The ability of exercisers to dissipate metabolically-produced heat depends largely on their ability to form and vaporize sweat. The magnitude of sweat production is proportional to the rate of energy expenditure.
Muscle water declines steadily with progressive dehydration. No direct evidence of tissue hypokalemia with heavy exercise and profuse sweating has been obtained. Plasma volume changes during days of repeated dehydration. Sodium is conserved, apparently through an increase in mineral corticoid function. Low potassium intake appears to reduce sodium loss and urine output during repeated days of heavy exercise. There is no evidence that heavy exercise on repeated days threatens muscle and plasma potassium stores, even when the dietary potassium intake is very low.
Costill1 indicates the body minimizes electrolyte losses during acute and repeated bouts of exercise and dehydration. In general, large sweat losses during training are adequately tolerated. Despite sizable excretion of ions in sweat, caloric intake and renal conservation of sodium minimize the threat of chronic dehydration, electrolyte deficiencies, or both.
Body water lost during exercise as a consequence of heat expenditure is accomplished at the expense of larger water losses from extracellular than from intracellular compartments. Furthermore, the losses in sweat and urine have little effect on potassium content of either plasma or muscle. With repeated days of dehydration and heavy exercise, plasma volume does increase and this relative increase of plasma water may result in a reading of fictitious anemia as a phenomenon of hemodilution. This may also produce an apparent hypokalemia that is also fictitious.
Skin Circulation during Exercise
Skin blood flow is the chief mechanism for transferring heat fromï circulatory system also must supply the increased metabolic requirements of exercising muscles. Roberts et al.2 examined the influence of body temperature on skin blood flow in exercise. Temperatures were measured in the esophagus and at eight skin sites in subjects who exercised on a cycle ergometer in three different positions. Cardiac output was measured by a CO2 re-breathing technique, and chest sweating was measured by resistance hygrometry.
Exercise increased internal body temperature and cutaneous blood flow at any given environmental and mean skin temperature. At high environmental temperatures, with skin temperature elevated, skin blood flow at any given internal temperature was higher than at cooler skin temperatures. At high levels of skin blood flow, peripheral vascular pooling and fluid loss through filtration led to reduced central venous pressure, which lowered cardiac stroke volume and required a higher heart rate to maintain a given cardiac output. Mechanisms for alleviating some of the cardiovascular strain include reflexes arising from receptors in working muscle that produce vasoconstriction in central and peripheral vascular beds. Reflexes arising from cardiac baroreceptors produce additional peripheral vasoconstriction when cardiac filling is impaired.
In the long term, physical conditioning and heat acclimatization lead to increased sweat output during thermal stress, cooler skin and core temperatures on exercise and a decrease in the level of skin blood flow needed for regulation of body temperature. An environment that inhibits evaporation will preclude large reductions in skin temperature.
The demand for skin blood flow is an important limiting factor in sustained exercise, particularly if the environment is warm or hot. With maximal cutaneous vasodilation, flow can reach 6-10L per minute, 25 percent or more of the total cardiac output.
Fatigability of Muscles
Local muscle fatigue causes a shift in the frequency spectrum of the surface electromyogram (EMG) toward lower frequencies. Sato et al.3 examined the functional differentiation of main human limb muscles with respect to fatigability for sustained isometric contraction by means of frequency analysis of the surface EMG. Fifty-eight fatigue studies were done on 12 muscles in seven normal subjects, four women and three men, aged 18-33.
Fatigability was estimated by use of contractions of half to two»thirds of maximum voluntary contraction (MVC) strength. The increase in slow wave ratio, or percentage of integrated amplitude in the frequency component at below 60 Hz to total activity, was calculated.
The triceps brachii was found to be more fatigable than the biceps brachii and brachioradialis; the extensor carpi ulnarisï the rectus femoris; and the tibialis anterior more than the gastrocnemius and soleus. There was no significant difference between the rectus femoris, vastus medialis and vastus lateralis. In general, the lower limb muscles, especially the knee extensors and calf muscles, were less fatigable than the upper limb muscles. In the upper limb, the extensors were more fatigable than the flexors. No consistent difference in fatigability was noted between one-joint and two-joint muscles.
Differential muscle fatigability could be due to differences in muscle fiber composition. Success in numerous activities appears related to fiber-type distribution in skeletal muscles. Changes in fiber composition have not been demonstrated to occur with any form of training. Long contraction times appear to correspond to fibers rich in mitochondria, or slow-twitch fibers. Rehab protocols would be wise to provide additional sets of work loads on those groups of musculature that fatigue quicker if endurance gains are required.
In the rehab clinic, fatigability of selected musculature that requires rehabilitation must be carefully observed (Figure 1). In order for injured musculature that fatigues quickly to regain normal strength and endurance, it is necessary to perform protocols that augment such strength and endurance loss. A common practice is to perform the strength-endurance exercise at the beginning and end of the exercise session.
- Costill DL. Ann NY Acad Sci 1977;301:160-174.
- Roberts MF, Wenger CB. Med Sci Sports 1979 (Spring):11-41.
- Sato H, Hayami A. J Orthop Sports Phys Ther
Kim Christensen, DC, DACRB, CCSP
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