Metabolism exercise effects

The transition time between each set varies with your level of conditioning. You should proceed from one exercise to the next as soon as you catch your breath or feel that you can produce a maximal level of effort. After an initial period of adjustment, you should be able to recover adequately within 1 to 3 minutes. Training with a minimal amount of recovery time between exercises will elicit a metabolic conditioning effect that cannot be approached by traditional multiple set programs. 

Overall, the results suggest that older males are more resistant to the anabolic effects of AA feeding, including having a dramatically shorter metabolic window (i.e., the period of heightened nutrient sensitivity to the post-exercise effects of RT). 

A further way in which metabolic control may be exercised is the artificial deprivation of required ions and cofactors, for example aconitase must have ferrous ions for activity. Conversely, addition of toxic ions is possible, for example aconitase is inhibited by cupric ions. Finally the use of metabolic analogues is possible. If monofluoroacetate is added to cells then monofluorocitrate is produced by titrate synthase and this compound inhibits the activity of aconitase. Great care has to be taken when using metabolic analogues, however, they are often less than 100% specific and may have unexpected and unwanted serious side effects. 

Hultman, E. Nilsson, L.H. (1971). Liver glycogen in man. Effect of different diet and muscular exercise. In Muscle Metabolism During Exercise (Pemow, B. Saltm, B., eds.), pp. 143-151, Plenum Press, New York. 

Spriet, L.L., Gledhill, N., Froese, A.B., Meyers, E.C. (1986). Effect of graded erythrocythemia on cardiovascular and metabolic responses to exercise. J. Appl. Physiol. 61, 1942-1948. 

Hypoperfusion of skeletal muscles leads to fatigue, weakness, and exercise intolerance. Decreased perfusion of the central nervous system (CNS) is related to confusion, hallucinations, insomnia, and lethargy. Peripheral vasoconstriction due to SNS activity causes pallor, cool extremities, and cyanosis of the digits. Tachycardia is also common in these patients and may reflect increased SNS activity. Patients will often exhibit polyuria and nocturia. Polyuria is a result of increased release of natriuretic peptides caused by volume overload. Nocturia occurs due to increased renal perfusion as a consequence of reduced SNS renal vasoconstrictive effects at night. In chronic severe HF, unintentional weight loss can occur which leads to a syndrome of cardiac cachexia. This results from several factors, including loss of appetite, malabsorption due to gastrointestinal edema, elevated metabolic rate, and elevated levels of proinflammatory cytokines. 

Perhaps the most intriguing perspective is that caffeine s major effects have little to do with muscles and fat metabolism but result from its psychostimulant effects, enhancing mood, improving attitude towards exercise, and thus motivating athletes to work harder and longer. This would account for its purported inability to alter strength, which may be a less psychologically malleable variable, while endurance performance is sometimes believed to be more amenable to force of will. 

Powers, S., Byrd, R., Tulley, R., and Callendar, T., Effects of caffeine ingestion on metabolism and performance during graded exercise, European Journal of Applied Physiology, 50, 301, 1983. 

Weir, J., Noakes, T.D., Myburgh, K., and Adams, B., A high carbohydrate diet negates the metabolic effects of caffeine during exercise, Medicine and Science in Sports and Exercise, 19, 100, 1987. 

Bond, V., Adams, R., Balkissoon, B., McRae, J., Knight, E., Robbins, S., and Banks, M., Effects of caffeine on cardiorespiratory function and glucose metabolism during rest and graded exercise, International Journal of Sports Medicine, 27, 47, 1987. 

The effect of the skeletal muscle pump is essential during exercise. Although a mass sympathetic discharge and venous vasoconstriction enhance VR, this mechanism alone is insufficient to increase VR and, therefore, CO to meet the metabolic demands of strenuous exercise. The skeletal muscle pump mobilizes the blood stored in these tissues and keeps it flowing toward the heart. As the number of muscles involved in the exercise increases, so does the magnitude of the increase in VR and CO. 

Resistance in the arterioles of the working muscles is regulated locally. As discussed previously, active hyperemia results in production of several factors that cause metabolic vasodilation. Exercising muscles generate COz, H+ and K+ ions, heat, and adenosine. The vasodilator effect of these locally produced substances overrides the vasoconstrictor effect of the sympathetic system in the muscle. As a result, local vascular resistance is decreased. The combination of increased driving pressure and decreased local vascular resistance causes an increase in blood flow to the working muscles. 

Beyond this point, during more severe exercise associated with anaerobic metabolism, minute ventilation increases faster than the rate of oxygen consumption, but proportionally to the increase in carbon dioxide production. The mechanism of the ventilatory response to severe exercise involves metabolic acidosis caused by anaerobic metabolism. The lactic acid produced under these conditions liberates an H+ ion that effectively stimulates the peripheral chemoreceptors to increase ventilation. 

During exercise, the increase in minute ventilation results from increases in tidal volume and breathing frequency. Initially, the increase in tidal volume is greater than the increase in breathing frequency. As discussed earlier in this chapter, increases in tidal volume increase alveolar ventilation more effectively. Subsequently, however, as metabolic acidosis develops, the increase in breathing frequency predominates. 

---