SECTION I CELLULAR PHYSIOLOGY Delayed Onset of Muscle Soreness The fitness of a group of individuals of various ages and both genders was assessed in a step test.The test consisted of stepping up and domn 18 inches (46 cm)15 times per minute,for 20 minutes.The stepping pattern produced shortening of the right quadriceps muscle during the step up.The descent was opposed by contraction of the left quadriceps muscle that was stretched by the force of gravity. The subjects reported feeling weakness in the left quadriceps muasele.The weakness lasted for approximately 2 hours,and naxinun voluntary force developeent was less than the preexercise value.Percutaneous electrical stimulation of the quadriceps elicited reduced forces.Pain developed in the left quadriceps 8 to 10 hours after the exercise.reached maximal intensity between 24 and 48 hours,and persisted for about a week.This delayed onset of mscular soreness (DOMS)induced by exercise was marked in activities that imposed negative work on the muscle:such activities include descending stairs.The magnitude of the soreness was unrelated to the overall fitness of the individuals,but specific traiming for this step test prevented soreness in subseguent tests. Evidence of muscle cell injury included an increase in serun levels of soluble proteins,such as creatine kinase and myoglobin.The time course vas similar to that of the soreness.Myofibrillar disorganization and sarcolemral disruption could be observed in biopsy samples from only the left quadriceps. 1.Have you experienced DOMS?What are the circurstances that lead to DOVS and increase its severity? 2.Why was DOntS experienced in only the left quadriceps muscle in this fairly moderate exercise? 3.Is an impaired adenosine triphosphate (ATP)supply or synthetic capacity a reasonable explanation for the fatigue of the left quadriceps musele?
SECTION I CELLULAR PHYSIOLOGY Delayed Onset of Muscle Soreness The fitness of a group of individuals of various ages and both genders was assessed in a step test. The test consisted of stepping up and down 18 inches (46 cm) 15 times per minute, for 20 minutes. The stepping pattern produced shortening of the right quadriceps muscle during the step up. The descent was opposed by contraction of the left quadriceps muscle that was stretched by the force of gravity. The subjects reported feeling weakness in the left quadriceps muscle. The weakness lasted for approximately 2 hours, and maximum voluntary force development was less than the preexercise value. Percutaneous electrical stimulation of the quadriceps elicited reduced forces. Pain developed in the left quadriceps 8 to 10 hours after the exercise, reached maximal intensity between 24 and 48 hours, and persisted for about a week. This delayed onset of muscular soreness (DOMS) induced by exercise was marked in activities that imposed negative work on the muscle; such activities include descending stairs. The magnitude of the soreness was unrelated to the overall fitness of the individuals, but specific training for this step test prevented soreness in subsequent tests. Evidence of muscle cell injury included an increase in serum levels of soluble proteins, such as creatine kinase and myoglobin. The time course was similar to that of the soreness. Myofibrillar disorganization and sarcolemmal disruption could be observed in biopsy samples from only the left quadriceps. 1. Have you experienced DOMS? What are the circumstances that lead to DOMS and increase its severity? 2. Why was DOMS experienced in only the left quadriceps muscle in this fairly moderate exercise? 3. Is an impaired adenosine triphosphate (ATP) supply or synthetic capacity a reasonable explanation for the fatigue of the left quadriceps muscle?
4.One hypothesis for the etiology of DolS is that increased netabolisn results in the accumulation of toxic waste products.Can this explain the soreness? 5.Exercise can raise the teaperature of an active ruscle by 5"C or nore.Is heat injury a plausible explanation for DOWS? 6.Are there clinical signs of muscle cell injury? 7.What is a plausible nechanisn for injury of muscle cells or their tendons? 8.What does DOIS sugcest about the adaptability of mascle fibers to use? 9.Pain is usually regarded (teleologically)as a signal to protect the organism fron injury.Is this a rational explanation for DOMS? 10.what nigcht be responsible for the slow developaent of stiffness and soreness? ANSVER 1.Almost anyone who "overuses"a muscle (i.e.,undertakes activity that leads to intense or sustained periods of force development)is likely to experience DOMS. The intensity of effort (nagnitude of forces imvolved)seems to be more important than the duration of the effort. 2.The forces imposed on the muscle by gravity would be higher because attached crossbridges can bear a load sone 1.6 times greater than the force that they can develop.Thus the forces on the coatracting notor units of the left quadriceps msele and its tendons would be greater than the forces in the comtralateral muscle. 3.This is unlikely because stretch of a contracting muscle does not result in ATP hydrolysis by crossbridge cycling.One might expect that glycogen depletion or some other factor that compromises ATP production.and thereby contraction.would be most pronounced in the right quadriceps,which has had a high metabolic rate during the exercise. 4.This seeas unlikely hecause the netabolisn of the right quadriceps ruscle would have beem much higher than that of the left.Furthermore,although metabolite accumulation micht contribute to temporary fatigue in voluntary contractions,no voluntary exercise induces cellular fatigue that would reduce the respoase to
4. One hypothesis for the etiology of DOMS is that increased metabolism results in the accumulation of toxic waste products. Can this explain the soreness? 5. Exercise can raise the temperature of an active muscle by 5°C or more. Is heat injury a plausible explanation for DOMS? 6. Are there clinical signs of muscle cell injury? 7. What is a plausible mechanism for injury of muscle cells or their tendons? 8. What does DOMS suggest about the adaptability of muscle fibers to use? 9. Pain is usually regarded (teleologically) as a signal to protect the organism from injury. Is this a rational explanation for DOMS? 10. What might be responsible for the slow development of stiffness and soreness? ANSWER 1. Almost anyone who "overuses" a muscle (i.e., undertakes activity that leads to intense or sustained periods of force development) is likely to experience DOMS. The intensity of effort (magnitude of forces involved) seems to be more important than the duration of the effort. 2. The forces imposed on the muscle by gravity would be higher because attached crossbridges can bear a load some 1.6 times greater than the force that they can develop. Thus the forces on the contracting motor units of the left quadriceps muscle and its tendons would be greater than the forces in the contralateral muscle. 3. This is unlikely because stretch of a contracting muscle does not result in ATP hydrolysis by crossbridge cycling. One might expect that glycogen depletion or some other factor that compromises ATP production, and thereby contraction, would be most pronounced in the right quadriceps, which has had a high metabolic rate during the exercise. 4. This seems unlikely because the metabolism of the right quadriceps muscle would have been much higher than that of the left. Furthermore, although metabolite accumulation might contribute to temporary fatigue in voluntary contractions, no voluntary exercise induces cellular fatigue that would reduce the response to
percutaneous stimulation.In addition,metabolic honeostasis is quickly restored, whereas the soreness and stiffness are not evident for many hours. 5.The efficieney of chenonechanical transduction by crossbridges is estinated to be some 40%to 45%at most.Thus over half of the energy liberated during ATP hydrolysis appears as heat.The rise in temperature results from the inability of the circulation to remove the heat at the sane rate that it is gemerated in a muscle. The absence of DootS in the shortening right quadriceps,with its high rate of ATP consunption.rules out heat injury as a causative factor. 6.Elevated serum creatine kinase and myoglobin levels must reflect muscle cell injury that allows leakage of these proteins from cells.The biopsy tissue sarples provide further support for focal injuries in the sore msele. 7.In the absence of traura.injury must reflect the imposition of forces that exceed the structural capacity of the affected cells to resist those forces.The highest forees in musele cells oceur when contracting cells are foreibly lengthened by imposed loads that result in negative work.Negative work is a normal part of muscle fumction,but it may cause injury in cells not regularly used in this way. 8.The cells are very adaptable and respond to use by hypertrophy and perhaps by cytoskeletal and extracellular connective tissue alterations that enable the cells not only to develop higher forces but also to withstand higher inposed loads. The safety factor is not great,and regular exercise is needed to maintain the capacity to deal with high forces without injury. 9.Pain as a signal to cease exercise in order to limit injury must be imediate. Thus no benefits for DOMS are evident except those that underlie the motivational "no pain,no gain"philosophy of athletes. 10.The sensation of pain depends on activation of afferent nerve fibers.Because the onset of pain roughly parallels the rise in serum creatine kinase and mroglobin, it seems likely that dying or injured cells release agents that can activate the pain receptors.Such factors could include serotonin.histamine,K+,pressure associated with edema,or inflamatory processes
percutaneous stimulation. In addition, metabolic homeostasis is quickly restored, whereas the soreness and stiffness are not evident for many hours. 5. The efficiency of chemomechanical transduction by crossbridges is estimated to be some 40% to 45% at most. Thus over half of the energy liberated during ATP hydrolysis appears as heat. The rise in temperature results from the inability of the circulation to remove the heat at the same rate that it is generated in a muscle. The absence of DOMS in the shortening right quadriceps, with its high rate of ATP consumption, rules out heat injury as a causative factor. 6. Elevated serum creatine kinase and myoglobin levels must reflect muscle cell injury that allows leakage of these proteins from cells. The biopsy tissue samples provide further support for focal injuries in the sore muscle. 7. In the absence of trauma, injury must reflect the imposition of forces that exceed the structural capacity of the affected cells to resist those forces. The highest forces in muscle cells occur when contracting cells are forcibly lengthened by imposed loads that result in negative work. Negative work is a normal part of muscle function, but it may cause injury in cells not regularly used in this way. 8. The cells are very adaptable and respond to use by hypertrophy and perhaps by cytoskeletal and extracellular connective tissue alterations that enable the cells not only to develop higher forces but also to withstand higher imposed loads. The safety factor is not great, and regular exercise is needed to maintain the capacity to deal with high forces without injury. 9. Pain as a signal to cease exercise in order to limit injury must be immediate. Thus no benefits for DOMS are evident except those that underlie the motivational "no pain, no gain" philosophy of athletes. 10. The sensation of pain depends on activation of afferent nerve fibers. Because the onset of pain roughly parallels the rise in serum creatine kinase and myoglobin, it seems likely that dying or injured cells release agents that can activate the pain receptors. Such factors could include serotonin, histamine, K+, pressure associated with edema, or inflammatory processes
