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).
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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