Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241112EnglishN2019January22HealthcareComparison of Effects of Continuous and Interval Training on Aerobic Capacity in Healthy, Non Exercising Young Individuals English0106Saba KhanEnglish Razia NagarwalaEnglish Ashok ShyamEnglish Parag SanchetiEnglishObjective: Participation in aerobic exercise generates increased cardiorespiratory fitness, which results in a protective factor for cardiovascular disease and all-cause mortality. Interval training might cause higher increases in cardiorespiratory fitness in comparison with continuous training; nevertheless, current evidence is not conclusive. This study tests the effect of interval training with moderate intensity continuous training on aerobic capacity (V02 max). Method: 40 young healthy subjects were recruited according to inclusion and exclusion criteria and were randomly allocated into a supervised 6 week endurance training program of 3 weekly sessions of either Interval training ( 5 minutes’ bout at 75%-80% HRMax with 2 minutes of active recovery at 40% -50% HRMax) and continuous training (40%- 60% HR Max) of walking on a treadmill for 30 minutes per session. Primary outcome measure was V02max; secondary outcome measure was resting heart rate, resting respiratory rate, blood pressure and Rating of Perceived Exertion. Results: Vo2max (ml/kg/min) improved significantly in both the groups.(P=0.000). There was reduction in resting heart rate, resting respiratory rate and resting blood pressure in both the groups post 6 weeks of training intervention. Rate of perceived exertion was unchanged in both the groups post training intervention. Conclusion: It was observed that both the groups showed significant improvements in aerobic capacity (Vo2max). There was reduction in resting heart rate, resting respiratory rate and resting blood pressure in both the groups post 6 weeks of training intervention. EnglishInterval training, Continuous training, VO2maxINTRODUCTION Exercise, in general, is one of the best preventive actions to fight illness and maintain health. There is an increasing evidence of cardiovascular problems in present  era, due to which importance of exercise for development of fitness is on rise. There is a slow decline in cardiovascular function with advancing age that is significantly accentuated by a sedentary lifestyle. ACSM has released a physical activity guideline to improve physical fitness. Hence it was recommended that “there should be accumulation of at least 30 minutes of moderate activity on most preferably all days of week.” [1]  Participation in aerobic exercise develops increased cardiorespiratory fitness, which protects from cardiovascular morbidity and mortality. Maximal oxygen consumption (VO2max) provides a measure of the maximal volume of oxygen that the body consumes via the respiratory system and is transported through the bloodstream to be used to release energy in the cell.  VO2max is currently the best indicator to assess Cardiorespiratory fitness and it is directly related to cardiovascular health, and its improvement has been linked to decreases in risk of death from cardiovascular disease. Laukkanen et al. studied the association between low levels of VO2max (37.1 ml/kg/min)[2] In a study conducted by Richard suminski etal, found that 28.1% of Asian college going students aged 18 to 25 years are physically inactive.[3] Low fitness levels are responsible for the highest proportion of deaths, followed by smoking had amongst the four cardiovascular lifestyle factors. Hence interventions to decrease the prevalence of low fitness and smoking can promote reduced mortality rates.[4] Intensity seems to be an important predictor of the effectiveness of fitness training programmes. Moderate-intensity continuous training methods and high-intensity interval training are typically prescribed to increase Cardiorespiratory fitness.  Continuous or long, slow distance training involves steady paced prolonged exercise at either moderate or high aerobic intensity, usually 60-80%Vo2max. Continuous exercise may increase Vo2max, capillary density, oxidative enzyme activity and plasma volume in untrained individuals. [5] Interval training consists of periods of high-intensity exercise alternated by periods of relative rest that makes it possible for patients to complete short work periods at higher intensities. Aerobic interval training is one of the most common training methods to improve athletes’ endurance and training performance. Continuous (CT) and interval training (IT) are both established exercise modalities used in the rehabilitation of patients with chronic diseases as well as to improve aerobic and anaerobic capacity of elite athletes. [6] The sedentary non exercising age group is most susceptible to develop cardiovascular problems hence this study aims to find out the effects of continuous and interval training  modes on Vo2max so as to predict which is more better for improving cardiovascular fitness so that we can make recommendations on how to improve fitness level in young population in the rehabilitation setting so as to maximize training effects and provide a shortened fitness program to promote a better, holistic feeling of health in young individuals. MATERIALS AND METHODS: Subjects  40 Sedentary (≤150 min of aerobic exercise a week) young individuals between 18-28 years of age were recruited to participate in this study. Prior to starting the program, all participants had to accept their voluntary participation by signing an informed consent form. The participants were made to answer PAR-Q (physical activity readiness Questionnaire) questionnaire and those who met the inclusion and exclusion criteria were included in the study. The inclusion criteria were Males and females in 18-28 years age group Healthy, non exercising, recreationally active adults without any co morbid illness. The exclusion criteria were subjects with Body mass index BMI>40, any neuro-musculoskeletal problems, cardiovascular and respiratory problems, Smokers and any other systemic illness. The subjects were randomly assigned into two groups, continuous training and interval training group. Study design Subjects were ascribed randomly using computer generated randomized table into two experimental groups: Continuous training (CT) or Interval training (IT) .20 subjects in each group. Prior to training the subjects were made to walk on treadmill (Trackmaster® model TMX 425C) and predicted Vo2max (Max aerobic capacity) was calculated according to modified Bruce protocol. The equation for calculation of Vo2Max using modified Bruce protocol is: VO2max = 3.5+ [0.1*speed] + [1.8*speed*grade][1] Training program: Subjects performed 3 training sessions per week in the laboratory over a 6 weeks period (18 sessions). CONTINUOUS TRAINING PROTOCOL consisted of  5min of warm up –stretching, spot jogging , 30 minutes of walking on treadmill (Trackmaster® model TMX 425C) at40%- 60% HR Max followed by 5 minutes of cool down which included stretching, spot jogging, breathing exercises. INTERVAL TRAINING PROTOCOL consisted of  5 minutes of warm up-stretching, spot jogging, 30 mins training including-5 minutes’ bout of treadmill exercise at 75%-80%  HRMax with 2 minutes of active recovery, i.e. treadmill walking at 40% -50% HRMax  followed by 5 minutes of cool down which included stretching, spot jogging, breathing exercise. The intensity of each interval training session was reached and adjusted manually throughout the session by a trained investigator manipulating the speed and incline of the treadmill to reach the target heart rate. Pre training and Immediate post training Heart rate (HR), Respiratory rate (RR), Blood pressure (BP) and Rating of perceived exertion (RPE) using Borg’s scale was obtained. (6-20 Borg’s scale) All the subjects underwent supervised training for 6 weeks, 3 times per week on alternate days. Post 6 weeks of training Vo2max (aerobic capacity) was again calculated using modified Bruce protocol on treadmill (Trackmaster® model TMX 425C). OUTCOME MEASURES The primary outcome measure was Pre training and post training Vo2max using Modified Bruce protocol on treadmill. The secondary outcome measures were pre training and post training vitals HR, RR, BP and Rate of perceived Exertion (RPE). STATISTICAL ANALYSIS: The statistical analysis was done by using SPSS software 16. P value was set at 0.05. The intra group pre and post test aerobic capacity (Vo2max), BP, HR, RR were analysed using paired t test. The inter group post test scores of aerobic capacity(Vo2max) , BP, HR, RR were analysed using unpaired t test. RESULTS: 40 patients (20 in each group) were enrolled and all completed the study, without any dropouts. As shown from table 1 and table 2, Vo2max improved significantly in continuous training and interval training groups respectively. TABLE 1 (VO2 max of cont. training) t(df)=- 12.50(19); p value=0.000. The p value was set at 0.05. The p value is less than 0.05 for intra group analysis for continuous training. Hence it is statistically significant TABLE 2 (VO2max of interval training group) t(df)= - 17.52(19); p value=0.000; pEnglishhttp://ijcrr.com/abstract.php?article_id=2553http://ijcrr.com/article_html.php?did=25531. ACSM guidelines for exercise testing and prescription. 9th Edition. 2.  Laukkanen JA, et al. Cardiovascular fitness as a predictor of mortality in men. Arch Intern Med. 2001;161(6):825–31. 3. Richard R. Suminski PhD, Rick Petosa PhD, Alan C. Utter PhD & James J. Zhang PhD. Physical Activity Among Ethnically Diverse College Students. Journal of American College Health Vol. 51, Iss. 2, 2002 4. Xuemei Sui,1 Hongjuan Li etal. Percentage of Deaths Attributable to Poor Cardiovascular Health Lifestyle Factors: Findings from the Aerobics Center Longitudinal Study. Epidemiology Research International, Volume 2013 (2013), Article ID 437465. 5. Mazoochi M, Fateminezhad SE, Mazoochi T. Effects of Continuous and Interval Training on Different Fitness Parameters in Athletes. World applied sciences journal. 2013; 28(3):312-5. 6. Daussin FN, Zoll J, Dufour SP, Ponsot E, et al Effect of interval versus Continuous training on cardiorespiratory and mitochondrial functions: relationship to aerobic performance improvements in sedentary subjects. American journal of physiology-regulatory, integrative and comparative Physiology. 2008 Jul 1; 295(1):R264-72 7. J. Myers, M. Prakash, V. Froelicher, D. Do, S. Partington, J.E. Atwood, Exercise capacity and mortality among men referred for exercise testing, N. Engl. J. Med. 346 (11)(2002) 793–801. 8. Pour-Abdi, Kh. et al. (2013). Effects of Short-Term Interval Training Courses on Fitness and Weight Loss of Untrained GirlsAnn Appl Sport Sci, 1(2): 1-9. 9. Esfarjani F1, Laursen PB. Manipulating high-intensity interval training: effects on VO2max, the lactate threshold and 3000 m running performance in moderately trained males. J Sci Med Sport. 2007 Feb;10(1):27-35. Epub 2006 Jul 28 10. Hottenrott K, Ludyga S, Schulze S. Effects of high intensity training and Continuous endurance training on aerobic capacity and body composition in recreationally active runners. Journal of sports science & medicine. 2012 Sep;11(3):483 11. Fox EL, Mathews DK. The Physiological Basis of Physical Education and Athletics. 3rd ed: Saunders College Publishing; 1981. 677 p. 12. Fisher G, Brown AW, Bohan Brown MM, Alcorn A, Noles C, Winwood L, et al. (2015) High Intensity Interval- vs Moderate Intensity- Training for Improving Cardiometabolic Health in Overweight or Obese Males: A Randomized Controlled Trial. PLoS ONE 10(10): e0138853. Journal. Pone.0138853 13. Brandon Swayer, Welsey J Tucker et al Effects of high-intensity interval training and moderate-intensity continuous training on endothelial function and cardiometabolic risk markers in obese adults. J Applied Physiol, 2016.115  2/japplphysiol.00024.2016. 14. Burgomaster KA, Howarth KR, Phillips SM, Rakobowchuk M, Macdonald MJ, McGee SL, et al. 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Oxygen uptake kinetics for various intensities of constant-load work. J Appl Physiol 33:351–356, 1972. 20. Kenny W. L. et al (1985) parasympathetic control of resting heart rate, relationship to aerobic power. Med. Sci. Sports Exer, 17:451 21. Marcos B. Almeida and Claudio Gil S. Araújo, Effects of aerobic training on heart rate, Rev Bras Med Esporte. Vol. 9, No. 2 – Mar/Abr, 2003. 22. Ve´ronique A. Cornelissen, Robert H. Fagard. Effects of Endurance Training on Blood Pressure, Blood Pressure–Regulating Mechanisms, and Cardiovascular Risk Factors, Hypertension. 2005;46:667-675. 23. William McArdle et al 2010,7th edition,Exercise Physiology.886-888. 24. Maeda S, Tanabe T, Otsuki T, et al: Moderate regular exercise increases basal production of nitric oxide in elderly women. Hypertens Res 2004; 27: 947–953. 25. Maeda S, Tanabe T, Miyauchi T, et al: Aerobic exercise training reduces plasma endothelin-1 concentration in older women. J Appl Physiol 2003; 95: 336–341. 26. 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Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241112EnglishN2019January22HealthcareAn Innovative Quinone (Pyrroloquinoline Quinone) and its Antiproliferative Effects English0710Flores-EncarnacionEnglish M.English Cabrera-Aguilar I.English Aguilar-Gutierrez G.R.English Cabrera-MaldonadoEnglish C.EnglishThe pyrroloquinoline quinine is a cofactor discovered in bacteria. It is associated with various bacterial soluble and membrane enzymes that directly oxidize sugars, alcohols, aldehydes. In higher organisms, it has been reported that pyrroloquinoline quinine acts as a potent free radical scavenger and it seems to intervene in different processes causing remarkable benefits. One of the most important effects is that pyrroloquinoline quinine induced apoptosis in different cancer cell lines. It is interesting to observe the role of pyrroloquinoline quinine as pro-apoptotic agent. This review shows the most relevant aspects of this cofactor and its antiproliferative effects. EnglishPyrroloquinoline quinone, PQQ, Cofactor, Effect, AntiproliferativeINTRODUCTION PQQ is a substance of quinoid nature discovered as a cofactor in different bacterial genera (Amador-Bravo, 2016; Ameyama et al., 1991; Choi et al., 2008; Misra et al., 2012). As a cofactor, it catalyzes the oxidation of organic compounds such as monosaccharides, alcohols and short chain aldehydes. It has been reported that PQQ is linked covalently and non-covalently to enzymes (Attwood et al., 1991; Flores-Encarnación et al., 2004; Goodwin and Anthony, 1998; Matsushita et al., 2002; Naveed et al., 2016). Due to its quinoid nature, PQQ has very active carbonyl groups, being a powerful antioxidant agent. It has been observed that the presence of PQQ in certain bacterial genera facilitates the activation of alternative metabolic pathways for the utilization of sugars; it also favors the production of high quantities of acidic substances in the external environment of bacteria by direct oxidation of sugars or alcohols (Choi et al., 2008). PQQ is a novel quinone of bacterial origin that has changed the vision regarding diseases such as cancer because PQQ has been proposed as a possible alternative for the treatment of this disease, according to results obtained in different cell lines. In recent years, the benefits of PQQ have been demonstrated when this substance is administered in plants or diet of different experimental animals(Amador-Bravo et al., 2016; Bauerly et al., 2011; Choi et al., 2008; Flores-Encarnación et al., 2014; Harris et al., 2013; Misra et al., 2012; Oteino et al., 2015). For example, it has a been attributed to PQQ the promotion of growth factors in tomato plantations, increasing amount of macronutrients and number of fruits. In rats, the use of a diet supplemented with PQQ showed a significant change in the learning (Amador-Bravo et al., 2016; Fukui et al., 2001; Harris et al., 2013; Ohwada et al., 2008). It has been reported that PQQ acts as a potent free radical scavenger; it suppresses the production of superoxide radicals(Hamagishi et al., 1988; Matsumoto et al., 1988; Zhang et al., 2013). PQQ has been described as a new vitamin and it seems to intervene in different processes in higher organisms causing remarkable benefits(McIntire, 1998). In recent years, the effect of PQQ on different cancer cell lines has been studied and it has been observed that PQQ induces apoptosis (Min et al., 2014). This review shows the most relevant aspects of PQQ and its antiproliferative effects. PQQ PQQ is a soluble anionic compound of low molecular weight, which has been classified as a new vitamin and as an essential nutrient, since it has been proven that it plays important roles: in cell proliferation, it is an antioxidant of lipid peroxidation and its beneficial effects have also been observed in cellular lesions (Shui et al., 2015; Azizi et al., 2014). PQQ is a nutrient that is well distributed in nature and serves as a non-covalent cofactor of redox reactions in certain bacterial dehydrogenase (named quinoproteins) (Flores-Encarnación et al., 2004; Matsushita et al., 2002; Tao et al., 2007). PQQ is not synthesized in mammals, however it has been found in several levels of concentration in plants, in certain foods, such as kiwi, egg, wine, even in human breast milk (Noji et al., 2007). It has been found that PQQ develops many important functions in humans and animals, including roles in nutrition, protection of the heart by ischemia, preventing damage to the liver by alcohol, sequestering free radicals from the body, increasing the level of nerve growth factor (in astrocytes) and inhibiting melanin production in melanoma cells (Fukui et al., 2001; Wang et al., 2014). PQQ as a vitamin PQQ has been proposed as a new vitamin because it had beneficial effects on healthy cells at low concentrations (nanomolar to micromolar order) (Chowanadisai et al., 2010; Steinberg et al., 2003). It is known that glutamate is the free amino acid more abundant in the central nervous system but excess glutamate can affect progenitor cells and induces apoptosis in neural trunkand other cells(Pavlovic et al., 2006). However, in vitro studies have shown that when the cells were cultured at different PQQ concentrations (3 nM to 30 mM), it was observed that PQQ favored cell proliferation and significantly attenuated cell damage induced by glutamate (Shui et al., 2015). On the other hand, it is known that vitamins perform their function in team and in certain specific places of the body. Some authors have studied the effect of PQQ and vitamin E in peripheral nerves such as sciatica. They discovered that PQQ together with vitamin E favored the fastest recovery from nerve damage (increasing the regeneration of axons). Therefore, those two agents were been proposed for an effective regeneration in peripheral nerve lesions (Azizi et al., 2014; Naveedet al., 2016).Tao et al., (2007) proposed to PQQ as a cardioprotective agent after observing a remarkable reduction of peroxides treating adult rat myocardium cells with H2O2 and PQQ. PQQ as growth promoter This novel quinone was proposed as a potent growth factor in mice and as a promoter of DNA synthesis in human fibroblasts(Amador-Bravo et al., 2016;Chowanadisai et al., 2010;Harris et al., 2013; Misra et al., 2012). Kumazawa et al., (2007) observed in NIH3T3mouse fibroblasts that PQQ increased cell proliferation through of signals related to Rats and it was observed that effect of PQQ derived from regulation of nitric oxide (NO) levels. Those studies contributed to expand understanding of cellular mechanisms, cell signaling and gene expression relevant to PQQ in mammals (Kumazawa et al., 2007). On the other hand, it has been reported that coenzymes such as PQQ showed a stimulating effect on the synthesis of nerve growth factor in mouse fibroblasts and BALBc/3T3 cell line, concluding that PQQ plays a important role in neuronal survival (Azizi et al., 2014; Misra et al., 2012; Murase et al., 1993). The effect of PQQ has also been studied in fibroblasts, myocytes and mouse brainmicrovascular endothelial cells, where it was observed that PQQ in nanomolar concentrations protected these cells from high glucose-induced damage, thus reducing apoptosis and increasing the number of mitochondria in the cells. Apparently the protective effect was due to intracellular expression of hypoxia-inducible factor 1 alpha subunit (HIF-1α) (Wang et al., 2014). It is known that liver fibrosis develops when there is chronic inflammation and destruction of liver cells, however it has been observed that PQQ has a suppressive, anti-oxidant and anti-fibrogenic effect. It has been reported that PQQ exerted a potent anti-fibrotic activity and reactive oxygen species (ROS) scavenging activity in Balb/C mouse models of liver fibrosis (Jia et al., 2015). In the majority of the studies that have been carried out, the effect of PQQ in nanomolar concentration has been tested, however in the last years other studies have been developed in different cell lines of malignant cells, showing that in micromolar quantities PQQ has apoptotic effects (Min et al., 2014). The antiproliferative effects of PQQ It has been reported that the murine melanoma cell line B16F1is characterized because melanocytes produce a large amount of tyrosinase enzyme. Tyrosinase is a key enzyme in melanin synthesis and that in high amounts produces hyperpigmentation of the skin and even cancer (melanoma) (Sato et al., 2008).Sato and Toriyama (2009) reported that PQQ between 12.5 to 25 μM inhibited the synthesis of mRNA that codes for tyrosinase involved in the production of melanin. These authors observed a decrease in cell proliferation and melanin production. Although the mechanism of action is still unknown, it has been proposed PQQ as a possible treatment against melanogenesis and hyperpigmentation disorders. In cell lines A-549 (adenocarcinoma of human lung), Neuro-2A (mouse neuroblastoma) and HCC-LM3 (human hepatocellular carcinoma), it has been observed that PQQ at concentrations 30 to 75 μM suppressed cell proliferation by inducing apoptosis. In addition, it was observed that PQQ increased the activity of caspase-3, produced cell cycle arrest in G0/G1 phase and produced the intracellular accumulation of reactive oxygen species (ROS) and the decline of ATP levels (Min et al., 2014). In the cell line A431 (human squamous cell carcinoma), it has been observed that PQQ at concentrations in the nanomolar order, promoted cell proliferation increasing growth up to 180%, however at concentrations in the micromolar order PQQ induced apoptosis (Kimura et al., 2012). In the cell line U937 (human promonocitic leukemia), it was reported that PQQ at concentrations of 50-100 μM induced a depletion of glutathione and, consequently, an increase in reactive oxygen species (ROS). The decrease in glutathione led to the cells suffering necrosis, indicating that PQQ increased cytotoxicity due to the change in the cellular redox state. Thus, glutathione depletion can change the mode of cell death to necrosis in the presence of PQQ. The modulation of intracellular glutathione could be a strategy to enhance the cytotoxicity of PQQ (Nunone et al., 2008; Shankar et al., 2013). As a scavenger of reactive oxygen species, PQQ appears to be a potent neuroprotector (Scanlon et al., 1997). Zhang et al. (2009 ) reported that the addition of 1 to 20 μM of PQQ in the human neuroblastoma cell line SH-SY5Y, together with the beta-amyloid protein (Aβ), prevents the damage caused by the latter, thus avoiding apotosis. Beta-amyloid proteins have been proposed as one of the causes of Alzheimer's disease that produces neurotoxicity (increasing the production of reactive oxygen species) and induces apoptosis of neurons (Zhang et al. (2013). The alpha-synuclein (α-syn) is a small soluble protein expressed primarily at presynaptic terminals in the central nervous system and it is related to several neurodegenerative diseases, including Parkinson’s disease (Amador-Bravo et al., 2016). The recent data suggest that α-syn has a role in regulating membrane stability and neuronal plasticity (Overk et al., 2014). When the α-syn is mutated the function is lostcausing the formation of bodies of Lewis, cytotoxicity, apoptosis in neurons of the substantia nigra and therefore Parkinson’s disease (Kim et al., 2010; Kobayashi et al., 2010;Overk et al., 2014; Recchia et al., 2004). On the other hand, the rotenone is a substance that has been used as a natural pesticide. Its use has increased in recent years. However, rotenone can cross the brain barrier by penetrating the cell membrane and acting as a potent inhibitor of mitochondrial complex I leading to cell death. It has been tested in several cellular models that PQQ added to different concentrations in the presence of rotenone, protects the cells from damage and delays their harmful effects (Qin et al., 2015). CONCLUSION PQQ is a novel cofactor that can act as a vitamin in nanomolar concentrations; at higher concentrations PQQ could be used for the treatment of certain diseases. PQQ can induce apoptosis in cancer cells, it is also protective of neurons, of myocardium and stimulates the cognitive system, among other things. However, PQQ can also have pro-oxidant characteristics and by binding to certain compounds can exacerbate cell toxicity. ACKNOWLEDGEMENTS Thank to PRODEP and Facultad de Medicina-BUAP for the facilities provided for the development of this work. CONFLICT OF INTEREST Authors have no conflict of interest. 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