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هدف: فشار دی‌اکسید کربن خون سرخرگی (PaCO2) از عوامل مهم در سازوکار شیمیایی کنترل تهویۀ ریوی (VE) است که تأثیر مستقیم یا غیرمستقیم یا بی‌تأثیر بودن آن هنوز مورد بحث است. هدف تحقیق حاضر بررسی تأثیر PaCO2 بر VE طی فعالیت منقطع کوتاه‌مدت و بازیافت پس ‌از این فعالیت و همچنین بررسی تأخیر زمانی در تحریک VE به‌وسیلۀ PaCO2 بود.روش­ها: ده آزمودنی مرد غیرفعال یک فعالیت منقطع کوتاه‌مدت (10ثانیه) با فشار کاری 200 وات را انجام دادند که شرایطی را به‌وجود می‌آورد که در آن از بین تمام عوامل شیمیایی تنها PaCO2 تغییر می‌کند. تهویۀ ریوی و گازهای تبادل تنفسی در طول مدت استراحت، گرم کردن، تمرین و دورۀ بازیافت اندازه‌گیری شد. PaCO2با استفاده از PETCO2 و حجم جاری پیش‌بینی شد. همبستگی عرضی برای نشان دادن ضریب همبستگی بین VE و PaCO2 پیش‌بینی‌شده با درنظر گرفتن تأخیرهای زمانی مختلف به‌دست آمد.نتایج: میزانPaCO2 پیش‌بینی‌شده از ثانیۀ 14 تا 28 دورۀ بازیافت و میزان VE از ثانیۀ 14 تا 90 دورۀ بازیافت به‌طور معنا‌داری بالاتر از میزان آن‌ها در زمان گرم کردن بود (05/0>p) و بالاترین ضریب همبستگی بین PaCO2 و VE با تأخیر زمانی 7 ثانیه به‌دست آمد (854/0=r).نتیجه‌گیری: نتایج نشان داد که در مردان غیرفعال طی فعالیت منقطع کوتاه‌مدت و بازیافت پس ‌از آن،PaCO2 موجب تحریک VE می‌شود و تأخیر زمانی 7 ثانیه در تحریک VE به‌وسیلۀPaCO2 وجود دارد.

We examined the agreement between heart rate deflection point (HRDP) variables with maximal lactate steady state (MLSS) in a sample of young males categorized to different body mass statuses using body mass index (BMI) cut-off points. One hundred and eighteen young males (19.9 ± 4.4 years) underwent a standard running incremental protocol with individualized speed increment between 0.3 and 1.0 km/h for HRDP determination. HRDP was determined using the modified Dmax method called S.Dmax. MLSS was determined using 2-5 series of constant-speed treadmill runs. Heart rate (HR) and blood lactate concentration (La) were measured in all tests. MLSS was defined as the maximal running speed yielding a La increase of less than 1 mmol/L during the last 20 min. Good agreement was observed between HRDP and MLSS for HR for all participants (±1.96; 95% CI = −11.5 to +9.2 b/min, ICC = 0.88; P < 0.001). Good agreement was observed between HRDP and MLSS for speed for all participants (±1.96; 95% CI = −0.40 to +0.42 km/h, ICC = 0.98; P < 0.001). The same findings were observed when participants were categorized in different body mass groups. In conclusion, HRDP can be used as a simple, non-invasive and time-efficient method to objectively determine submaximal aerobic performance in nonathletic young adult men with varying body mass status, according to the chosen standards for HRDP determination.

Purpose Effort sense has been suggested to be involved in the hyperventilatory response during intense exercise (IE). However, the mechanism by which effort sense induces an increase in ventilation during IE has not been fully elucidated. The aim of this study was to determine the relationship between effort-mediated ventilatory response and corticospinal excitability of lower limb muscle during IE. Eight subjects performed 3 min of cycling exercise at 75-85 % of maximum workload twice (IE1st and IE2nd). IE2nd was performed after 60 min of resting recovery following 45 min of submaximal cycling exercise at the workload corresponding to ventilatory threshold. Vastus lateralis muscle response to transcranial magnetic stimulation of the motor cortex (motor evoked potentials, MEPs), effort sense of legs (ESL, Borg 0-10 scale), and ventilatory response were measured during the two IEs. The slope of ventilation (l/min) against CO2 output (l/min) during IE2nd (28.0 +/- 5.6) was significantly greater than that (25.1 +/- 5.5) during IE1st. Mean ESL during IE was significantly higher in IE2nd (5.25 +/- 0.89) than in IE1st (4.67 +/- 0.62). Mean MEP (normalized to maximal M-wave) during IE was significantly lower in IE2nd (66 +/- 22 %) than in IE1st (77 +/- 24 %). The difference in mean ESL between the two IEs was significantly (p < 0.05, r = -0.82) correlated with the difference in mean MEP between the two IEs. The findings suggest that effort-mediated hyperventilatory response to IE may be associated with a decrease in corticospinal excitability of exercising muscle.

The purpose of the present study was to examine how oscillation of tissue oxygen index (TOI) in non-exercising exercise is affected during high-intensity and low-intensity exercises. Three exercises were performed with exercise intensities of 30% and 70% peak oxygen uptake ((V)over doto(2)peak) for 12 min and with exercise intensity of 70% (V)over doto(2)peak for 30 s. TOI in non-exercising muscle (biceps brachii) during the exercises for 12 min was determined by nearinfrared spectroscopy. TOI in the non-exercising muscle during the exercises was analyzed by fast Fourier transform (FFT) to obtain power spectra density (PSD). The frequency at which maximal PSD appeared (Fmax) during the exercise with 70% (V)over doto(2)peak for 12 min (0.00477 +/- 0.00172 Hz) was significantly lower than that during the exercise with 30% (V)over doto(2)peak for 12 min (0.00781 +/- 0.00338 Hz). There were significant differences in blood pH and blood lactate between the exercise with 70% V.o2peak and the exercise with 30% (V)over doto(2)peak. It is concluded that TOI in nonexercising muscle oscillates during low-intensity exercise as well as during high-intensity exercise and that the difference in Fmax between the two exercises is associated with the difference in increase in blood lactate derived from the exercise.

Time delay in the mediation of ventilation (V(.)E) by arterial CO(2) pressure (PaCO(2)) was studied during recovery from short impulse-like exercises with different work loads of recovery. Subjects performed two tests including 10-s impulse like exercise with work load of 200 watts and 15-min recovery with 25 watts in test one and 50 watts in test two. V(.)E, end tidal CO(2) pressure (PETCO(2)) and heart rate (HR) were measured continuously during rest, warming up, exercise and recovery. PaCO(2) was estimated from PETCO(2) and tidal volume (V(T)). Results showed that predicted arterial CO(2) pressure (PaCO(2 pre)) increased during recovery in both tests. In both tests, V(.)E increased and peaked at the end of exercise. V(.)E decreased in the first few seconds of recovery but started to increase again. The highest correlation coefficient between PaCO(2 pre) and V(.)E was obtained in the time delay of 7 s (r=0.854) in test one and in time delays of 6 s (r=0.451) and 31 s (r=0.567) in test two. HR was significantly higher in test two than in test one. These results indicate that PaCO(2 pre) drives V(.)E with a time delay and that higher work intensity induces a shorter time delay.

The purpose of the present study was to compare oscillation of skin blood flow with that of deoxygenation in muscle during light exercise in order to determine the physiological significance of oscillations in deoxygenation. Prolonged exercise with 50% of peak oxygen uptake was performed for 60 min. Skin blood flow (SBF) was measured using a laser blood flow meter on the right vastus lateralis muscle. Deoxygenated haemoglobin/myoglobin (DHb/Mb) concentration in the left vastus lateralis were measured using a near-infrared spectroscopy system. SBF and DHb/Mb during exercise were analysed by fast Fourier transform. We classified frequency bands according to previous studies (Kvernmo et al. 1999, Kvandal et al. 2006) into phase I (0.005-0.0095 and 0.0095-0.02 Hz), phase II (0.02-0.06 Hz: phase II) and phase III (0.06-0.16 Hz). The first peak of power spectra density (PSD) in SBF appeared at 0.0078 Hz in phase I. The second peak of PSD in SBF appeared at 0.035 Hz. The third peak of PSD in SBF appeared at 0.078 Hz. The first peak of PSD in DHb/Mb appeared at 0.0039 Hz, which was out of phase I. The second peak of PSD in DHb/Mb appeared at 0.016 Hz. The third peak of PSD in DHb/Mb appeared at 0.035 Hz. The coefficient of cross correlation was very low. Cross power spectra density showed peaks of 0.0039, 0.016 and 0.035 Hz. It is concluded that a peak of 0.016 Hz in oscillations of DHb/Mb observed in muscle during exercise is associated with endothelium-dependent vasodilation (phase I) and that a peak of 0.035 Hz in DHb/Mb is associated with sympathetic nerve activity (phase II). It is also confirmed that each peak of SBF oscillations is observed in each phase.

The aim of the present study was to compare the frequency of oxygenation determined in the vastus lateralis by near-infrared spectroscopy (NIRS) in light exercise with that at rest. A subject rested in a recumbent position for 5 min and changed body position to a sitting position on a cycle ergometer for 9 min. Then exercise with low intensity (work rate of 60% of maximal oxygen uptake) was carried out for 30 min. Total hemoglobin and myoglobin (THb/Mb) suddenly decreased after the start of exercise and gradually increased until 6 min. Oxygenated hemoglobin and myoglobin (Hb/MbO2) suddenly decreased and returned to a steady state after the start of exercise. The difference between Hb/MbO2 and THb/Mb showed a sudden decrease and then a steady state. This difference was analyzed by fast Fourier transform. The peak frequencies of the power spectrum density (PSD) were 0.0169 + 0.0076 Hz at rest and 0.0117 + 0.0042 Hz in exercise. The peak frequency of PSD was significantly decreased in exercise. In exercise, the range of frequencies was expanded. It is concluded that there are oscillations at rest as well as in exercise and that the frequency of peak PSD becomes lower in exercise than at rest.

The aim of the present study was to compare the oscillations of oxygenation in skeletal muscle between early and late phases in prolonged exercise. During prolonged exercise at 60 % of peak oxygen uptake (V o2) for 60 min and at rest, oxygenated hemoglobin/myoglobin (Hb/MbO2) and total Hb/Mb (THb/Mb) were determined by near-infrared spectroscopy in the vastus lateralis. Power spectra density (PSD) for the difference between Hb/MbO2 and THb/Mb (−HHb/MbO2: deoxygenation) was obtained by fast Fourier transform at rest, in the early phase (1-6 min) and in the late phase (55-60 min) in exercise. Peak PSD in the early phase was significantly higher than that at rest. There were at least three peaks of PSD in exercise. The highest peak was a band around 0.01 Hz, the next peak was a band around 0.04 Hz, and the lowest peak was a band around 0.06 Hz. PSD in the early phase was not significantly different from that in the late phase in exercise. Heart rate (HR) showed a continuous significant increase from 3 min in exercise until the end of exercise. Skin blood flow (SBF) around the early phase was significantly lower than that around the late phase. It was concluded that oscillation of oxygenation in the muscle oxygen system in the early phase is not different from that in the late phase in prolonged exercise despite cardiovascular drift.

We investigated ventilation ((V) over dotE) control factors during recovery from light impulse-like exercise (100 watts) with a duration of 20 s. Blood ions and gases were measured at rest and during recovery. (V) over dotE, end tidal CO2 pressure (PETCO2) and respiratory exchange ratio (RER) were measured continuously during rest, exercise and recovery periods. Arterial CO2 pressure (PaCO2 (pre)) was estimated from PETCO2 and tidal volume (V-T). RER at 20 s of exercise and until 50 s during recovery was significantly lower than RER at rest. Despite no change in arterialized blood pH level, PaCO2 (pre) was significantly higher in the last 10 s of exercise and until 70 s during recovery than the resting value. (V) over dotE increased during exercise and then decreased during recovery; however, it was elevated and was significantly higher than the resting value until 155 s (p

To determine that whether arterial carbon dioxide (PaCO2) affects ventilation (VE) during recovery from impulse-like exercises of various intensities, subjects performed four impulse-like tests with different workloads. Each test consisted of a 20-sec impulse-like exercise at 80 rpm and 60-min recovery. Blood samples were collected at rest and during recovery to measure blood ions and gases. VE was measured continuously during rest, exercise and recovery periods. A significant curvilinear relationship was observed between VE and pH during recovery from the 300 and 400 watts tests in all subjects. VE was elevated during recovery from the 100 watts test despite no change in any of the humoral factors. Arterialized carbon dioxide (PaCO2) kinetics showed fluctuation, being increased at 1 min and decreased at 5 min during recovery, and this fluctuation was more enhanced with increase in exercise intensity. There was a significant relationship between VE and PaCO2 during recovery from the 300 and 400 watts tests in all subjects. The results of the present study demonstrate that pH and neural factors drive VE during recovery from impulse-like exercise and that fluctuation in PaCO2 controls VE as a feedback loop and this feedback function is more enhanced as the work intensity increases.

The purpose of this study was to examine the effects of blood lactate level (La) on oxygen uptake ( ·VO2) kinetics during recovery after short-term exercise with maximal effort (sprint). Three sprints were performed on a cycle ergometer with a load of 8% of body weight at maximal rotation rate. ·VO2 kinetics and oxygen debt were determined after three sprint tests: one 10-s cycling sprint, five repeated 10-s cycling sprints with 6-min intervals and one 30-s cycling sprint. There was no significant difference between peak power outputs in the 10-s sprint and five sprints. There was no difference in ·VO2 kinetics during recovery from one sprint and during recovery after five sprints. La peaked at 5 min. The peak value of La was significantly lower in one sprint (4.41 ± 0.9 mM) than in five sprints (7.01 ± 2.2 mM). Thus, despite a difference in La, there was no difference between ·VO2 kinetics during recovery after one sprint and after five sprints. There was a significant difference in ·VO2 between the five sprints and 30-s sprint from 70 s to 320 s during recovery, but there were no significant differences in La after 5 min of recovery. There were two phases in ·VO2. They consisted of fast oxygen debt and slow oxygen debt. There were also no differences in slow and fast oxygen debts between the two 10-s sprints despite significant differences in blood lactate during recovery. Peak La in the five sprints was not significantly different from that in the 30-s sprint (8.68 ± 1.2 mM). However, slow oxygen debt was significantly greater in the 30-s sprint than in the five sprints. It is concluded that · VO2 kinetics during recovery are not affected by an increase in blood lactate.

To clarify the ventilatory kinetics during recovery after impulse-like exercise, subjects performed one impulse-like exercise test (one-impulse) and a five-times repeated impulse-like exercises test (five-impulse). Duration and intensity of the impulse-like exercise were 20 sec and 400 watts (80 rpm), respectively. Although blood pH during recovery (until 10 min) was significantly lower in the five-impulse test than in the one-impulse test, ventilation (.VE) in the two tests was similar except during the first 30 sec of recovery, in which it was higher in the five-impulse test. In one-impulse, blood CO2 pressure (PCO2) was significantly increased at 1 min during recovery and then returned to the pre-exercise level at 5 min during recovery. In the five-impulse test, PCO2 at 1 min during recovery was similar to the pre-exercise level, and then it decreased to a level lower than the pre-exercise level at 5 min during recovery. Accordingly, PCO2 during recovery (until 30 min) was significantly lower in the five-impulse than in one-impulse test..VE and pH during recovery showed a curvilinear relationship, and at the same pH, ventilation was higher in the one-impulse test. These results suggest that ventilatory kinetics during recovery after impulse-like exercise is attributed partly to pH, but the stimulatory effect of lower pH is diminished by the inhibitory effect of lower PCO2.

The purpose of this study was to examine whether ventilation kinetics are related to blood lactate level after 5 min in recovery after a sprint. Subjects performed two tests, one test consisting of one sprint with maximal effort and the other test consisting of five repeated sprints with time intervals of 6 min. The recovery period from the last sprint was 30 min. Oxygen uptake during recovery from one sprint was the same as that during recovery from five repeated sprints. Ventilation after 50 sec in recovery after one sprint was the same as that in recovery after five repeated sprints despite the significantly higher blood lactate levels during recovery from five repeated sprints than that from a single sprint. There was an exponential relationship between ventilation and blood lactate after 5 min in recovery. The curve shifted to the right in the case of five repeated sprints. End tidal CO[sub]2[/sub] pressure after one sprint was higher than that after five repeated sprints during recovery. From these results, it seems that ventilation control related to blood lactate level is modified by end tidal CO[sub]2[/sub] pressure.

The purpose of this study was to determine the relationship between oxygen uptake ( •VO2) and the oxygen supply system during incremental load in the supine position. Each subject (n=6) performed an incremental-load supine exercise test (20 W min-1). •VO2 and heart rate (HR) were measured breath-by-breath during exercise. Oxygenation level was obtained from the inactive biceps brachii muscle using near-infrared spectroscopy (NIRS). •VO2 and HR increased linearly in proportion to increase in work rate (WR) after a time delay. The linear relationships between •VO2 and WR and between HR and WR below the ventilatory threshold (VT, 112.9±11.7 W) were extrapolated to WR above the VT. Estimated HR was not significantly different from that measured above VT. Oxygenation level slightly decreased after the VT and decreased exponentially after the respiratory compensation point (RCP, 175.8±21.3 W). Oxygenation level decreased from 100�0at warming-up exercise (10 W) to 63.3±14.0�0at exhaustion. In this study, HR and oxygenation level were regarded as oxygen supply to the whole body in the supine position and oxygen supply to inactive muscle, respectively. Therefore, an increase in HR suggests a linear increase in oxygen supply to active muscle through exercise. In addition to the effect of HR, a decrease in oxygenation level in inactive muscle could induce an increase in oxygen supply to active muscle. However, •VO2 showed a linear increase throughout the exercise in the supine position. Judging from the present indirect indicators of HR and oxygenation level, it is unlikely that •VO2 kinetics is determined by oxygen supply to active muscle in the supine position.

The purpose of this study was to determine the relationship between oxygen uptake (VO2) kinetics and oxygen supply system during constant-load exercise in the supine position. The main exercises which were carried in supine position were moderate at an intensity corresponding to 80% of ventilatory threshold (VT) and heavy at an intensity corresponding to 20% of the difference between VT and peak VO2. Oxygenation level was obtained from inactive muscle by near-infrared spectroscopy (NIRS). This index is used to express the distribution of oxygen supply to inactive muscle during exercise [19]. After an exponential rise in VO2 (primary component), VO2 during moderate exercise reached a steady state, while during heavy exercise it continued to increase gradually (slow component). The HR kinetics which reflected systemic O2 supply in the supine position was similar to that of VO2 in main exercise tests. However, time constants of primary and slow components in VO2 were not significantly related to those in HR in each exercise mode. Furthermore, oxygenation level decreased after about 0.5 min from the onset of exercise and showed a minimum value at about 2 min and then recovered to the initial level during moderate and heavy exercises. Since there were no significant correlation coefficients in the time constant between VO2 and HR in each component in each exercise mode and since O2 supply to active muscle is affected by systemic O2 supply and distribution of O2 supply to inactive muscle, it is unlikely that VO2 is related to O2 supply to active muscle in supine position.

It was hypothesized that an oscillation of tissue oxygen index (TOI) determined by near-infrared spectroscopy during recovery from exercise occurs due to feedback control of adenosine triphosphate and that frequency of the oscillation is affected by blood pH. In order to examine these hypotheses, we aimed 1) to determine whether there is an oscillation of TOI during recovery from exercise and 2) to determine the effect of blood pH on frequency of the oscillation of TOI. Three exercises were performed with exercise intensities of 30 % and 70 % peak oxygen uptake (V(.)o(2)peak) for 12 min and with exercise intensity of 70 % V(.)o(2)peak for 30 s. TOI during recovery from the exercise was analyzed by fast Fourier transform in order to obtain power spectra density (PSD). There was a significant difference in the frequency at which maximal PSD of TOI appeared (Fmax) between the exercises with 70 % V(.)o(2)peak for 12 min (0.0039+/-0 Hz) and for 30 s (0.0061+/-0.0028 Hz). However, there was no significant difference in Fmax between the exercises with 30 % (0.0043+/-0.0013 Hz) and with 70 % V(.)o(2)peak for 12 min despite differences in blood pH and blood lactate from the warmed fingertips. It is concluded that there was an oscillation in TOI during recovery from the three exercises. It was not clearly shown that there was an effect of blood pH on Fmax.

The purpose of the present study was to examine 1) whether O(2) uptake (VO(2)) oscillates during light exercise and 2) whether the oscillation is enhanced after impulse exercise. After resting for 1 min on a bicycle seat, subjects performed 5-min pre-exercise with 25 watts work load, 10-s impulse exercise with 200 watts work load and 15-min post exercise with 25 watts work load at 80 rpm. VO(2) during pre-exercise significantly increased during impulse exercise and suddenly decreased and re-increased until 23 s after impulse exercise. In the cross correlation between heart rate (HR) and VO(2) after impulse exercise, VO(2) strongly correlated to HR with a time delay of -4 s. Peak of power spectral density (PSD) in HR appeared at 0.0039 Hz and peak of PSD in VO(2) appeared at 0.019 Hz. The peak of the cross power spectrum between VO(2) and HR appeared at 0.0078 Hz. The results suggested that there is an oscillation in O(2) uptake during light exercise that is associated with the oscillation in O(2) consumption in active muscle. The oscillation is enhanced not only by change in O(2) consumption but also by O(2) content transported from active muscle to the lungs.

The purpose of the present study was to examine how end tidal CO(2) pressure (PETCO(2)) is controlled in impulse exercise. After pre-exercise at 25 watts for 5 min, impulse exercise for 10 sec with 200 watts followed by post exercise at 25 watts was performed. Ventilation (VE) significantly increased until the end of impulse exercise and significantly re-increased after a sudden decrease. Heart rate (HR) significantly increased until the end of impulse exercise and then decreased to the pre-exercise level. PETCO(2) remained constant during impulse exercise. PETCO(2) significantly increased momentarily after impulse exercise and then significantly decreased to the pre-exercise level. PETCO(2) showed oscillation. The average peak frequency of power spectral density in PETCO(2) appeared at 0.0078 Hz. Cross correlations were obtained after impulse exercise. The peak cross correlations between VE and PETCO(2), HR and PETCO(2), and VE and HR were 0.834 with a time delay of -7 sec, 0.813 with a time delay of 7 sec and 0.701 with a time delay of -15 sec, respectively. We demonstrated that PETCO(2) homeodynamics was interactively maintained by PETCO(2) itself, CO(2) transportation (product of cardiac output and mixed venous CO(2) content) into the lungs by heart pumping and CO(2) elimination by ventilation, and it oscillates as a result of their interactions.

We investigated this hypothesis that arterial CO2 pressure (PaCO2) drives ventilation (V.E) with a time delay duringrecovery from short impulse-like exercise (10 s) with work load of 200 watts. V.E and end tidal CO2 pressure (PETCO2) were measured continuously during rest, warming up, exercise and recovery periods. PaCO2 was predicted (PaCO2 pre) from PETCO2 and tidal volume (VT). PETCO2 and PaCO2 pre peaked at 20 s of recovery. V.E increased and peaked at the end of exercise and then decreased during recovery; however, it peaked again at 30 s of recovery, which was 10 s later than the peak of PaCO2 pre. The relationship between V. E and PaCO2pre was not significant by using data of them obtained at the same time but was significant by using data of V.E obtained 10 s later for data of PaCO2 pre. The results support our hypothesis that PaCO2 drives V.E with a time delay., {"references":["J.A. 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The aim of this study was to investigate muscle damage and inflammatory response following eccentric exercise as well as the effect of carbohydrate supplement on these responses in untrained men.Eighteen healthy untrained men were randomly allocated into two carbohydrate (age 21/33+/-0/7 years) and placebo (age 20/66+/-1/22 years) groups. Forty-five repetitions of eccentric elbow flexion were performed with 90% of one maximum repetition by each subject. The exercises were done as three sets of 15 repetitions with 3 minutes rest between sets. Venous blood samples were obtained at pre-exercise, immediately, 8h, and 24h after exercise. Subjects consumed a 6% carbohydrate or placebo drink immediately following the exercise session, every hour, for 10 hours.CK activities and IL-6 levels were significantly greater than per-exercise in immediately, 8 h and 24 h after exercise in both groups (P0.05). No significant increases was observed in CRP levels immediately, 8 h and 24 h after exercise versus baseline, in both groups (P0.05), but in 8 h versus immediately after exercise, the augmentation in the carbohydrate group was significant(P0.05). Blood glucose increased significantly 8 h after exercise versus baseline in both groups (P0.05). There was significant difference in serum IL-6 between two groups in 8 h and 24 h after exercise (P0.05) and it was greater in carbohydrate group. There was no significant difference in serum CK, CRP, and glucose between two groups (P0.05).According to results, carbohydrate increased the inflammatory (IL-6) response following resistance exercise, but had no effects on CRP and CK.