Stiffness, Pain, and Sleep Following Exercise

Post-exercise Stiffness It is to be expected thai many rehab patients will experience .stiff, painful, slow-functioning leg muscles after an exer­cise, and myoglobinemia has been reported in many endurance activi­ties. Hansen. ct at., determined the degree of leakage of myoglobin and other muscle proteins into the cir­culation during various types of mus­cular activity.1 Sixteen highly-trained marathon runners, age 19-44 years. were examined, along with nine non-runners of similar age, and six rowers, age 15-24 years. All subjects were men. The runners trained lor 100 km to 350 km per week, and had maximal oxygen uptake values of 72-90 ml oxy­gen per minute, per kilogram of body weight. The nonrunners had maximal oxygen uptake values of about 40 ml. and the rowers" values were at 60-75 ml. Four runners were examined, after running 17-27 km on a hilly course, at a mean rate of 17.4 km per hour. Six runners and six nonrunners were com­pared during and after a noncompeti-tive test run of 27 km. or 12 km. respectively. Runners also participat­ed in 15 km and 30 km events. The rowers were examined after hard row­ing for 1-1/2 hours. Runners returned from the 17-27 km race with plasma-free hemoglobin val­ues of 2.4-10 mole/L. High transierrin iron-binding capacity and low hapto-globin values also were noted. The runners received iron daily, and had normal serum iron levels. All the run­ners had abnormally high serum myo-globin values immediately alter the race. Minimal myoglo-binuria was observed for 24 hours. No runner had significant proteituiria. Serum lactic dehydroge-nase. crcatinine kinuse. and alkaline phosphatase values were increased. Nonrunners had a greater increase in serum myo-globin levels than did the runners. Most runners had increased values of serum creutinine kinase B after the competitive run. in contrast to those values after noncompetitive runs or rowing. The rowers had elevations of serum enzymes and serum myoglobin similar to those seen in the runners. Free plasma hemoglobin was present in all the rowers. Both distance running and rowing damage skeletal muscle cells. The myopathic condition resolves within 24 hours, except for soreness in leg muscles. The changes after competi­tive running are consistent with some leakage of muscle proteins from myocardial cells. Neither myoglobine-mia nor hemoglobinemia appears to explain adequately the iron deficiency that occurs in athletes. This study makes a careful compari­son of the biochemical damage sus­tained by muscle in athletes and nonathletes after running, and in row­ers after rowing. The fact that protein leaks from the muscles of rowers makes a traumatic explanation unlike­ly. This phenomenon is possible after endurance exercise within the clinic. Nutritional intervention is helpful. Exercise-Induced Soreness Acute soreness develops during exercise and is related by Abraham2 to stress-induced ischemia. Pain occurs when exercise is intense enough to produce muscle ischemia, and the muscle cannot remove metabolic waste products such as lactic acid and potas­sium quickly enough. Critical concen­trations of these substances can stimu­late pain, which continues until exer­cise intensity is reduced or work ceas­es, both of which result in increased blood How. Delayed muscle soreness develops 24-48 hours alter exercise. It has been attributed to torn tissues, spasm and the strain placed on the elastic compo­nent of muscle by eccentric work. Increases in urinary myoglobin excre­tion have been associated with exer­cise-induced muscle soreness, but they may also follow exercise when sore­ness does not develop. The relation­ship between exercise-induced muscle soreness and urinary hydroxyproline excretion can be compared. Signifi­cant correlation is apparent between the time of maximum hydroxyproline excretion and the day when the most soreness is reported. Delayed soreness appears to be linked to an irritation of the connective tissue in muscles. Exercise-Delayed Soreness Exercise that uses untrained muscles results in delayed muscle soreness-'and increased muscle enzyme activities in untrained individuals.4 Tiidus5 exam­ined the time course of these effects and the importance of the intensity and duration of exercise in untrained indi­viduals of both sexes, age 20-45 years. All exercised less than once a week. A dynamic leg extension apparatus was used. Six persons performed sets of up-to-ten contractions to establish the time course of post-exercise serum enzyme changes and muscle soreness. Twenty-one subjects then performed exercise at various intensities and dura­tions at ten-day intervals. The most severe muscle soreness and the highest serum creatine phosphoki-nase (CPK). lactic dehydrogenase. and glutamic oxaloacetic trunsaminase activities occurred 48 hours and 8-to-24 hours after exercise, respectively, in the pilot study. Increasing intensity and duration of exercise resulted in corresponding increases in enzyme activities and muscle soreness. High-intensity, brief exercise led to greater enzyme activities and more muscle soreness than low-intensity exercise of long duration. The serum CPK activity correlated significantly with the change of degree of muscle soreness. The findings suggest that exercise-induced muscle damace leads to leak- age of muscle enzyme into the blood, and physiologic reactions to the muscle damage that result in a sensation of muscle soreness. Studies in rate have shown myofibrillar disruption, macrophage and fibroblast accumula­tion, and necrosis in exercised muscles in association with serum enzyme ele­vations. The exercise-induced changes may be casually related to delayed muscle soreness. What is important is that the enzyme elevation and subjec­tive symptoms of soreness are signals of profound cellular change, which includes cellular disruption, fibroblas-tic change, and necrosis. Sleep and Exercise Slow-wave sleep (SWS) has been suggested to be a restorative phase of sleep, and exercise has been hypothe­sized to create a demand for SWS pro­portional to energy expenditure. Bun-ncll6 used a quantified submaximal exercise procedure, carried out to voli­tional exhaustion, to test the exercise-SWS hypothesis. Measures of total caloric expenditure permitted compar­isons on individual energy costs and changes in SWS. Five women and four men. age 21-30 years, participated in the study. All were moderately active, but none engaged in vigorous physical training. Four patients typically exer­cised regularly. Recordings were made on adaptation and baseline nights, and for two nights after an afternoon exer- cise bout in which the subjects walked on a treadmill for fifty-minute periods , at 50c/c to 7Qc/r of maximal oxygen I uptake, to the point of volitional i exhaustion. j The duration of SWS before the j onset of rapid eye movement (REM) j sleep increased markedly on the exer- j cise night. Moderate increases in stage j 4 sleep and total SWS were observed. I An increased latency to first REM ! onset and decreased duration of the first REM period were also found. Ini- j tial REM cycle length decreased. The j increases in SWS before the onset of ! REM sleep averaged twenty-four min- j utes in women and six minutes in men. '■ In women, this increase correlated with total caloric expenditure during exer­cise, with a coefficient o\' 0.85. Heart rate and cardiac output during sleep were .significantly increased on the exercise night. A significant fall in nocturnal urinary cortisol excretion fol­lowed exercise. The findings suggest that exhaus­tive exercise affects sleep primarily in the early part of the night. An increase in SWS pressure is observed, at the expense of REM sleep. The increase in SWS in the first non-REM period is consistently greater in women than in CoiUimwd on Page 46 REHABILITATION ..from Page 35 men. Any explanation of the increase in SWS alter exhaustive exercise must lake into account the apparently greater effect of exercise intensity, compared with caloric expenditure, itself. An explanation that holds that SWS reflects primarily neural functioning seems to account for the changes in both SWS and REM sleep. The metabolic and biochemical alterations induced by vigorous exer­cise have not been identified precisely. It is of some interest that, in rats that swim to exhaustion, there is a \5c/c increase in whole brain serotonin, and a 20% drop in norepinephrine levels. Whether this pattern is reduplicated or paralleled in the higher vertebrates remains to be seen. The main points are well documented: slow wave sleep is increased early on. REM sleep is decreased, and the effect is greater in women than in men. Kim D. Christensen. DC, CCSP, DACRB. is co-director of the SportsMedicine & Rehab Clinics of Washington. He is a popular speaker, and participates as a team physician and consultant to high school and uni­versity athletic programs. He is cur­rently a postgraduate faculty member of numerous chiropractic colleges and is the president of the American Chiro­practic Association (ACA) Rehab Council. Dr. Christensen is the author of numerous publications and texts on musculoskeletal rehabilitation and nutrition. He can be reached at Chiro­practic Rehabilitation Assoc, 18604 NW 64th Ave.. Ridgejield. WA 98642. References Hanson KN. Bjene-Knudsen J. Brodtha- gen U. Jordal R. Paulcv PE. Muscle cell leakage due to long-distance training. Eur J Appl Physiol Ocaip Phyxiol 19X2: 4X(2):177-18X. Abraham WM. Pin.sic inn Sportsined 1979:7(Oct):57-6(). Ernst E. Does posi-exeieise massage treatment reduce delayed onset muscle soreness? A systematic review, lir J Sports Meil 1998: 32(3):212-214. Vincent HK. Vincent KR. The effect of training status on the serum creatine kinase response, soreness and muscle function following resistance exercise. hit J Sports Med 1997: 18(6):431-437. Tiidus PM. lanu/zo CD. Effects of inten­ sity and duration of muscular exercise on delayed soreness and serum enzyme activities. 5c/ Spoils E.xerc 1983: 15(61:461-465. Bunnell DE. Bcvier W. Horvath SM. Effects of exhaustive exercise on the sleep of men and women. Psychophysi- oloxy 1983:2011 ):5<)-5X.w