Competitive swimming performance frequently requires a swimmer to complete multiple bouts of high-intensity exercise within 1 meet. Each of these intense exercise bouts results in significant metabolic disturbances. Fuel sources including creatine phosphate and carbohydrates are rapidly consumed, and metabolic products are made, especially lactic acid. The body begins to recover immediately after the exercise bout because fuels are being stored back into the exercised skeletal muscle and the metabolic products are being cleared from the muscle and blood. But full recovery from these metabolic disturbances, including the return of blood and muscle lactate to resting levels, can take up to 60 minutes or more (21,28). It is quite possible that a swimmer will complete 2 or more intense events separated by no more than 30 minutes and thus be unable to sufficiently recover before the next event. There is concern that elevated muscle and blood lactate levels after 1 event, if not reduced to near resting levels before the next event, may negatively affect subsequent performance (3,9).
The high blood and muscle lactate levels resulting from high-intensity exercise can potentially be detrimental to subsequent sports performance for a variety of reasons. Excessive lactate levels can produce a severe burning sensation that some have observed to decrease swimming speed (20). Physiologically, the greatest consequence of lactate production is the associated elevation of hydrogen ion concentration [H+] and low pH observed in the muscle and blood. The high [H+] can contribute directly to muscular fatigue by affecting the contractile process. It can reduce the force of contraction by inhibiting calcium release from the sarcoplasmic reticulum or by interfering with the binding of calcium and troponin (10,14,26). This direct action of high [H+] on the contractile mechanism is important during exercise but is likely less important during recovery. Force production recovers almost fully while muscle pH remains depressed during recovery, suggesting that the high [H+] may indirectly affect performance by impairing energy metabolism (27). Most of the energy required for a 200-yard swimming sprint is supplied by fast anaerobic glycolysis. For maximal performance in this event, it is important that fast anaerobic glycolysis operates at a maximal rate dependent on the full activation of its associated enzymes. However, 2 of the important rate-limiting enzymes in glycolysis, phosphofructokinase and lactic dehydrogenase, are both inhibited by elevated [H+] (3,4,18,19). If lactate and [H+] are elevated from a previous sprint, subsequent performance is likely to be diminished in part by the direct effect on the contractile process and indirectly through the inhibition of rate-limiting glycolytic enzymes. Therefore, it follows that removing lactic acid faster during recovery from 1 exercise bout should benefit the performance of any subsequent exercise bouts that rely on glycolytic metabolism such as a 200-yard swimming event (4,17).
The activity performed during the recovery period after intense exercise can impact the rate of lactate removal from the muscle and blood. Active exercise recovery or warm-down has been shown numerous times to speed the removal of blood lactate compared with a passive resting recovery (3,4,7,9,13,21,34). This holds true in a variety of exercise modes including running, cycling, and swimming. In general, active exercise recovery can double the rate of lactate removal, thereby cutting in half the time required for blood lactate to return to near resting levels when compared with passive resting recovery (4,5,7,8,15,21). Faster lactate removal with active exercise recovery is believed to be caused by greater lactate oxidation as an energy source by the exercising muscle (4,5,30). The exercise also maintains a greater skeletal muscle blood flow (12), which may help transport the lactate out of the exercised muscles and distribute it to nonexercised muscles and other tissues throughout the body where it can be used for fuel or converted to glucose and restored back into the muscle (11).
During competitive swimming performance, the preference would be to use a swimming recovery or warm-down between events. However, in cases where there is no pool available for a sufficient swimming recovery, alternative recovery treatments must be sought. Studies have been published on swimmers using active recovery treatments other than swimming, including walking (29), running (7), and rowing (9). These treatments, although affective, may be limited in their practicality or may not be popular with swimmers. Another alternative treatment that has not yet been studied is low-frequency transcutaneous electrical stimulation of large muscles during recovery. The muscular contractions created in response to the electrical stimulation result in a greater energy demand and potentially in greater blood flow and lymphatic drainage in the contracting muscles. Theoretically, this could result in some of the same benefits expected from the active exercise recovery and facilitate faster blood lactate removal. Therefore, the purpose of this study was to evaluate the effectiveness of submaximal swimming recovery and transcutaneous electrical muscle stimulation in promoting blood lactate removal after a maximal effort swim compared with a passive resting recovery.
Experimental Approach to the Problem
Sprint swimming performance requires a significant contribution from anaerobic energy sources including glycolytic metabolism. A consequence of producing energy by way of glycolytic metabolism is the production and accumulation of muscle and blood lactate. Elevated lactate levels are related to muscular fatigue and potentially to reduced swimming performance. Most sprint and middle-distance competitive swimmers perform multiple bouts of intense exercise over the course of a 2- to 3-hour swimming competition, resulting in the production of significant amounts of lactate. It is important that these swimmers use appropriate recovery methods between events to maximize the clearance of muscle and blood lactate. Previous studies have demonstrated the benefits of an active exercise recovery in reducing blood lactate when compared with a passive resting recovery. There is reason to believe that other types of recovery treatments may also be beneficial in speeding the removal of lactate but have not been studied to the same extent as active exercise recovery. One such recovery treatment is transcutaneous electrical muscle stimulation. The rationale for electrical muscle stimulation speeding the removal of lactate hinges on its ability to create low-frequency submaximal muscle contractions that potentially promote increased blood flow through and lymphatic drainage from the exercised muscle. This investigation was designed to compare the effects of 3 types of recovery treatments, passive resting, active submaximal swimming, and transcutaneous electrical muscle stimulation, on the time course of blood lactate after high-intensity swims. On 3 separate days, swimmers completed a maximal 200-yard frontcrawl sprint and then completed 1 of the 3 recovery treatments in random order. Blood samples were drawn immediately after the sprint and then again at 10 and 20 minutes into recovery to study the effect of the 3 recovery treatments.
Thirty competitive swimmers (19 men and 11 women) from high school and collegiate swim teams volunteered for the study. Their mean (±SD) age, height, and weight were 17.7 ± 2.9 years, 175.6 ± 8.8 cm, and 67.4 ± 10.7 kg, respectively. Participants in this study trained on a year-round basis. Data were collected in May, considered to be 1 to 3 weeks postseason. Swimmers were selected for the study based on their previous swimming performance. Only swimmers who had swum a 200-yard frontcrawl in competition in under 1:53.50 (men) or 2:04.00 (women) at least once in the previous 12 months were selected. These times were the time standards for boys' and girls' 200-yard freestyle as identified by the California Interscholastic Federation, Southern Section (6).
The study was approved by the university institutional review board. Swimmers were recruited through age-group swim teams and consisted of high school and community college athletes. All adult subjects signed an informed consent document. All minor subjects signed a minor assent form, and their parent or legal guardian signed a parental consent form before participation.
The subjects were tested individually on 3 occasions, each separated by a minimum of 24 hours. All 3 testing sessions were completed within 3 weeks. All subjects were required to wear a swimsuit that exposed the lower extremities 5 to 7 cm inferior to the greater trochanter and exposed the lumbar spine to accommodate the placement of electrodes for the purpose of transcutaneous electrical muscle stimulation.
One complete testing session consisted of the following parts. The subjects began with a 1,200-to 1,500-yard warm-up swim at a self-selected pace followed by a 2-minute passive resting recovery. They then completed a 200-yard maximal frontcrawl sprint begun from a dive followed by a 3-minute resting recovery, after which a blood sample was drawn to determine a “peak” blood lactate value. They then completed 1 of 3 recovery treatments in randomized order. Treatment 1 was a 20-minute seated resting recovery during which subjects sat passively in a chair near the pool deck. Treatment 2 was a 20-minute active recovery during which the subjects swam 100-yard repeats at approximately 65% of their 200-yard sprint speed. Times for the 100-yard repeats ranged from 1:18 to 1:29 for the men and 1:28 to 1:39 for the women. Treatment 3 was a 20-minute session of electrical muscle stimulation. A blood sample was drawn 10 minutes into the treatment session to determine a “mid-recovery” blood lactate value, and a final blood sample was drawn after the 20-minute recovery treatment to determine a “postrecovery” blood lactate value. One “baseline” blood lactate was determined for each subject before the warm-up swim on the first testing day only. This 1 value was used as the baseline for all 3 recovery treatments.
Administration of Electrical Muscle Stimulation
Transcutaneous electrical muscle stimulation was administered using an H-wave Home Model P-4 electrical stimulator (Electronic Waveform Laboratory, Inc., Huntington Beach, CA, USA). The H-wave stimulator is capable of producing a biphasic, exponentially decaying waveform up to a peak current of 35 mA at frequency settings ranging from low frequency (2 Hz) to high frequency (70 Hz). The “intensity” of the signal can be controlled on a 10-point scale ranging from the lowest setting of 0 (0 mA) to the highest setting of 10 (35 mA). According to the manufacturer, low-frequency stimulation (2 Hz) is used to reduce peripheral edema, and high-frequency stimulation (70 Hz) is used to reduce peripheral pain. The low-frequency setting (2 Hz) was selected for use in this study in an attempt to elicit a peripheral muscle pump action by electrically inducing low-tension, nonfatiguing muscle contractions at approximately 10% of maximum voluntary contraction (16,25).
Electrical muscle stimulation was administered primarily to muscles in the region of the anterior thighs and lower back of the subject. These muscles, the rectus femoris, latissimus dorsi, and triceps, were chosen because of their significant involvement in swimming. Electrodes were placed bilaterally at the origins and insertions of the rectus femoris (5 cm inferior to the greater trochanter, midshaft; 5 cm superior to the superior patellar border, midshaft) and latissimus dorsi muscles (posterior aspect of the upper arm, midshaft; 5 cm lateral to the spinous processes of L3 and L4) (Figure 1). Because of the placement of the electrodes on the upper arm at the insertion of the latissimus dorsi, secondary contractions of the triceps were also elicited. With the subject seated in a chair near the pool deck, the H-wave stimulator was set to 2 Hz, and the intensity level was gradually increased until the subject felt a “mild tapping” on their skin or until mild muscular contractions were visible. At this point, the intensity was increased further until the subjects felt a “strong, yet comfortable contraction.” After 2 to 3 minutes, the subjects often became used to the contractions, and the intensity was increased again (typically to an intensity value of 7-10) to elicit strong yet comfortable contractions.
Determination of Blood Lactate
Blood lactate values were determined using an Accutrend Portable Lactate Analyzer (Boehringer Mannheim, Indianapolis, IN, USA) that was calibrated and operated according to the manufacturer's specifications. A portable analyzer was selected so that blood lactate measurements could be made poolside. The analyzer works by placing a sample of whole blood on a test strip and inserting it into the analyzer for it to react with lactate oxidase. Lactate concentration is then determined from reflectance photometry in the range of 0.7 to 26.0 mmol·L−1. The reliability and validity of the Accutrend analyzer have been reported in previous studies. Pinnington and Dawson (23) showed the analyzer to be reliable (intraclass correlation coefficient [ICC] r = 0.995) and to demonstrate good association (ICC r = 0.853) with the Analox LM3 analyzer (Analox Instruments, Ltd., London, UK).
Blood samples were drawn either from the posterior-inferior aspect of the earlobe or the lateral aspect of the fingertip midway between the nail plate and the inferior distal phalanx. The sample sites were wiped with isopropyl alcohol swabs and punctured with a spring-loaded lancet device followed by 2 to 3 seconds of a “milking” technique (alternating pressure and release 6-8 mm from the puncture site) to promote blood flow from the wound. Blood droplets approximately 3 mm in diameter were applied directly to the test strips for the determination of blood lactate (mmol·L−1). For subsequent blood samples, if wiping the previous wound with an alcohol swab and milking the area elicited an adequate flow of blood to collect an adequate sample, no further puncture was necessary. However, if the previous site did not yield an adequate sample, a new site was selected and used for subsequent sampling.
Descriptive statistics (mean and SD) were calculated for subject characteristics (age, height, and weight) and blood lactate values (by treatment and time). Factorial (2 × 3 × 3) analysis of variance with repeated measures (ANOVA-RM) was used to test for any main effects, repeated measures effects, or interaction between the differences in blood lactate values between 2 sexes (male and female), 3 recovery treatments (rest, swimming, and electrical stimulation), and 3 repeated times (peak, mid-recovery, and postrecovery). Post hoc analysis of any significant effects identified by the ANOVA-RM was done using one-way ANOVA to compare recovery treatments and repeated times followed up by Scheffé confidence interval procedures. An alpha level of 0.05 was chosen for all statistical comparisons. The statistical analyses were conducted using StatView statistical software (SAS Institute, Inc., Cary, NC, USA).
All subjects were instructed to swim each trial of the 200-yard frontcrawl as fast as possible. The mean (±SD) 200-yard swim time for the men was 1:50.0 ± 4.0 seconds and for the women was 2:01.6 ± 3.9 seconds. Both of these mean times are faster than the desired standard times of 1:53.5 and 2:04.0 that were used for recruiting the men and women, respectively. The mean peak blood lactate for all subjects after the 200-yard maximal frontcrawl across all trials was 6.17 ± 2.16 mmol·L−1, ranging from 2.4 to 13.2 mmol·L−1. Analysis of variance revealed no significant (p = 0.518) interaction between sex and recovery treatment, and therefore all further statistical analysis was done on the group as a whole regardless of sex. Mean blood lactate values are presented in mmol·L−1 (Figure 2) and in relative terms as the percent of remaining blood lactate using the peak blood lactate as the reference (Figure 3).
Analysis revealed a significant (p < 0.05) interaction between recovery and time for blood lactate (mmol·L−1). A significant drop in blood lactate was observed (Figure 2) with resting recovery from peak (6.32 ± 2.17 mmol·L−1) to postrecovery (4.11 ± 1.35 mmol·L−1). A significant drop in blood lactate was observed with electrical stimulation from peak (6.25 ± 1.99 mmol·L−1) to mid-recovery (4.46 ± 1.79 mmol·L−1) and from mid-recovery to postrecovery (3.12 ± 1.41 mmol·L−1). Similarly, a significant drop in blood lactate was observed with swimming recovery from peak (5.96 ± 2.35 mmol·L−1) to mid-recovery (3.50 ± 1.57 mmol·L−1) and from mid-recovery to postrecovery (1.60 ± 0.57 mmol·L−1). At mid-recovery, blood lactate was significantly lower with swimming recovery (3.50 ± 1.57 mmol·L−1) when compared with electrical stimulation (4.46 ± 1.79 mmol·L−1) and resting recovery (5.18 ± 1.93 mmol·L−1). At postrecovery, blood lactate was significantly lower with both swimming recovery (1.60 ± 0.57 mmol·L−1) and electrical stimulation (3.12 ± 1.41 mmol·L−1) when compared with resting recovery (4.11 ± 1.35 mmol·L−1) and was significantly lower with swimming recovery when compared with electrical stimulation.
Analysis revealed a significant (p < 0.05) interaction between recovery and time for remaining blood lactate (%). Remaining blood lactate was significantly lower from peak to mid-recovery and from mid-recovery to postrecovery in all 3 recovery treatment groups (Figure 3). At mid-recovery, remaining blood lactate was significantly lower with electrical stimulation (71.4 ± 18.1%) when compared with resting recovery (82.6 ± 12.9%) and lower with swimming recovery (59.3 ± 14.6%) than both resting recovery and electrical stimulation. The same was true at postrecovery; remaining blood lactate was significantly lower with electrical stimulation (50.1 ± 16.0%) when compared with resting recovery (66.8 ± 13.4%) and lower with swimming recovery (29.5 ± 10.7%) than both resting recovery and electrical stimulation.
Mean (±SD) blood lactates of all swimmers in this study increased from a baseline value of 1.44 ± 0.34 mmol·L−1 to a peak value of 6.17 ± 2.16 mmol·L−1 after a 200-yard swim. These values are in close agreement with the results of similar studies by Beckett and Steigbigel (3), who reported a baseline blood lactate of 1.35 ± 0.36 mmol·L−1 and peak blood lactates after a 200-yard and 400-yard swim of 7.53 ± 1.67 and 6.86 ± 1.95 mmol·L−1, respectively, and McMaster et al. (21), who reported peak blood lactates of 6.60 ± 1.46 mmol·L−1 and 6.45 ± 2.74 mmol·L−1 after 200-yard swims. Felix et al. (9) reported slightly lower blood lactates of approximately 1 mmol·L−1 at baseline and peak values of approximately 4.2 to 5.3 mmol·L−1 after a 200-yard swim in women only. The mean blood lactate after 20 minutes of resting recovery (4.11 ± 1.35 mmol·L−1) was significantly lower (p < 0.05) than the peak lactate value but was still significantly elevated over baseline. This value is similar to previous studies that reported blood lactate values of 4.60 ± 1.91 mmol·L−1 after 20 minutes (21) and 3.05 ± 1.19 mmol·L−1 after 30 minutes of resting recovery (3). It is clear that when swimmers passively rest after a 200-yard swim, blood lactate is still significantly elevated, in some cases above 4 mmol·L−1, for at least 20 to 30 minutes, and may still be elevated above resting levels for over 60 minutes. This elevated blood lactate is believed by many to potentially have a detrimental effect on subsequent physical performance, such that faster and more complete removal of blood lactate after exercise would be particularly beneficial with regard to athletic competition (3,4,9,21,22,31).
Blood lactate was reduced after the 200-yard maximal frontcrawl swim most effectively by using a submaximal swimming recovery (Figure 2). The swimming recovery, modeled after recommendations by McMaster et al. (21), consisted of swimming 100-yard repeats at 65% of each swimmer's maximum 200-yard velocity. Peak blood lactate (5.96 ± 2.35 mmol·L−1) dropped significantly (p < 0.05) to 3.50 ± 1.57 mmol·L−1 after 10 minutes of recovery, which was significantly lower than with electrical muscle stimulation or with resting recovery. It dropped significantly further to 1.60 ± 0.57 mmol·L−1 after 20 minutes of recovery, which was again significantly lower than the other 2 treatments. The blood lactate value after 20 minutes of resting recovery was not significantly different (p = 0.965) from the baseline value. In terms of the remaining blood lactate, only 29.5 ± 10.7% of the peak lactate value remained after 20 minutes with the swimming recovery, compared with 50.1 ± 16.0% and 66.8 ± 13.4% of lactate remaining for electrical muscle stimulation and resting recovery, respectively (Figure 3). The superior effect of the swimming recovery in reducing blood lactate confirms several previous studies that found similar results with different forms of active exercise recovery. Beckett and Steigbigel (3) found that completion of a 1,000-yard warm-down swim at 60% effort reduced blood lactate more than 30 minutes of sitting on the pool deck (3). McMaster et al. (21) compared the effect of passive recovery to submaximal swimming recovery on blood lactate for 20 minutes after a 200-yard maximal swim. The treatments consisted of sitting on the pool deck or swimming 100-yard repeats at a velocity 65% of the best effort. Similarly to the current study, blood lactate was reduced from a peak value of 6.45 ± 2.74 mmol·L−1 to 2.20 ± 1.44 mmol·L−1 with the active recovery, compared with a reduction from a peak of 6.60 ± 1.46 mmol·L−1 to 4.60 ± 1.91 mmol·L−1 after the passive recovery (21). In a follow-up study, the same authors were interested in the effect of exercise intensity during recovery and whether swimming recovery performed at lower intensity (100-yd repeats at 55% of best velocity) or higher intensity (100-yd repeats at 75% of best velocity) had a beneficial effect on lactate clearance. All 3 of the recovery intensities (55%, 65%, and 75% velocity) proved to be effective at lowering blood lactates, with none of the intensities displaying superiority. Subjectively, the swimmers believed the 55% velocity was “too sluggish,” the 75% velocity was “too fast,” and the 65% intensity was “the best” (22). From the 2 studies combined, it was concluded that recovery swimming at 65% of best effort velocity has important implications for enhancing recovery during competition when repeated performance is required (21,22).
The mode of exercise used during active recovery is also of interest. Denadai et al. (7) studied 3 recovery modes including passive sitting, moderate intensity running, and moderate intensity swimming on lactate removal after 250-m swims at maximal speed with a 2-minute rest in between. Both active recovery conditions removed blood lactate faster than passive sitting, with the running recovery being the most effective treatment. They believed that using an exercise mode for recovery different than the original exercise mode increased the speed of blood lactate removal (7). Felix et al. (9) studied the effect of passive recovery, swimming at 65% of lifetime best velocity in 200-yard freestyle, and rowing at 60% of age-predicted maximal heart rate on blood lactate after a maximal 200-yard swim. Both active recovery modes reduced blood lactate more than passive recovery, with little difference between swimming and rowing recovery. They recommended use of a rowing ergometer as an alternate recovery treatment when swimming recovery was not available during competition (9). Siebers and McMurray (29) compared self-selected rates of swimming recovery and walking recovery and the effect of each on lactate removal after 2 minutes of swimming ergometer exercise. They found that the swimming recovery reduced the lactate concentration by 53.3 ± 3.0% compared with 38.5 ± 3.0% for the walking recovery. No significant difference was found, however, between 200-yard swim times after the swimming and walking recoveries (29). Other studies have also demonstrated that elevated blood lactate levels do not adversely affect subsequent cycling or swimming performance (29,32,33,34). Two of these studies by Toubekis et al. (32,33) found 50-m sprint swimming performance after 6 minutes of recovery from 8 repetitions of 25-m sprints to be unaffected by recovery treatments even when blood lactate levels were significantly different. Swimming performance may have been unaffected partly because of the short sprint distance (50-m) and limited recovery time (6 min), which would place more emphasis on phosphagen metabolism and less emphasis on glycolysis for supplying the energy required for the sprint. Although conflicting evidence exists, it is still logical to believe that elevated blood lactate levels can adversely affect 200-yard swimming performance. Should subsequent research confirm the importance of residual muscle and blood lactate on subsequent performance, then, in addition to facilitating lactate removal, the performance benefits of exercise recovery may also be confirmed.
The ability of active exercise recovery to speed the removal of muscle and blood lactate compared with passive resting recovery is explained primarily by increased lactate oxidation within the exercising muscle (4,5,12,30). Increased blood flow resulting from the exercise recovery may also facilitate lactate transport out of the muscle to other tissues for oxidation or resynthesis to glucose (12,30). Theoretically, a valid alternative to active exercise recovery may be transcutaneous electrical muscle stimulation. Low-frequency electrical stimulation results in strong contractions of large skeletal muscles that should increase the energy demand and promote increased blood flow similar to active exercise recovery. Previous studies using similar stimulation protocols have investigated the effect of electrical muscle stimulation on acute and chronic changes in cardiovascular function and aerobic fitness. Banerjee et al. (2) demonstrated that rhythmic muscle contractions of the quadriceps, hamstrings, gluteal, and calf muscles induced by electrical stimulation at 4 Hz resulted in physiologic responses consistent with light to moderate physical exercise in healthy, sedentary adults. Peak heart rate and oxygen uptake with 3 minutes of electrically induced muscle contractions were 101 ± 12 bpm and 14.9 ± 4.3 ml·kg·min−1, respectively (2). Chronic application of electrical muscle stimulation done for 40 minutes per session, 5 sessions per week, for 6 weeks, resulted in a significant aerobic training effect as evidenced by a 10% increase in peak oxygen uptake (1). Poole et al. (24) also showed electrical muscle stimulation at 40 mA acutely increased pulse, blood pressure, energy expenditure, and glucose uptake.
Electrical muscle stimulation during recovery from a 200-yard maximal swim in the current study had a significant effect on blood lactate (Figure 2). From a peak value of 6.25 ± 1.99 mmol·L−1, blood lactate dropped significantly (p < 0.05) to 4.46 ± 1.79 mmol·L−1 after 10 minutes and dropped significantly again to 3.12 ± 1.41 mmol·L−1 after 20 minutes of recovery. At 20 minutes of recovery, the value for blood lactate with electrical stimulation (3.12 ± 1.41 mmol·L−1) was significantly lower compared with passive resting recovery (4.11 ± 1.35 mmol·L−1) but was still significantly higher compared with active swimming recovery (1.60 ± 0.57 mmol·L−1). These results suggest that a passive resting recovery is the least effective treatment for removing blood lactate after a 200-yard swim. When possible, a 20-minute warm-down swim at a velocity 65% of the best 200-yard time would be the preferred recovery treatment because it reduces blood lactate the most. However, if an appropriate warm-down swim is not possible, 20 minutes of electrical muscle stimulation appears to offer a valid alternative treatment option for reducing blood lactate. In addition, other electrical muscle stimulation protocols not yet tested may prove even more effective in reducing blood lactate than the protocol used in this study. Stimulating a greater muscle mass or stimulating at a higher intensity may elicit better results.
In many sports, including swimming, track and field, and wrestling, competition and training require multiple bouts of maximal intensity exercise resulting in significant physiologic and metabolic disturbances. These disturbances can have detrimental effects on the performance of subsequent heats and events in swimming and track and field and on subsequent matches in wrestling. Ideally, an athlete would like to be fully recovered before competing in another heat, event, or match that requires high-intensity exercise. The potential for being fully recovered is influenced by both the length of time an athlete has to recover between exercise bouts and the activity performed during this recovery period. An athlete who passively rests during recovery, such as sitting in a chair or lying on the ground, will fully recover, but it may take over 60 minutes. When the recovery time between exercise bouts is limited to less than 60 minutes, athletes frequently use an active exercise recovery or other alternate treatments to help speed the rate of recovery. Continuing to actively exercise during recovery has the benefit of using some of the metabolic products made during the intense exercise, especially lactate, as a fuel source. The elevated muscle blood flow maintained by the recovery exercise may also promote the removal of lactate and other metabolic products from the exercised muscles but likely to a lesser degree. An athlete will typically have the ability to exercise recover between competitive events by swimming, stationary cycling, running, or walking. There may be situations, however, in which the athlete has limited access to a pool, stationary bike, or opportunities to run or walk, is physically or psychologically exhausted and not motivated to continue to exercise, or simply seeks an alternate recovery treatment. In these situations, using electrical stimulation to produce strong low-frequency muscle contractions while otherwise resting may be of benefit in helping reduce muscle and blood lactate before subsequent performance.
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