Cramp Training Induces a Long-Lasting Increase of the Cramp Threshold Frequency in Healthy Subjects.

OBJECTIVE: A low cramp threshold frequency (CTF) is associated with an increased cramp susceptibility. Recent data indicate that the CTF can be substantially increased by a cramp training consisting of electrically induced muscle cramps (EIMCs). This study investigated if four cramp training sessions induce sustained effects on the CTF. METHODS: In ten healthy male subjects, EIMCs were induced in the gastrocnemius medialis of one leg (intervention leg, IL) twice a week, while the opposite leg served as control leg (CL). The stimulation protocol consisted of three sets of six bipolar rectangular wave pulsed currents (5 sec on, 10 sec off) at 30 Hz above the individual CTF. RESULTS: After four cramp training sessions (2 weeks) the CTF differed (p < 0.001) from pre-values in the IL (pre: 19.2 ± 1.4 Hz post 29.8 ± 8.0 Hz) but not in the CL (pre: 18.2 ± 1.5 Hz post 19.6 ± 2.8 Hz; p > 0.05). Thereafter, the CTF remained elevated in the IL for 22 days (22 days post: 22.2 ± 3.2 Hz; p < 0.05) when compared to pre and was significantly (p < 0.05) higher than that of the CL 5, 10, and 14 days after the intervention. CONCLUSION: The applied cramp training induced a long-term CTF increase of 14 days.

Low-Intensity Sprint Training With Blood Flow Restriction Improves 100-m Dash.

Behringer, M, Behlau, D, Montag, JCK, McCourt, ML, and Mester, J. Low-intensity sprint training with blood flow restriction improves 100-m dash. J Strength Cond Res 31(9): 2462-2472, 2017-We investigated the effects of practical blood flow restriction (pBFR) of leg muscles during sprint training on the 100-m dash time in well-trained sport students. Participants performed 6 × 100-m sprints at 60-70% of their maximal 100-m sprinting speed twice a week for 6 weeks, either with (intervention group [IG]; n = 12) or without pBFR (control group [CG]; n = 12). The 100-m dash time significantly decreased more in the IG (-0.38 ± 0.24 seconds) than in the CG (-0.16 ± 0.17 seconds). The muscle thickness of the rectus femoris increased only in the IG, whereas no group-by-time interactions were found for the muscle thickness of the biceps femoris and the biceps brachii. The maximal isometric force, measured using a leg press, did not change in either group. However, the rate of force development improved in the IG. Growth hormone, testosterone, insulin-like growth factor 1, and cortisol concentrations did not significantly differ between both groups at any measurement time point (pre, 1 minute, 20 minutes, 120 minutes, and 24 hours after the 6 all-out sprints of the first training session). The muscle damage marker h-FABP increased significantly more in the CG than in the IG. The pBFR improved the 100-m dash time significantly more than low-intensity sprint interval training alone. Other noted benefits of training with pBFR were a decreased level of muscle damage, a greater increase of the rectus femoris muscle thickness, and a higher rate of force development. However, the tested hormones were unable to explain the additional beneficial effects.

Polyamines, myosin heavy chains, and collagen specific amino acids after a repeated bout of eccentric exercise.

We investigated alternatives to commonly used biomarkers of exercise-induced tissue damage. Over 5 days following two bouts of 100 drop-to-vertical jumps (inter-bout rest period of 3 weeks), myosin heavy chain 1, hydroxylysine (HYL), hydroxyproline (HYP), spermine (SPM) and spermine synthase (SMS) were measured in the serum of 10 participants. HYL significantly increased from 5.92 ± 1.49 ng/mL to 6.48 ± 1.47 ng/mL at 24 h. A similar trend was observed for bout 2, but without reaching significance. SPM significantly increased only after bout 1 from 0.96 ± 0.19 ng/mL at pretest to a peak level of 1.12 ± 0.26 ng/mL at 24 h, while B2 increments remained non-significant. Myosin heavy chain 1, HYP and SMS values remained below the detection limit of the applied enzyme-linked immunosorbent assay (ELISA) kit. Though HYL and SM increased after the intervention, both markers showed a large standard deviation (SD) combined with small increments. Therefore, none of the investigated biomarkers provides a meaningful alternative to commonly used damage markers.

Effects of stimulation frequency, amplitude, and impulse width on muscle fatigue.

INTRODUCTION: We investigated the effect of stimulation intensity (in percent of maximal tolerated stimulation current, mTSC), frequency, and impulse width on muscle fatigue. METHODS: Using a randomized crossover design, 6 parameter combinations (80% mTSC, 80 Hz, 400 µs; 60% mTSC, 80 Hz, 400 µs; 80% mTSC, 20 Hz, 400 µs; 60% mTSC, 20 Hz, 400 µs; 80% mTSC, 80 Hz, 150 µs; 60% mTSC, 80 Hz, 150 µs) were tested in both legs of 13 athletic men (age 26 ± 2.3). The slope of the linear regression line over all tetani (FIS) and the number of tetani whose force was above 50% of the initial tetanus (FIN) were used to quantify fatigue. RESULTS: FIS and FIN were significantly lower in high-frequency protocols. No effects on FIS and FIN were found for intensity and impulse width. CONCLUSIONS: Stimulation frequency, but not impulse width or intensity, affected fatigue kinetics.

Are Electrically Induced Muscle Cramps Able to Increase the Cramp Threshold Frequency, When Induced Once a Week?

The cramp threshold frequency (CTF) is known to be positively correlated with the individual cramp susceptibility. Here we assessed CTF changes after two bouts of electrically induced muscle cramps (EIMCs). The EIMCs (6×5 sec) were unilaterally induced twice (separated by one week) in the gastrocnemius of an intervention group (n=8), while 5 participants served as control. The CTF increased from 25.1±4.6 Hz at baseline to 31.4±9.0 Hz and 31.7±8.5 Hz 24 h after bout 1 and 2 (P<0.05). Thereafter, the CTF declined following both bouts to reach values of 28.0±6.7 Hz and 29.1±7.7 Hz after 72 h after bout 1 and 2. Creatine kinase (CK) activity and perceived discomfort during cramps was lower after bout 2 (P<0.05). CTF, CK, and discomfort did not change in CG. That is, a single bout of EIMCs induces a 24 h CTF increment and a second bout sustains this effect, while perceived discomfort and muscle damage decreases. This short term effect may help athletes to reduce the cramp susceptibility for an important match.

Exhaustive exercise--a near death experience for skeletal muscle cells?

In sports medicine, muscle enzymes in the blood are frequently used as an indicator of muscle damage. It is commonly assumed that mechanical stress disrupts plasma membrane to an extent that allows large molecules, such as enzymes, to leak into the extracellular space. However, this does not appear to fully explain changes in muscle enzyme activity in the blood after exercise. Apart from this mechanically induced membrane damage, we hypothesize that, under critical metabolic conditions, ATP consuming enzymes like creatine kinase (CK) are "volitionally" expulsed by muscle cells in order to prevent cell death. This would put themselves into a situation comparable to that of CK deficient muscle fibers, which have been shown in animal experiments to be virtually infatigable at the expense of muscle strength. Additionally we expand on this hypothesis with the idea that membrane blebbing is a way for the muscle fibers to store CK in fringe areas of the muscle fiber or to expulse CK from the cytosol by detaching the blebs from the plasma membrane. The blebbing has been shown to occur in heart muscle cells under ischaemic conditions and has been speculated to be an alternative pathway for the expulsion of troponin. The blebbing has also been seen skeletal muscle cells when intracellular calcium concentration increases. Cytoskeletal damage, induced by reactive oxygen species (ROS) or by calcium activated proteases in concert with increasing intracellular pressure, seems to provoke this type of membrane reaction. If these hypotheses are confirmed by future investigations, our current understanding of CK as a blood muscle damage marker will be fundamentally affected.

Serum Cartilage Oligomeric Matrix Protein: is There a Repeated Bout Effect?

The primary aim of the present study was to investigate if there is a repeated bout effect for cartilage tissue, evident in the marker serum cartilage oligomeric matrix protein (sCOMP). Ten healthy male subjects (26.4±3.14 years) performed two high impact interventions (100 drop jumps with a 30 second interval) carried out at a 3 week interval. After each intervention, sCOMP and muscle soreness were assessed on 8 and 6 occasions respectively. Muscle soreness was determined via a visual analog scale with a maximum pain score of 10. sComp levels did not show a blunted response after the second bout (Bout 1: 12.2±3.3 U/L(-1); Bout 2: 13.1±4.0 U/L(-1); P>0.05). Remarkably, sCOMP increased from baseline levels by 16% after bout 1 and 15% after bout 2. Muscle soreness was blunted following the second intervention (Bout 1: 5.0±1.8; Bout 2: 1.6±0.8). Unlike the known repeated bout effect for muscle damage markers, sCOMP levels do not show a blunted response after two similar loading interventions. This information on biomarker behavior is essential to clinicians attempting to use this marker as an indicator of cartilage damage associated with the development or progression of osteoarthritis.

A promising approach to effectively reduce cramp susceptibility in human muscles: a randomized, controlled clinical trial.

BACKGROUND: To investigate if the cramp threshold frequency (CTF) can be altered by electrical muscle stimulation in a shortened position. METHODS: A total of 15 healthy male sport students were randomly allocated to an intervention (IG, n = 10) and a non-treatment control group (CG, n = 5). Calf muscles of both legs in the IG were stimulated equally twice a week over 6 weeks. The protocol was 3×5 s on, 10 s off, 150 µs impulse width, 30 Hz above the individual CTF, and was at 85% of the maximal tolerated stimulation energy. One leg was stimulated in a shortened position, inducing muscle cramps (CT), while the opposite leg was fixated in a neutral position at the ankle, hindering muscle cramps (nCT). CTF tests were performed prior to the first and 96 h after the 6(th) (3 w) and 12(th) (6 w) training session. RESULTS: After 3 w, the CTF had significantly (p<0.001) increased in CT calves from 23.3±5.7 Hz to 33.3±6.9 Hz, while it remained unchanged in nCT (pre: 23.6±5.7 Hz, mid: 22.3±3.5 Hz) and in both legs of the CG (pre: 21.8±3.2 Hz, mid: 22.0±2.7 Hz). Only CT saw further insignificant increases in the CTF. The applied stimulation energy (mA² • µs) positively correlated with the effect on the CTF (r = 0.92; p<0.001). CONCLUSIONS: The present study may be useful for developing new non-pharmacological strategies to reduce cramp susceptibility. TRIAL REGISTRY: German Clinical Trials Register DRKS00005312.