Ethnographic Study Summary

However, there are semi-effective ways to counter the aging process of one’s metabolism. Some of the most effective ways a person can increase their energy rate, therefore increase their metabolic rate is through physical exercise. Exercise develops one's muscle mass and body fat, resulting in an increase in BMR and metabolic rate. Performing aerobic workouts, sometimes known as cardio-exercise requires pumping of oxygenated blood by the heart to deliver oxygen to working muscles. Aerobic exercise stimulates the heart rate and breathing rate to increase in a way that can be sustained for the exercise session (3). On the flip side, anaerobic exercise is short-lasting, high-intensity activity, where your body's demand for oxygen exceeds the oxygen supply available. Anaerobic exercise relies on energy sources that are stored in the muscles and, unlike aerobic exercise, is not dependent on oxygen from the air (2). Both forms of exercise can be effectively utilized to increase one’s metabolism and combat body

These can range from lifting very heavy weights, to intricate tasks such as playing a piano, to pumping blood non-stop for a lifetime. To accommodate such wide variation, muscles have high plasticity and can adapt to changing activity levels and environments. For example, endurance exercise increases the oxidative capacity and makes muscle more fatigue resistant while disuse leads to muscle atrophy [1]. The pathways underlying these changes and muscle plasticity are therefore of great interest.

Possible explanations for differences between our findings and other published data could be attributed to age, exercise protocol and intensity of exercise. Serum creatine kinase (CK) and lactate dehydrogenase (LDH) are an indication of the degree of metabolic adaptation to physical training of skeletal muscles. These enzymes are involved in muscle metabolism, and their serum concentration is normally very low. They increase considerably after intensive exercise. Changes in serum activity of muscle enzymes have been reported in normal subjects and athletes after strenuous exercise. The amount of enzyme efflux from muscle tissue to serum can be influenced by physical exercise. These results showed that the use of BCAA didn 't reduce serum CK activity 24 and 48 hrs after heavy resistance exercise. Serum CK activity was elevated in all groups after exercise and was highest in the placebo group. It was obvious in BCAA group that the Ck and LDH levels were non-significantly lower than the control one indicating that the muscle soreness is lower (higher muscle fitness). The positive action of BCAA in lowering the muscle soreness could be referred to

For example; increases in 100 and 200m swimming performance (22) and increases in 2000m rowing performance (18) as well as increases in cycling capacity (17) have been demonstrated (for reviews see Refs. 10, 16). However, the precise mechanisms by which carnosine may elicit increases in exercise performance and capacity remain to be fully elucidated. During high intensity exercise, hydrogen cation (H+) accumulation is significantly increased, which results in significantly decreased intracellular pH (23). Furthermore, H+ accumulation is reported to disrupt the ability of the muscle’s contractile machinery to function (8, 12). Due to carnosine’s imidazole ring having a pKa of 6.83, it is well acknowledged that carnosine is a perfectly suited intracellular pH buffer across the entire physiological range (4). Therefore, during high intensity exercise where H+ accumulation is likely to be the biggest contributing factor that limits exercise performance, carnosine’s ability to increase intracellular buffering capacity and maintain muscular function, is suggested to be the most pertinent mechanism by which carnosine evokes an ergogenic effect (27). Hill et al., (17) suggested increased intracellular buffering capacity resulting from an increase in muscle carnosine concentrations explained a significant increase (TWD: +16.2%) in cycling capacity following 10 weeks of BA

Resistance training until failure was first introduced during World War II as a way to speed up injury rehabilitation of soldiers. (Sampson, 2015, p. 1) Several studies have suggested repeating an exercise to the point where neuromuscular system can no longer produce adequate force to overcome a specific workload. Training to failure acutely causes motor damage but in turn causes increased motor unit recruitment, elevates mechanical stress. (Cardoso De Souza, 2013, p. 2) Metabolic by products (H+, Lactate, Pi, Cr, K+) accumulate inside and outside of the muscle fibers during fatigue. (Folland, 2002, p. 1) Recent studies suggest that metabolic accumulation during high resistance training to failure can have a positive muscle neuromuscular adaptations

This essay is based on research done over a study of mitochondrial myopathy, which is a disease of the muscular system. This is a consideration of the short communication article titled; “Short- and long-term effects of endurance training in patients with mitochondrial myopathy”, published by the European Journal of Neurology 2009. This was a collaborative project authored by; T.D. Jeppesen, M. Duno, M. Schwartz, T Krag, J. Rafiq, F. Wibrand, and J. Vissing. Hosted by; Neuromuscular Research Unit, Depatment of Neurology, and the Copenhagen Muscle Center; and “Department of Clinical Genetics, University of Copenhagen, Rigshospitalet, Copenhagon, Denmark. The purpose of this research was to determine whether endurance training was safe for patients with mitochondrial myopathy.

The aim of this study was to investigate the modulation of satellite cell content and myonuclear number in cells, following 30 and 90 days of resistance training and which was then followed by 3, 10, 30, 60 and 90 days of detraining (which is an extended break from regular activity). Fifteen men (age: 24 ± 1 years) considered to be healthy, gave consent to participate in the experiment. All subjects were participating in any organised sports and had not performed any heavy resistance training for at least 1 year before this study commenced. The participants were subject to a training programme that was based around heavy resistance for 3 months. The training programme showed lots of progress which involved, watching load levels closely so that

At rest our body’s energy expenditure results from our basal metabolic rate (sleeping metabolic rate) and our arousal (wakefulness). At the onset of exercise, VO2 cannot initially support or new metabolic demands at sub-maximal level, so an oxygen deficit is created and must be compensated by our anaerobic metabolic systems. As exercise continues, for about 3-5 minutes, our aerobic system syncs in and supplements VO2, and a steady state is achieved. Heart rate increases as exercise increases in order to support an increase in VO2 and the metabolic demands required to pump more blood; this represents and linear relationship. Heart rate and VO2 are also linearly related, as the maintenance of a steady state during exercise is largely dependent on the heart’s ability to stimulate the metabolic activities that result in increased ventilation and a subsequent increase in VO2.

Lactate threshold and the increase of lactic acid in muscles throughout intense exercise has become a major interest for athletes, coaches and clinicians, it is to be noted that lactate is ‘’the product of, not the cause of muscle contraction’’,(Myers, J et al, 1997).Lacate threshold gives a good insight as to how long an individual can endure a particular intensity. Resting value for amount of lactic acid is 1 mmol/liter. Just over a heart rate of 90% of the maximum gives a good estimate of threshold intensity. This 24 year olds maximal heart rate is about 176 bpm, therefore from observing the two graphs we can note that his threshold intensity occurs approximately at 210 watts.(high performance sports conditioning)

The purpose of the maximal oxygen consumption test is to assess a participant’s aerobic power and fitness. Maximal oxygen is defined as the “single highest oxygen consumption elicited during graded exercise to exhaustion” (Adams, 2014). However, peak oxygen is measured “during a specific test, but it may not truly be the highest or maximal oxygen consumption possible” (Adams, 2014). To simplify, every test will show values for peak oxygen consumption; however every test does not always show a value for maximal oxygen consumption. This could happen if a participant is not able to fully reach the point of exhaustion due to physical pain symptoms or lack of motivation. Maximal oxygen consumption is important to understand aerobic fitness because it utilizes many systems in the body such as pulmonary, muscular, and cardiovascular. According to an article in the Journal of Human Kinetics, “maximal aerobic power is commonly accepted as the best measure of the cardiovascular systems’ functional limits (Rowell, 1974) and has been shown to predict mortality from all causes in healthy (Blair et al., 1989; 1996) and unhealthy individuals (Myers et al., 2002)” (Hamlin et al., 2012). For this lab, the maximal oxygen consumption test used was the Vo2 Max Bruce Protocol test and the equipment used was a Woodway treadmill.

Aerobic training has higher oxygen consumption (VO2), oxidizes more lipids (when compared to strength training), and utilizes carbohydrates as fuel energy. In more recent studies, it is suggested that strength training (ST) plays a significant role in regulating body weight once weight loss has occurred (4). It is also suggested that ST results in unique effects that aerobic exercise alone cannot achieve (4). Viewing ST alone and how it affects weight loss, it is concluded that weight loss occurs due to muscle hypertrophy. During ST, resting metabolic rate increases due to the increase in muscle mass, this in turn increases the total daily energy expenditure. When an individual is trying to lose weight through means of exercises, ST can complement aerobic training and aid in more efficient weight loss.

The aim of the present study is to investigate the influence of aerobic capacity to the level of fitness of anaerobic exercises. In the following experiment, subjects are requested to perform push-ups and step-ups. The anaerobic level of fitness is determined by the maximum number of push-ups done by the individuals whereas the aerobic capacity is indicated by the change in pulse rates. It is hypothesized that subjects with higher aerobic capacity will be more anaerobically fit (HA), whereas the null hypothesis is that subjects with higher aerobic capacity will not be more anaerobically fit (Ho)

Maximal oxygen consumption or VO2 max refers to the single maximum oxygen consumption that an individual can utilize during graded-intensity exercise. VO2 max can be assessed through properly administered submaximal oxygen consumption test which can include exercise test modes of treadmill, cycle ergometer or step test. In an individual, VO2 max can be determined by the cardiovascular system 's ability to deliver oxygenated blood to working muscles and then the muscle 's ability to extract that oxygen from the blood and generate energy for work. Influencing factors can include genetics, decline of VO2 max with aging, and finally aerobic training can positively influence an individual 's VO2 max and overall aerobic fitness. Individuals with high VO2 maxes often have greater overall aerobic fitness, which includes high efficiency, or running economy, better glycogen storage and is often an indicator of success when completing aerobic tasks of over 20 minutes. On the contrary, a low VO2 max can predict poor overall aerobic fitness which can include cardiovascular disease and problems with transporting oxygen to working muscles. (3) In these laboratory exercise test, submaximal intensity exercises were used to determine an individual 's predicted VO2 max which allowed the assessment of their overall aerobic fitness and the ability to compare the correlations between tests.

Kozakowska et al., (2015) findings show that it is possible for exercises to support special adaptations as regards to the group and vigor of the physical activity engaged. Based on their findings, they hypothesize that the adaptations occur to protect the muscles from disproportionate ROS generation, hence, enhancing the motor activities (Kozakowska et al., 2015). Their findings show that light exercises and warm-up regimens reduced erythrocyte MDA and raised erythrocyte SOD performance in patients with MD who engaged in regular light workouts. This study is corroborated by the study done by Al-Naama et al., (2015) whose findings were that low-intensity exercises was adequate to improve MDA levels and carbonyl protein – which is

High intensity, prolonged exercises increases oxidation of amino acids for fuelling our body and protein is used as an energy. Protein makes a greater contribution to total energy production during endurance exercise when muscle glycogen levels are low.