Effects of cold water immersion on the symptoms of exercise-induced muscle damage.

Cryotherapy is an effective treatment for acute sports injury to soft tissue, although the effect of cryotherapy on exercise-induced muscle damage is unclear. The aim of this study was to assess the effects of cold water immersion on the symptoms of exercise-induced muscle damage following strenuous eccentric exercise. After performing a bout of damage-inducing eccentric exercise (eight sets of five maximal reciprocal contractions at 0.58 rad x s(-1)) of the elbow flexors on an isokinetic dynamometer, 15 females aged 22.0+/-2.0 years (mean +/- s) were allocated to a control group (no treatment, n = 7) or a cryotherapy group (n = 8). Subjects in the cryotherapy group immersed their exercised arm in cold water (15 degrees C) for 15 min immediately after eccentric exercise and then every 12 h for 15 min for a total of seven sessions. Muscle tenderness, plasma creatine kinase activity, relaxed elbow angle, isometric strength and swelling (upper arm circumference) were measured immediately before and for 3 days after eccentric exercise. Analysis of variance revealed significant (P < 0.05) main effects for time for all variables, with increases in muscle tenderness, creatine kinase activity and upper arm circumference, and decreases in isometric strength and relaxed elbow angle. There were significant interactions (P<0.05) of group x time for relaxed elbow angle and creatine kinase activity. Relaxed elbow angle was greater and creatine kinase activity lower for the cryotherapy group than the controls on days 2 and 3 following the eccentric exercise. We conclude that although cold water immersion may reduce muscle stiffness and the amount of post-exercise damage after strenuous eccentric activity, there appears to be no effect on the perception of tenderness and strength loss, which is characteristic after this form of activity.     

Delayed onset muscle soreness: mechanisms and management.

This review describes the phenomenon of delayed onset muscle soreness (DOMS), concentrating upon the types of muscle contraction most likely to produce DOMS and the theories underlying the physiological mechanisms of DOMS. Ways of attempting to reduce the effects of DOMS are also summarized, including the application of physical and pharmacological therapies to reduce the effects of DOMS and training for reduction or prevention of DOMS.     

Longitudinal monitoring of power output and heart rate profiles in elite cyclists

Power output and heart rate were monitored for 11 months in one female (V(.)O(2max): 71.5 mL · kg?1 · min?1) and ten male (V(.)O(2max): 66.5 ± 7.1 mL · kg?1 · min?1) cyclists using SRM power-meters to quantify power output and heart rate distributions in an attempt to assess exercise intensity and to relate training variables to performance. In total, 1802 data sets were divided into workout categories according to training goals, and power output and heart rate intensity zones were calculated. The ratio of mean power output to respiratory compensation point power output was calculated as an intensity factor for each training session and for each interval during the training sessions. Variability of power output was calculated as a coefficient of variation. There was no difference in the distribution of power output and heart rate for the total season (P = 0.15). Significant differences were observed during high-intensity workouts (P < 0.001). Performance improvements across the season were related to low-cadence strength workouts (P < 0.05). The intensity factor for intervals was related to performance (P < 0.01). The variability in power output was inversely associated with performance (P < 0.01). Better performance by cyclists was characterized by lower variability in power output and higher exercise intensities during intervals.     

Eccentric exercise-induced muscle damage dissociates the lactate and gas exchange thresholds

We tested the hypothesis that exercise-induced muscle damage would increase the ventilatory (V(E)) response to incremental/ramp cycle exercise (lower the gas exchange threshold) without altering the blood lactate profile, thereby dissociating the gas exchange and lactate thresholds. Ten physically active men completed maximal incremental cycle tests before (pre) and 48 h after (post) performing eccentric exercise comprising 100 squats. Pulmonary gas exchange was measured breath-by-breath and fingertip blood sampled at 1-min intervals for determination of blood lactate concentration. The gas exchange threshold occurred at a lower work rate (pre: 136 ± 27 W; post: 105 ± 19 W; P < 0.05) and oxygen uptake (VO(2)) (pre: 1.58 ± 0.26 litres · min(-1); post: 1.41 ± 0.14 litres · min(-1); P < 0.05) after eccentric exercise. However, the lactate threshold occurred at a similar work rate (pre: 161 ± 19 W; post: 158 ± 22 W; P > 0.05) and VO(2) (pre: 1.90 ± 0.20 litres · min(-1); post: 1.88 ± 0.15 litres · min(-1); P > 0.05) after eccentric exercise. These findings demonstrate that exercise-induced muscle damage dissociates the V(E) response to incremental/ramp exercise from the blood lactate response, indicating that V(E) may be controlled by additional or altered neurogenic stimuli following eccentric exercise. Thus, due consideration of prior eccentric exercise should be made when using the gas exchange threshold to provide a non-invasive estimation of the lactate threshold.     

The effect of exercise-induced muscle damage on isometric and dynamic knee extensor strength and vertical jump performance

In this study, we assessed the effect of exercise-induced muscle damage on knee extensor muscle strength during isometric, concentric and eccentric actions at 1.57 rad · s -1 and vertical jump performance under conditions of squat jump, countermovement jump and drop jump. The eight participants (5 males, 3 females) were aged 29.5 - 7.1 years (mean - s ). These variables, together with plasma creatine kinase (CK), were measured before, 1 h after and 1, 2, 3, 4 and 7 days after a bout of muscle damaging exercise: 100 barbell squats (10 sets 2 10 repetitions at 70% body mass load). Strength was reduced for 4 days ( P ? 0.05) but no significant differences ( P > 0.05) were apparent in the magnitude or rate of recovery of strength between isometric, concentric and eccentric muscle actions. The overall decline in vertical jump performance was dependent on jump method: squat jump performance was affected to a greater extent than countermovement (91.6 - 1.1% vs 95.2 - 1.3% of pre-exercise values, P ? 0.05) and drop jump (95.2 - 1.4%, P ? 0.05) performance. Creatine kinase was elevated ( P ? 0.05) above baseline 1 h after exercise, peaked on day 1 and remained significantly elevated on days 2 and 3. Strength loss after exercise-induced muscle damage was independent of the muscle action being performed. However, the impairment of muscle function was attenuated when the stretch-shortening cycle was used in vertical jumping performance.     

Knee joint neuromuscular activation performance during muscle damage and superimposed fatigue

This study examined the concurrent effects of exercise-induced muscle damage and superimposed acute fatigue on the neuromuscular activation performance of the knee flexors of nine males (age: 26.7 ± 6.1 years; height 1.81 ± 0.05 m; body mass 81.2 ± 11.7 kg [mean±s]). Measures were obtained during three experimental conditions: (i) 'fatigue-muscle damage', involving acute fatiguing exercise performed on each assessment occasion plus a single episode of eccentric exercise performed on the first occasion and after the fatigue trial; (ii) 'fatigue', involving the fatiguing exercise only; and (iii) 'control' consisting of no exercise. Assessments were performed prior to (pre) and at 1 h, 24 h, 48 h, 72 h, and 168 h relative to the muscle damaging eccentric exercise. Repeated-measures analyses of variance (ANOVAs) showed that muscle damage elicited reductions of up to 38%, 24% and 65% in volitional peak force, electromechanical delay and rate of force development compared to baseline and controls, respectively (F ([10, 80]) = 2.3 to 4.6; P < 0.05) with further impairments (6.2% to 30.7%) following acute fatigue (F ([2, 16]) = 4.3 to 9.1; P < 0.05). By contrast, magnetically-evoked electromechanical delay was not influenced by muscle damage and was improved during the superimposed acute fatigue (～14%; F ([2, 16]) = 3.9; P < 0.05). The safeguarding of evoked muscle activation capability despite compromised volitional performance might reveal aspects of capabilities for emergency and protective responses during episodes of fatigue and antecedent muscle damaging exercise.     

Heart rate and perceived muscle pain responses to a functional walking test in McArdle disease

Abstract

The aim of this study was to assess a 12-min self-paced walking test in patients with McArdle disease. Twenty patients (44.7 ±11 years; 11 female) performed the walking test where walking speed, distance walked, heart rate (HR) and perceived muscle pain (Borg CR10 scale) were measured. Median (interquartile range) distance walked was 890 m (470–935). From 1 to 6 min, median walking speed decreased (from 75.0 to 71.4 m?min^–1) while muscle pain and %HR reserve increased (from 0.3 to 3.0 and 37% to 48%, respectively). From 7 to 12 min, walking speed increased to 74.2 m?min^–1, muscle pain decreased to 1.6 and %HR reserve remained between 45% and 48%. To make relative comparisons, HR and muscle pain were divided by walking speed and expressed as ratios. These ratios rose significantly between 1 and 6 min (HR:walking speed P = .001 and pain:walking speed P < .001) and similarly decreased between 6 and 11 min (P = .002 and P = .001, respectively). Peak ratios of HR:walking speed and pain:walking speed were inversely correlated to distance walked: r_s (HR) = ?.82 (P < .0001) and r_s (pain) = ?.55 (P = .012). Largest peak ratios were found in patients who walked < 650 m. A 12-min walking test can be used to assess exercise capacity and detect the second wind in McArdle disease.