In the sport of cycling there was an average increase in participation by master racers in USCF (United States Cycling Federation) events of approximately 50% from 1990–1995 (17). This increase in participation in competitive cycling events increases the risk of injuries that can lead to periods of detraining or modified activity. Fractures of the clavicle are a common injury sustained by racing cyclists, with the middle third of the bone as the most common site of fracture seen by physicians (7). Most of these clavicular fractures heal without complication when managed with immobilization using a sling or figure-eight bandage (7). Some, however, occasionally cause lesions of the brachial plexus (1). One purpose of this study was to describe a patient in whom a fracture of the clavicle caused by a crash while racing resulted in brachial plexus impingement and surgery, forcing the athlete into a detraining period lasting 32 d. The major focus, however, was to describe this athlete’s physiological adaptations to a progressive retraining program.
Little is known on the time-course of retraining of young endurance athletes following injury, and even less is known about detraining and retraining of master athletes. Several studies of bed rest, which represents the most extreme form of detraining, have demonstrated significant reductions in aerobic power (V̇O2max), with the degree of decline directly related to the number of days of inactivity (2,3,9,13). Convertino (2) recently evaluated the results of 19 studies of bed rest and found an average daily decline in V̇O2max of approximately 0.9% over a 30-d period. Although this loss is similar in men and women and independent of age, individuals with a high initial aerobic power appear to undergo greater absolute decline in V̇O2max with bed rest (3). When normal daily physical activity is maintained following the cessation of a 6-month period of high intensity endurance training, the physiologic decrements of detraining are attenuated by approximately 50% compared with those observed with bed rest (6).
Although there is an abundance of data on the physiological effects of deconditioning in both the young nonathlete and in recreational athletes (6,14), information is limited on the time-course of retraining in nonathletic older adults (16), and none specifically examines the time-course of retraining in the master athlete in peak condition. Indeed, such a study design is improbable, for competitive athletes at the peak of their training are usually unwilling to voluntarily undergo a detraining period. This case study presents a unique situation in which the subject of another research study had undergone performance testing just 2 d before an injury and subsequent surgery that led to a detraining period lasting approximately 1 month. The primary purpose of this study was to examine the effects of detraining and the time-course of retraining in a highly trained female master cyclist.
This study was approved by the university’s Committee on the Protection of Human Subjects, and written informed consent was obtained from the subject. The physical characteristics of the subject before the injury are shown in Table 1. Although she had been cycle training for 9 yr, for 13 yr before that she trained and competed in running events ranging from 5 km to marathon distances. As a master competitor she had placed in the top five at the United States Cycling Federation (USCF) Masters National Road Championships over the past 4 yr. She also consistently places in the top two or three positions at state and national level NORBA (National Off-Road Bicycle Association) mountain bike events.
Table 2 illustrates the timeline of the study. Baseline data were collected 2 d before the injury as part of another research study. The injury consisted of a right clavicular fracture sustained during a criterium race (Fig. 1A). Following the injury, the athlete continued her training for 8 d on an indoor trainer and then resumed road training on day 9, at first on the rear of a tandem, then 1 wk later on her own bicycle. During this time she did not reduce the intensity or the volume of her training. Twenty-two days after the injury she developed complications of the right shoulder consisting of nearly complete loss of range of motion and numbness and tingling in the right hand. Two days later she was diagnosed with brachial plexus impingement and referred for surgery. Surgery was performed 26 d postinjury, after which the subject began a detraining period that lasted 32 d. Thus, the detraining period did not begin until approximately 4 wk after the initial injury. Retesting was conducted initially on day 32 postsurgery (Day 0 of retraining). The retraining period began at this time and follow-up data were collected again on days 14, 28, 42, and 77 of the retraining period.
The surgery consisted of reducing the fracture, removing a bone fragment that was impinging upon the brachial plexus, and stabilizing the clavicle with a steel plate and seven screws (Fig. 1B). Following surgery the subject lost complete function of the shoulder, elbow, and hand. She was then diagnosed with probable contusion of the brachial plexus and told that function should gradually return to normal. Range of motion of the shoulder and elbow, but not the hand, returned within approximately 4–5 d. Strength and function of the hand gradually began to improve after approximately 10 d, with full strength and function resuming after 8 wk.
During the first 2 wk after surgery, the athlete engaged in no structured exercise and minimal daily physical activity. From day 15–21 postsurgery she walked daily for approximately 20–30 min at very low intensity (RPE = 3–4 on 10-point scale), then from day 22–30 she resumed indoor riding on a stationary wind trainer for approximately 15–30 min every other day at low intensity (RPE = 4–5).
Retesting was conducted initially on day 32 postsurgery. The athlete then began a structured retraining program, gradually progressing from approximately 40% of her usual training volume and intensity to 100% over the next 11 wk (Table 3). By the 11th week of retraining she had reached her normal training regimen for that phase of her year-round program. The outcome variables examined were aerobic power (V̇O2max), lactate threshold (LT), power output at 4 mM lactate (LT4 mM), peak lactate, peak power output (PPO), leg fatigue at 110% of PPO (PPO110), and body composition (% fat and fat-free mass (FFM)) measured by hydrodensitometry.
V̇O2max and lactate threshold.
V̇O2max and LT were determined on an electrically-braked cycle ergometer (Lode Excalibur, Groningen, The Netherlands), which was equipped with the subject’s own pedals to allow use of her own cleated shoes. Before exercise a baseline blood sample was obtained, by finger prick using 50-μL heparanized capillary tubes, and analyzed immediately, in duplicate, for whole blood lactate with the YSI Sport Lactate Analyzer (YSI Incorp., Yellow Springs, OH). The analyzer was calibrated with standard solutions (5 mM and 15 mM HLA+) before each test. The subject then warmed up for 10–15 min at approximately 75 W at her preferred cadence. Following the warm-up the resistance was increased to 100 W for the first stage, which was 4 min in duration. The protocol consisted of 25 W increments every 3 min thereafter (19). During the last 30 s of each stage a blood sample was obtained. Once the subject completed a workload at a blood lactate level of 4 mM or greater, she was allowed 4–5 min of active recovery before beginning the V̇O2max protocol, which consisted of continuous cycling, beginning at a work rate one stage lower than that at LT and increasing by 25 W every minute until she reached the PPO attained on the previous test. Thereafter, 15- to 20-W increases were made until exhaustion, which was defined as the point at which the subject could no longer turn the cranks. Lactate threshold was defined as the power output and V̇O2 attained just before a curvilinear increase in blood lactate and an absolute rise in lactate of 1 mM or more (20).
During the entire procedure the subject breathed through a one-way valve (Hans Rudolph, Kansas City, MO), which was connected by tubing to a VMAX 29 metabolic cart (Sensormedics, Corp, Anaheim, CA). Gas analyzers were calibrated before each testing session using ambient air and two separate gas concentrations. Minute ventilation (V̇E) was measured by the metabolic cart via a mass flow sensor, which was calibrated before each testing session with a 3-L calibration syringe.
Heart rate was monitored using a Uniq CIC heart rate monitor (Polar CIC, Inc, Port Washington, NY) taped to the handlebar of the ergometer. Heart rate was recorded during the last 10 s of each stage of exercise.
Muscular resistance to fatigue (PPO110).
Following a 10–15 min rest, the subject performed a fatigue test at 110% of PPO achieved on the initial (preinjury) V̇O2max test. This absolute power output was used for each subsequent testing period. The resistance was initially set at 100 W while the subject increased her cadence to greater than 120 rpm. The power output was quickly increased to 303 W (110% PPO). The subject then pedaled until her cadence fell below 70 rpm. Endurance time was measured with a stopwatch to the closest hundredth of a second. The reliability of the time taken for the investigator to increase the power output from 100 W to 303 W was later tested by having the same investigator perform 10 trials in succession. The mean, SD and range of scores for the 10 trials were 2.80 ± 0.44; 2.31–3.85 s. Thus, a change in score for PPO110 was considered meaningful if the time was ± 2.0 s.
Body density was measured by hydrodensitometry. Residual lung volume was assessed by the oxygen dilution technique (21). Percent fat was estimated from the Siri equation (15) and fat-free mass (FFM) was then computed.
Table 4 displays the physiological data at each time point, while Figure 2 illustrates the changes in aerobic power and LT4 mM throughout the retraining period. The V̇O2max of the subject decreased 25.7% over the 4-week detraining period, while the power output at LT and at LT4 mM decreased 16.7% and 18.9%, respectively. Peak power output measured from the graded exercise test decreased 18.2%, while PPO110 decreased 16.6%. Percentage of body fatness increased 2.1 percentage points, while fat-free mass decreased nearly 2 kg.
After 2 wk of retraining, all variables except the LT and LT4mM had improved considerably; however, V̇O2peak was still 14.8% lower, while PPO and PPO110 were 12.7% and 5.7% lower than preinjury values. By the fourth week of retraining, LT had returned to the preinjury value, but LT4 mM remained 12.4% lower, while V̇O2max was just 2.3% lower than the preinjury value. Body composition had improved slightly at this point. Lactate threshold had returned to its preinjury level; however, the LT4 mM was still 12% lower than that at baseline.
At 6 wk of retraining a similar pattern as that at 4 wk was observed. V̇O2peak and LT had reached their preinjury values, but PPO and LT4 mM were still 5.5% and 12.4% lower than at preinjury, while PPO110 was just 3.9% lower. By the final measurement at 11 wk, PPO and PPO110 had returned to their preinjury values, but LT4 mM remained 5.5% below its baseline value.
Although these data are from a single subject, this report is the first of its kind in the master athlete. A strength of this report is having baseline (preinjury) data collected at the peak of the subject’s competitive season just 2 d before the injury. Without such baseline data it would be impossible to quantify the actual amount of physiological decline or to accurately describe the timeline of retraining to the preinjured state.
The clinical data represent a fairly rare case in that clavicular fracture typically does not require surgery (7). Since the symptoms of brachial plexus impingement are usually delayed (1), it is unknown whether the athlete’s early return to road training (9 d postinjury) may have induced the impingement or whether the location of the fragmented bone was such that this would have occurred anyway. Either way, athletes need to be cautioned regarding the risks of resuming training too soon. False assumptions are often made by cyclists that if they are able to hold onto the handlebars of their bike with little or no pain then it is acceptable to resume cycle training with a clavicular fracture. These athletes need to be made aware of the possible complications of this injury.
The results indicate that approximately 11 wk were required for the athlete to return to her preinjured level of fitness. The large (25%) decrease in aerobic power was somewhat surprising. Although complete bed rest results in a loss in aerobic power of approximately 1% per day over a 30-d period (2), the cessation of training but maintenance of normal physical activity results in much smaller losses in V̇O2max (6). Although the subject remained in a supine or semisupine position for the first 2 wk of the detraining period, the observed decline in her aerobic power was still approximately 10% greater than that reported in earlier literature (2,6). Although measurements were not made during the 32 d of detraining, it is likely that much of the decrease in V̇O2max occurred during those first 2 wk of detraining when she remained in bed, with a further loss over the next 2 wk (6).
Possible underlying mechanisms for the loss in aerobic power with detraining have been proposed by others (2,6), who suggest that the early, rapid decline in V̇O2max is a result of a decrease in stroke volume attributed to a decrease in blood volume (12), with a later decline in arterial-venous O2 difference (6). The large decrease in V̇O2max despite a 5–8 beats·min−1 increase in HRmax in our subject after detraining is suggestive of a large decrease in stroke volume. This is further supported by data from Coyle et al. (6), who showed very little change in arterio-venous O2 difference in the early phase of detraining, followed by approximately a 7% decline after 84 d of detraining in previously highly trained subjects. The decrease in oxygen extraction by skeletal muscle was explained by a large decrease in mitochondrial enzyme activity after 56 d of detraining (6). Thus, it appears that cardiac mechanisms are responsible for the early changes that occur with detraining, with peripheral changes occurring more slowly, especially in athletes who have had years of endurance training (6).
The large increase we observed in HRmax with 32 d of detraining and early in the retraining period has also been demonstrated following bed rest (3) and with a detraining period as short as 15 d (10) and as long as 84 d (6). Elevations in plasma norepinephrine following 16 d of bed rest have been reported (8). If increased sympathetic secretion of norepinephrine also occurs with detraining, this could explain the elevation in the maximal heart rate of our subject.
No studies could be found that examined changes in lactate threshold with detraining and retraining. A 25- and 35-W decrease from baseline in power output at LT and LT4 mM, respectively, were noted. After 4 wk of retraining, the LT had returned to its preinjury value, but LT4 mM was still 23 W lower than the preinjury value. Although no performance testing was conducted in the present study, the decrease in LT and LT4 mM would likely reflect a decrease in performance, particularly in events such as the 40 km time trial, which has been shown to correlate highly with various blood lactate measures (5,12).
The changes in muscular resistance to fatigue (PPO110) during retraining appear to parallel those of peak power output. That is, they decreased 17–18% with detraining, then steadily improved over the retraining period. Since it was decided to use 110% of the preinjury peak power output for all retesting, the actual absolute power output remained constant at 303 W throughout the retraining period. Thus, the subject was performing this test at a higher relative power output during the retraining phase. The improvement in PPO110 after just 2 wk of retraining was surprising, given that the training at this time consisted of mostly moderate, steady-state endurance exercise. Since the contribution from anaerobic sources to the energy requirements of approximately 60 s of all-out effort is estimated at approximately 50–60% (11), it would be expected that improvement in this variable would require high intensity efforts for a duration of 1–2 min.
The overall pattern of retraining demonstrated a steady improvement in aerobic power over 6 wk, but essentially little or no change in power output corresponding to LT and LT4 mM until after 4–6 wk of retraining. This may reflect a differential adaptation rate between central and peripheral systems. This could also be a result of the intensity at which the subject trained. For the first 2–3 wk her exertion was kept at a moderate intensity, with very few hard efforts (Table 3). By week 4 she had increased the intensity with interval training during two of her weekly training sessions. Although moderate intensity endurance training could be expected to increase V̇O2max, it has been shown in runners that training above the lactate threshold induced greater changes in velocity of running at LT and at LT4 mM than did training at or below the lactate threshold (18). Others have also shown that high intensity interval training raises the lactate threshold (4)
In conclusion, these data illustrate the timeline of retraining in a female master cyclist following an injury sustained at the peak of her competitive season. With a structured, progressive program increasing in volume and intensity biweekly, this master athlete reached her preinjury level of fitness in approximately 11 wk. The clinical data illustrate the need for caution when resuming cycling with clavicular fracture. Cyclists should be informed of the risks associated with this injury to prevent complications and further loss of training.
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