Completion of an Ironman triathlon results in muscle damage, indicated by reductions in muscle function and muscle soreness. However, the time course of recovery from this damage has received little attention. The purpose of this case study was to examine the time course of changes in blood markers of muscle damage and inflammation, muscle function, muscle soreness, and economy of motion following an Ironman event. An experienced well-trained male triathlete aged 35 years completed the Western Australian Ironman triathlon in 11 h 38 min 41 s (winner’s time: 8 h 3 min 56 s). Before and on several occasions in the 15 days after the event, the participant performed an incremental cycling test to exhaustion, running economy test at 12 km · h (2% incline), maximal isometric knee flexion and extension at 90° knee flexion, and maximal squat and countermovement jumps. Venous blood samples and muscle soreness were also assessed. Maximal oxygen consumption, efficiency of motion, maximal muscle strength, and jump performance were all markedly reduced (4.5–54%) following the event, but returned to baseline within 15, 8, 2, and 8 days following the event, respectively. Muscle soreness and blood markers peaked 2–24 h after the race but returned to baseline within 8 days. In conclusion, although the Ironman triathlon induces marked muscle damage, a trained triathlete recovered almost completely within approximately one week, without the use of any therapeutic interventions after the event.
Figure 1. Schematic time line of measurements before and after the Ironman triathlon event.
Figure 2. Running economy expressed as oxygen consumption, gross cycling efficiency, and maximal oxygen consumption during cycling before (pre) and 3, 8, and 15 days after the Ironman event.
Figure 3. Maximal isometric strength of the knee extensors (MVCKE) and knee flexors (MVC-KF), grip strength, squat jump (SJ) height, and counter movement jump (CMJ) height before and in the 15 days after the Ironman event.
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Figure 2. Changes (mean + s) in (a) _ V O 2 , (b) minute ventilation ( _ V E ), (c) respiratory exchange ratio (RER), (d) heart rate (HR), and (e) rating of perceived exertion (RPE) during 5 min of level running, and (f) blood lactate concentration (LA) 3 min after 5 min of level running at 70%, 80%, and 90% _ V O 2max before (pre), and 2 and 5 days after, downhill running (DHR). *Significant (P 5 0.05) interaction (intensity 6 time) effect. # Significant (P 5 0.05) difference from baseline (pre) values.
In this study, we tested the hypothesis that running economy assessed at a high intensity [e.g. 90% maximal oxygen capacity (VO2(max))] would be affected more than at a lower intensity (e.g. 70% VO2(max)) after downhill running. Fifteen untrained young men performed level running at 70, 80, and 90% VO2(max) (5 min for each intensity) before and 2 and 5 days after a 30-min downhill run (gradient of -16%) at the intensity of their pre-determined 70% VO2(max). Oxygen consumption, minute ventilation, respiratory exchange ratio, heart rate, rating of perceived exertion, and blood lactate concentration were measured during the level runs together with kinematic measures (e.g. stride length and frequency) using high-speed video analysis. Downhill running resulted in significant (P < 0.05) decreases in maximal isometric strength of the knee extensors, the development of muscle soreness, and increases in plasma creatine kinase activity and myoglobin concentration, which lasted for 5 days after downhill running. Significant (P < 0.05) changes in all running economy and kinematic measures from baseline were evident at 2 and 5 days after downhill running at 80% and 90% VO2(max), but not at 70% VO2(max). These results suggest that running economy assessed at high intensity is affected more than at low intensity (lower than the lactate threshold).
Table 1 Physiological characteristics for participant group (n = 7)
Fig. 2 Changes in RPE at each 60 s interval during the timetrial at baseline (black), 48 h (open) and 168 h (grey) following 100 jumps. Values expressed as mean ± SEM. Asterisks indicates significant difference between 60 s time interval (P \ 0.05)
Table 2 Changes in cardio-respiratory, perceptual, blood lactate and pedal force responses during cycling intensities corresponding to 60%P max and 80%P max following jumping exercise
The effect of exercise-induced muscle damage on perceived exertion and cycling endurance performance
This study evaluated the effects of exercise-induced muscle damage (EIMD) on fixed-load cycling and 5-min time-trial performance. Seven recreational athletes performed two submaximal fixed-load exercise bouts followed by a 5-min time-trial before, 48 and 168 h following 100 counter-movement jumps. Measurements of V(O)(2) heart rate, RER and blood lactate concentration remained unchanged during the fixed-load bouts following jumping exercise. However, VE and VE/VO2 increased (P < 0.05) at 48 h. RPE values were higher at 48 h as were the ratio of RPE:HR and RPE:VO2 (P < 0.05). In the time-trial, mean VO2 peak power output, mean power output, distance covered and post exercise blood lactate were lower at 48 h (P < 0.05). RPE remained unchanged between trials. These findings indicate that the ventilatory equivalent for oxygen and perceived exertion at sub maximal work rates are increased 48 h following eccentric exercise. Furthermore, RIMS increase.
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