTEN inhibition. These results suggest that through inhibition of myostatin, MOTS-c could be a potential therapy for insulin resistance-induced skeletal muscle atrophy as well as other muscle wasting phenotypes including sarcopenia.
    Keywords:  FOXO1; MOTS-c; high-fat-diet; muscle atrophy; myostatin
  12. Am J Physiol Heart Circ Physiol. 2021 Feb 12.
    Weeks KL, Tham YK, Yildiz SG, Alexander Y, Donner DG, Kiriazis H, Harmawan CA, Hsu AT, Bernardo BC, Matsumoto A, DePinho RA, Abel ED, Woodcock EA, McMullen JR.
      The insulin-like growth factor 1 receptor (IGF1R) and phosphoinositide 3-kinase p110a (PI3K) are critical regulators of exercise-induced physiological cardiac hypertrophy, and provide protection in experimental models of pathological remodeling and heart failure. Forkhead box class O1 (FoxO1) is a transcription factor which regulates cardiomyocyte hypertrophy downstream of IGF1R/PI3K activation in vitro, but its role in physiological hypertrophy in vivo was unknown. We generated cardiomyocyte-specific FoxO1 knockout (cKO) mice and assessed the phenotype under basal conditions and settings of physiological hypertrophy induced by 1) swim training, or 2) cardiac-specific transgenic expression of constitutively active PI3K (caPI3KTg+). Under basal conditions, male and female cKO mice displayed mild interstitial fibrosis compared with control (CON) littermates, but no other signs of cardiac pathology were present. In response to exercise training, female CON mice displayed an increase (~21%) in heart weight normalized to tibia length vs untrained mice. Exercise-induced hypertrophy was blunted in cKO mice. Exercise increased cardiac Akt phosphorylation and IGF1R expression, but was comparable between genotypes. However, differences in Foxo3a, Hsp70 and autophagy markers were identified in hearts of exercised cKO mice. Deletion of FoxO1 did not reduce cardiac hypertrophy in male or female caPI3KTg+ mice. Cardiac Akt and FoxO1 protein expression were significantly reduced in hearts of caPI3KTg+ mice, which may represent a negative feedback mechanism from chronic caPI3K, and negate any further effect of reducing FoxO1 in the cKO. In summary, FoxO1 contributes to exercise-induced hypertrophy. This has important implications when considering FoxO1 as a target for treating the diseased heart.
    Keywords:  Foxo1; cardiac hypertrophy; exercise; forkhead box protein; heart disease
  13. Int J Sci Res Methodol. 2020 Sep;16(3): 61-77
    Gulick CN, Peddie MC, Jowett T, Hackney AC, Rehrer NJ.
      Insulin-like growth factor 1 (IGF-1) is a dichotomous hormone. While beneficial for growth/repair, and regulating muscle hypertrophy, high concentrations of IGF-1 are associated with increased risk of cancer and mortality. Factors thought to mediate IGF-1 include dietary protein and exercise. The purpose of this study was to analyze acute effects of dietary protein and/or exercise on plasma free IGF-1 and the time-course thereof to inform individuals who may benefit from increased IGF-1 (muscle growth/repair) or reduced IGF-1 (risk/diagnosis of cancer). Twenty-four participants (11 females, 24.9±4.6y) completed the three-way crossover study consisting of: (1)a high protein (42g) meal; (2)exercise (20min with four 30sec sprints); and (3)exercise followed by a high protein meal. Blood samples were collected fasted at rest, immediately after rest (or 5min after exercise), and at regular intervals throughout a 5h recovery. An additional fasted venipuncture was performed the morning following each condition (24h after baseline). Free IGF-1 was higher at immediately after exercise in the exercise condition (p=0.04). In the protein condition the 24h IGF-1 was 17.5% higher (p=0.02) than baseline. IGF-1 did not change over time in response to exercise with protein. The data gleaned from this study can enhance the knowledge of the time-course effects from protein and/or exercise on IGF-1. This study can provide a foundation for future research to investigate optimal timing and dosage to enhance muscle protein synthesis for athletes, as well as investigate whether consistent high protein meals may chronically elevate IGF-1 and increase the risk of deleterious health outcomes.
    Keywords:  diet; insulin-like growth factor; physical activity; somatotropin
  14. Int J Environ Res Public Health. 2021 Jan 31. pii: 1261. [Epub ahead of print]18(3):
    Domin R, Dadej D, Pytka M, Zybek-Kocik A, Ruchała M, Guzik P.
      Different forms of physical activity-endurance, resistance or dynamic power-stimulate cytokine release from various tissues to the bloodstream. Receptors for exercise-induced cytokines are present in muscle tissue, adipose tissue, liver, brain, bones, cardiovascular system, immune system, pancreas, and skin. They have autocrine, paracrine and endocrine activities. Many of them regulate the myocyte growth and differentiation necessary for muscle hypertrophy and myogenesis. They also modify energy homeostasis, lipid, carbohydrate, and protein metabolism, regulate inflammation and exchange information (crosstalk) between remote organs. So far, interleukin 6 and irisin have been the best studied exercise-induced cytokines. However, many more can be grouped into myokines, hepatokines and adipomyokines. This review focuses on the less known exercise-induced cytokines such as myostatin, follistatin, decorin, brain-derived neurotrophic factor, fibroblast growth factor 21 and interleukin 15, and their relation to various forms of exercise, i.e., acute vs. chronic, regular training in healthy people.
    Keywords:  brain-derived neurotrophic factor; decorin; exercise; exercise-induced cytokines; fibroblast growth factor 21; follistatin; hepatokines; interleukin 15; myokines; myostatin
  15. Int J Environ Res Public Health. 2021 Jan 31. pii: 1262. [Epub ahead of print]18(3):
    Alarcón-Gómez J, Calatayud J, Chulvi-Medrano I, Martín-Rivera F.
      Cardiovascular complications are important causes of morbidity and mortality of Type 1 Diabetes Mellitus (T1DM) people. Regular exercise is strongly recommended to these patients due to its preventive action against this type of disease. However, a large percentage of patients with T1DM people present a sedentary behavior, mainly, because of the fear of a post-exercise hypoglycemia event and lack of time. High-intensity interval training (HIIT) is an efficient and safe methodology since it prevents hypoglycemia and does not require much time, which are the main barriers for this population to doing exercise and increasing physical conditioning. Nineteen sedentary adults (37 ± 6.5 years) with T1DM were randomly assigned to 6 weeks of either HIIT, 12 bouts first 2 weeks, 16 bouts in weeks 3 and 4, and 20 bouts in the last two weeks x 30-s intervals interspersed with 1-min rest periods, performed thrice weekly or to control group, which did not train. VO2max, body composition, heart rate variability (HRV), and fasting glucose were measured as cardiovascular risk factors. We suggest that the 6-week HIIT program used in the present study is safe since no severe hypoglycemia was reported and is an effective strategy in improving VO2max, body composition, HRV, and fasting glucose, which are important cardiovascular risk factors in T1DM people.
    Keywords:  exercise; high-intensity interval training; type 1 diabetes
  16. Perspect Public Health. 2021 Feb 12. 1757913920985898
    Nagpal TS, Everest C, Goudreau AD, Manicks M, Adamo KB.
      AIMS: An increasingly popular exercise modality for women is high-intensity interval training (HIIT). Limited research has assessed HIIT during pregnancy, and as a result, pregnant women may inquire about HIIT on their own through online searches. The purpose of this study was to systematically search and critically evaluate online resources that women may access when inquiring about performing HIIT during pregnancy.METHODS: Following previously published methodology, we systematically examined the online search engine Google with the terms 'HIIT' and 'pregnancy'. Using the 2019 Canadian Guideline for Physical Activity throughout Pregnancy as a reference, we identified evidence-based safety recommendations that apply to all prenatal exercise regimes. All selected links were assessed for whether or not they included evidence-based exercise and pregnancy safety recommendations. Descriptive analyses were performed to report the frequency of each construct.
    RESULTS: Seventy-six links were retrieved, and 33 relevant links were selected for inclusion. The majority of the retrieved links recommended that women should consult a healthcare provider before beginning any exercise programme (67%), and modify the intensity and types of exercises in the active HIIT bout based on general pregnancy-related changes (73%) and individual comfort level (55%). Just under half of the links recommended modifying intensity based on prepregnancy activity level (46%), offered trimester-specific recommendations (42%), and only 12% mentioned contraindications to exercise.
    CONCLUSION: Publicly accessible information online on HIIT during pregnancy does not routinely adhere to evidence-based safety recommendations for prenatal exercise. Further research on HIIT during pregnancy and public dissemination of findings is required.
    Keywords:  Internet; evaluation; exercise; high-intensity interval training; pregnancy