Kazuaki SHIMAMOTO, Katsuyuki ANDO, Toshiro FUJITA, Naoyuki HASEBE, Jitsuo HIGAKI, Masatsugu HORIUCHI, Yutaka IMAI, Tsutomu IMAIZUMI, Toshihiko ISHIMITSU, Masaaki ITO, Sadayoshi ITO, Hiroshi ITOH, Hiroshi IWAO, Hisashi KAI, Kazuomi KARIO, Naoki KASHIHARA, Yuhei KAWANO, Shokei KIM-MITSUYAMA, Genjiro KIMURA, Katsuhiko KOHARA, Issei KOMURO, Hiroo KUMAGAI, Hideo MATSUURA, Katsuyuki MIURA, Ryuichi MORISHITA, Mitsuhide NARUSE, Koichi NODE, Yusuke OHYA, Hiromi RAKUGI, Ikuo SAITO, Shigeyuki SAITOH, Kazuyuki SHIMADA, Tatsuo SHIMOSAWA, Hiromichi SUZUKI, Kouichi TAMURA, Norio TANAHASHI, Takuya TSUCHIHASHI, Makoto UCHIYAMA, Shinichiro UEDA, Satoshi UMEMURA, on behalf of The Japanese Society of Hypertension Committee for Guidelines for the Management of Hypertension

/pdf/the-japanese-society-of-hypertension-guidelines-for-the-39bqgfj2cl.pdf

The Japanese Society of Hypertension guidelines for the management of hypertension (JSH 2014)

Areas of general agreement: Total creatine kinase (CK) levels depend on age, gender, race, muscle mass, physical activity and climatic condition. High levels of serum CK in apparently healthy subjects may be correlated with physical training status, as they depend on sarcomeric damage: strenuous exercise that damages skeletal muscle cells results in increased total serum CK. The highest postexercise serum enzyme activities are found after prolonged exercise such as ultradistance marathon running or weight-bearing exercises and downhill running, which include eccentric muscular contractions. Total serum CK activity is markedly elevated for 24 h after the exercise bout and, when patients rest, it gradually returns to basal levels. Persistently increased serum CK levels are occasionally encountered in healthy individuals and are also markedly increased in the pre-clinical stages of muscle diseases. Areas that are controversial: Some authors, studying subjects with high levels of CK at rest, observed that, years later, subjects developed muscle weakness and suggested that early myopathy may be asymptomatic. Others demonstrated that, in most of these patients, hyperCKemia probably does not imply disease. In many instances, the diagnosis is not formulated following routine examination with the patients at rest, as symptoms become manifest only after exercise. Some authors think that strength training seems to be safe for patients with myopathy, even though the evidence for routine exercise prescription is still insufficient. Others believe that, in these conditions, intense prolonged exercise may produce negative effects, as it does not induce the physiological muscle adaptations to physical training given the continuous loss of muscle proteins. Growing points: High CK serum levels in athletes following absolute rest and without any further predisposing factors should prompt a full diagnostic workup with special regards to signs of muscle weakness or other simple signs that, in both athletes and sedentary subjects, are not always promptly evident. These signs may indicate subclinical muscle disease, which training loads may evidence through the onset of profound fatigue. It is probably safe to counsel athletes with suspected myopathy to continue to undertake physical activity at a lower intensity, so as to prevent muscle damage from high intensity exercise and allow ample recovery to favour adequate recovery.

Creatine kinase monitoring in sport medicine

The autonomic nervous system.

Regional limb blood flow has been measured with dilution techniques (cardio-green or thermodilution) and ultrasound Doppler. When applied to the femoral artery and vein at rest and during dynamical exercise these methods give similar reproducible results. The blood flow in the femoral artery is approximately 0.3 L min(-1) at rest and increases linearly with dynamical knee-extensor exercise as a function of the power output to 6-10 L min[-1] (Q= 1.94 + 0.07 load). Considering the size of the knee-extensor muscles, perfusion during peak effort may amount to 2-3 L kg(-1) min(-1), i.e. approximately 100-fold elevation from rest. The onset of hyperaemia is very fast at the start of exercise with T 1/2 of 2-10 s related to the power output with the muscle pump bringing about the very first increase in blood flow. A steady level is reached within approximately 10-150 s of exercise. At all exercise intensities the blood flow fluctuates primarily due to the variation in intramuscular pressure, resulting in a phase shift with the pulse pressure as a superimposed minor influence. Among the many vasoactive compounds likely to contribute to the vasodilation after the first contraction adenosine is a primary candidate as it can be demonstrated to (1) cause a change in limb blood flow when infused i.a., that is similar in time and magnitude as observed in exercise, and (2) become elevated in the interstitial space (microdialysis technique) during exercise to levels inducing vasodilation. NO appears less likely since NOS blockade with L-NMMA causing a reduced blood flow at rest and during recovery, it has no effect during exercise. Muscle contraction causes with some delay (60 s) an elevation in muscle sympathetic nerve activity (MSNA), related to the exercise intensity. The compounds produced in the contracting muscle activating the group IIl-IV sensory nerves (the muscle reflex) are unknown. In small muscle group exercise an elevation in MSNA may not cause vasoconstriction (functional sympatholysis). The mechanism for functional sympatholysis is still unknown. However, when engaging a large fraction of the muscle mass more intensely during exercise, the MSNA has an important functional role in maintaining blood pressure by limiting blood flow also to exercising muscles.

Skeletal muscle blood flow in humans and its regulation during exercise

Anaerobic tests are divided into tests measuring anaerobic power and anaerobic capacity. Anaerobic power tests include force-velocity tests, vertical jump tests, staircase tests, and cycle ergometer tests. The values of maximal anaerobic power obtained with these different protocols are different but generally well correlated. Differences between tests include factors such as whether average power or instantaneous power is measured, active muscle mass is the same in all the protocols, the legs act simultaneously or successively, maximal power is measured at the very beginning of exercise or after several seconds, inertia of the devices and body segments are taken into account. Force-velocity tests have the advantage of enabling the estimation of the force and velocity components of power, which is not possible with tests such as a staircase test, a vertical jump, the Wingate test and other long-duration cycle ergometer protocols. Maximal anaerobic capacity tests are subdivided into maximal oxygen debt test, ergometric tests (all-out tests and constant load tests), measurement of oxygen deficit during a constant load test and measurement of peak blood lactate. The measurement of the maximal oxygen debt is not valid and reliable enough to be used as an anaerobic capacity test. The aerobic metabolism involvement during anaerobic capacity tests, and the ignorance of the mechanical efficiency, limit the validity of the ergometric tests which are only based on the measurement of work. The amount of work performed during the Wingate test depends probably on glycolytic and aerobic power as well as anaerobic capacity. The fatigue index (power decrease) of the all-out tests is not reliable and depends probably on aerobic power as well as the fast-twich fibre percentage. Reliability of the constant load tests has seldom been studied and has been found to be rather low. In theory, the measure of the oxygen deficit during a constant load test is more valid than the other tests but its reliability is unknown. The validity and reliability of postexercise blood lactate as a test of maximal anaerobic capacity are probably not better than that of the current erogmetric tests. The choice of an anaerobic test depends on the aims and subjects of a study and its practicability within a testing session.

Standard Anaerobic Exercise Tests

The aim of this study was to clarify the relationship between sympathetic outflow to skeletal muscle and oxygen uptake during dynamic exercise. Muscle sympathetic nerve activity (MSNA) was recorded from the right median nerve microneurographically in eight healthy volunteers during leg cycling at four different intensities in a seated position for a 16-min bout. Work loads selected were 20, 40, 60, and 75% of maximal oxygen uptake (VO2max). Heart rate and blood pressure were measured during each exercise test. MSNA burst frequency was suppressed by 28% during cycling at 20% VO2max (23 vs. 33 bursts/min for control). Thereafter, it increased in a linear fashion with increasing work rate, with a significantly higher burst frequency during 60% VO2max than the control value. Both heart rate and mean blood pressure rose significantly during 20% VO2max from the control value and increased linearly with increased exercise intensity. During light exercise, MSNA was suppressed by arterial and cardiopulmonary baroreceptors as a result of the hemodynamic changes associated with leg muscle pumping. The baroreflex inhibition may overcome the muscle metaboreflex excitation to induce MSNA suppression during light exercise. These results suggest that during light exercise MSNA is inhibited, perhaps due to loading of the cardiopulmonary and arterial baroreflexes, and that during heavier exercise the increase in MSNA occurs as muscle metaboreflexes are activated.

Muscle sympathetic nerve responses to graded leg cycling

We tested the hypotheses that arterial baroreflex (ABR) control over muscle sympathetic nerve activity (MSNA) in humans does not remain constant throughout a bout of leg cycling ranging in intensity from very mild to exhausting. ABR control over MSNA (burst incidence, burst strength and total MSNA) was evaluated by analysing the relationship between beat-to-beat spontaneous variations in diastolic arterial pressure (DAP) and MSNA in 15 healthy subjects at rest and during leg cycling in a seated position at five workloads: very mild (10 W), mild (82 ± 5.0 W), moderate (126 ± 10.2 W), heavy (156 ± 14.3 W), and exhausting (190 ± 21.2 W). The workload was incremented every 6 min. The linear relationships between DAP and MSNA variables were significantly shifted downward during very mild exercise, but then shifted progressively upward as exercise intensity increased. During heavy and exhausting exercise, moreover, the DAP–MSNA relationships were also significantly shifted rightward from the resting relationship. The sensitivity of ABR control over burst incidence and total MSNA was significantly lower during very mild exercise than during rest, and the sensitivity of the burst incidence control remained lower than the resting level at all higher exercise intensities. By contrast, the sensitivity of the total MSNA control recovered to the resting level during mild and moderate exercise, and was significantly increased during heavy and exhausting exercise (versus rest). We conclude that, in humans, ABR control over MSNA is not uniform throughout a leg cycling exercise protocol in which intensity was varied from very mild to exhausting. We suggest that this non-uniformity of ABR function is one of the mechanisms by which sympathetic and cardiovascular responses are matched to the exercise intensity.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.2007.150060

Modulation of the control of muscle sympathetic nerve activity during incremental leg cycling.

We investigated the time-dependent modulation of arterial baroreflex (ABR) control of muscle sympathetic nerve activity (MSNA) that occurs during isometric handgrip exercise (IHG) Thirteen healthy

Time-dependent modulation of arterial baroreflex control of muscle sympathetic nerve activity during isometric exercise in humans.

Blood lactate was determined in 19 untrained subjects after maximal treadmill exercise lasting for about 1 min. It was found that blood lactate increases after exercise, reaching a maximum level 6–9 min after the cessation of exercise, and the average time for the appearance of the peak blood lactate concentration was 7.65 min. Peak blood lactate concentration at 7.65 min (CLA7.65), which was calculated by substituting t (7.65) into the equation for the lactate recovery curve for each subject, agreed well with the observed peak blood lactate concentration (r=0.98, p<0.001). In addition, correlations of r=−0.65, r=−0.78, r=−0.79 were found between CLA7.65 and the running times of 100 m, 200 m, and 400 m sprints, respectively. These results suggest that CLA7.65 may be used as a valid indicator of anaerobic work capacity in man.

Peak blood lactate after short periods of maximal treadmill running.

The purpose of this study was to elucidate the influence of inspiratory muscle fatigue on muscle sympathetic nerve activity (MSNA) and blood pressure (BP) response during submaximal exercise. We hy...

Mitsuru Saito

Papers

Muscle sympathetic nerve responses to graded leg cycling

Modulation of the control of muscle sympathetic nerve activity during incremental leg cycling.

Time-dependent modulation of arterial baroreflex control of muscle sympathetic nerve activity during isometric exercise in humans.

Peak blood lactate after short periods of maximal treadmill running.

Inspiratory muscle fatigue increases sympathetic vasomotor outflow and blood pressure during submaximal exercise