During exercise

Some P-adrenoceptor blockers have intrinsic sympathomimetic activity (ISA) or partial agonist activity (PAA). They activate P-adrenoceptors before blocking them. Theoretically, patients taking P-adrenoceptor blockers with ISA should not have cold extremities because the dmg produces minimal decreases in peripheral blood flow (smaller increases in resistance). In addition, these agents should produce minimal depression of heart rate and cardiac output, either at rest or during exercise (36). 

Calcium channel blockers reduce arterial blood pressure by decreasing calcium influx, resulting in a decrease in intracellular calcium (236,237). The arterial smooth muscle tone decreases, thereby decreasing total peripheral resistance. The increase in vascular resistance in hypertension is found to depend much on calcium influx. Calcium channel blockers reduce blood pressure at rest and during exercise. They decrease the transmembranous calcium influx or entry that lead to a net decrease of intracellular calcium and therefore the vascular tone falls, as does blood pressure. 

Anderson, S. D., and Schoeffel, R. E. (1982). Respiratory heat and W ater loss during exercise in patients with asthma Effect of repeated exercise challenge. E r. /. Respir. Dis. 63, 472-480. 

Paulsson, B., Bende, M., and Ohim, P. (1985). Nasal mucosal blood flow at rest and during exercise. Acta Otolaryngol. (Stockh.) 99, 140-143. 

Hargreaves, M., 1997. Interactions between muscle glycogen and blood glucose during exercise. Exercise and Sport Sciences Reviews 25 21-39. 

The Costs of Locomotion. Because oxygen is required for energy-producing metabolic reactions (respiration), there is a direct correlation between the amount of oxygen consumed and the metabolic rate. Not surprisingly, metabolic rates increase with activity. During exercise, a person will consume fifteen to twenty times more oxygen than when at rest. 

Lactic acid is produced by muscles during exercise. Calculate the pH and pOH of each of the following aqueous solutions of lactic acid, CH3CH(OH)COOH (a) 0.12 M ... 

During exercise below 60% VO2 max, there is greater reliance on fuel sources from outside the muscle (plasma glucose and FFAs). Since exercise can be sustained for 3-5 hours at 50% VO2 max and over eight hours at or below 40%... 

Asmussen, E. (1971). Muscle metabolism during exercise in man A historical survey. In Muscle Metabolism During Exercise (Pemow, B. Saltin, B., eds.), pp. 1-12. Plenum Press, New York. 

Bergstrom, J. Hultman, E. (1967). A study of the glycogen metabolism during exercise in man. Scand. J. Clin. Lab. Invest. 19,218-228. 

Costill, D.L., Coyle, E., Dalsky, G., Evans, W., Fink, W., Hoopes, D. (1977). Effects of elevated plasma FFA and insulin on muscle glycogen usage during exercise. J. Appl. Physiol. 43.695-699. 

Lindinger, M.I. Sjdgaard, G. (1991). Potassium regulation during exercise and recovery. Sports Med. 11,382-401. 

Thomson, J.M., Stone, J.A., Ginsburg, A.D., Hamilton, P. (1982). Oj transport during exercise following blood reinfusion. J. Appl. Physiol. 50, 864-868. 

Salo, D.C., Donovan, C.M., Davies, K.J, (1991). Hsp70 and other possible heat shock or oxidative stress proteins are induced in skeletal muscle, heart, and liver during exercise. Free Radic. Biol. Med 11,239-246. 

Muscle phosphorylase is distinct from that of Hver. It is a dimer, each monomer containing 1 mol of pyridoxal phosphate (vitamin Bg). It is present in two forms phos-phoiylase a, which is phosphorylated and active in either the presence or absence of 5 -AMP (its allosteric modifier) and phosphorylase h, which is dephosphorylated and active only in the presence of 5 -AMP. This occurs during exercise when the level of 5 -AMP rises, providing, by this mechanism, fuel for the muscle. Phosphorylase a is the normal physiologically active form of the enzyme. 

Grootveld, M., Henderson, E.B., Farrell, A.J., Blake, D.R, Parkes, H.G. and Haycock, P. (1991). Oxidative damage to hyaluronate and gjucose in synovial fluid during exercise of the inflamed rheumatoid joint detection of abnormal low-molecular-mass metabolites by proton NMR spectroscopy. Biochem. J. 273, 459-467. 

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