Taketoshi Morimoto

Extracellular Water May Mask Actual Muscle Atrophy During Aging

BACKGROUND Skeletal muscle tissue holds a large volume of water partitioned into extracellular water (ECW) and intracellular water (ICW) fractions. As the ECW may not be related to muscle strength directly, we hypothesized that excluding ECW from muscle volume would strengthen the correlation with muscle strength. METHODS A total of 119 healthy men aged 20-88 years old participated in this study. Knee isometric extension strength, vertical jump, and standing from a chair were measured as indices of muscle strength and power in the lower extremities. The regional lean volume (LV), total water (TW), ICW, and ECW in the lower leg were estimated by anthropometry (skinfold and circumference measurements) and segmental multifrequency bioelectrical impedance spectroscopy (S-BIS). Then, we calculated the ECW/TW and ICW/TW ratios. RESULTS Although ICW and the LV index decreased significantly with age (p < .001), no significant changes in ECW were observed (p = .134). Consequently, the ECW/TW ratio increased significantly (p < .001) with age (young adult, 27.0 +/- 2.9%; elderly, 34.3 +/- 4.9%; advanced elderly, 37.2 +/- 7.0%). Adjusting for this by including the ICW/TW ratio in our models significantly improved the correlation between the LV index and strength-related measurements and correlated with strength-related measurements independently of the LV index (p < .001). CONCLUSIONS The ECW/TW ratio increases in the lower leg with age. The results suggest that the expansion of ECW relative to ICW and the LV masked actual muscle cell atrophy with aging.

Effect of an exercise-heat acclimation program on body fluid regulatory responses to dehydration in older men.

We examined if an exercise-heat acclimation program improves body fluid regulatory function in older subjects, as has been reported in younger subjects. Nine older (Old; 70 +/- 3 yr) and six younger (Young; 25 +/- 3 yr) male subjects participated in the study. Body fluid regulatory responses to an acute thermal dehydration challenge were examined before and after the 6-day acclimation session. Acute dehydration was produced by intermittent light exercise [4 bouts of 20-min exercise at 40% peak rate of oxygen consumption (VO(2 peak)) separated by 10 min rest] in the heat (36 degrees C; 40% relative humidity) followed by 30 min of recovery without fluid intake at 25 degrees C. During the 2-h rehydration period the subjects drank a carbohydrate-electrolyte solution ad libitum. In the preacclimation test, the Old lost approximately 0.8 kg during dehydration and recovered 31 +/- 4% of that loss during rehydration, whereas the Young lost approximately 1.2 kg and recovered 56 +/- 8% (P < 0.05, Young vs. Old). During the 6-day heat acclimation period all subjects performed the same exercise-heat exposure as in the dehydration period. Exercise-heat acclimation increased plasma volume by approximately 5% (P < 0.05) in Young subjects but not in Old. The body fluid loss during dehydration in the postacclimation test was similar to that in the preacclimation in Young and Old. The fractional recovery of lost fluid volume during rehydration increased in Young (by 80 +/- 9%; P < 0.05) but not in Old (by only 34 +/- 5%; NS). The improved recovery from dehydration in Young was mainly due to increased fluid intake with a small increase in the fluid retention fraction. The greater involuntary dehydration (greater fluid deficit) in Old was accompanied by reduced plasma vasopressin and aldosterone concentrations, renin activity, and subjective thirst rating (P < 0.05, Young vs. Old). Thus older people have reduced ability to facilitate body fluid regulatory function by exercise-heat acclimation, which might be involved in attenuation of the acclimation-induced increase in body fluid volume.We examined if an exercise-heat acclimation program improves body fluid regulatory function in older subjects, as has been reported in younger subjects. Nine older (Old; 70 ± 3 yr) and six younger (Young; 25 ± 3 yr) male subjects participated in the study. Body fluid regulatory responses to an acute thermal dehydration challenge were examined before and after the 6-day acclimation session. Acute dehydration was produced by intermittent light exercise [4 bouts of 20-min exercise at 40% peak rate of oxygen consumption (V˙o 2 peak) separated by 10 min rest] in the heat (36°C; 40% relative humidity) followed by 30 min of recovery without fluid intake at 25°C. During the 2-h rehydration period the subjects drank a carbohydrate-electrolyte solution ad libitum. In the preacclimation test, the Old lost ∼0.8 kg during dehydration and recovered 31 ± 4% of that loss during rehydration, whereas the Young lost ∼1.2 kg and recovered 56 ± 8% ( P < 0.05, Young vs. Old). During the 6-day heat acclimation period all subjects performed the same exercise-heat exposure as in the dehydration period. Exercise-heat acclimation increased plasma volume by ∼5% ( P < 0.05) in Young subjects but not in Old. The body fluid loss during dehydration in the postacclimation test was similar to that in the preacclimation in Young and Old. The fractional recovery of lost fluid volume during rehydration increased in Young (by 80 ± 9%; P < 0.05) but not in Old (by only 34 ± 5%; NS). The improved recovery from dehydration in Young was mainly due to increased fluid intake with a small increase in the fluid retention fraction. The greater involuntary dehydration (greater fluid deficit) in Old was accompanied by reduced plasma vasopressin and aldosterone concentrations, renin activity, and subjective thirst rating ( P < 0.05, Young vs. Old). Thus older people have reduced ability to facilitate body fluid regulatory function by exercise-heat acclimation, which might be involved in attenuation of the acclimation-induced increase in body fluid volume.

Role of plasma osmolality in the delayed onset of thermal cutaneous vasodilation during exercise in humans

To elucidate the role of increased plasma osmolality (Posmol), which occurs during exercise in the regulation of cutaneous vasodilation (CVD) during exercise, we determined the relationship between the change in esophageal temperature (DeltaTes) required to elicit CVD (DeltaTes threshold for CVD) and Posmol during light and moderate exercise (30 and 55% of peak oxygen consumption, respectively) and passive body heating. Then we compared the relationship with the data obtained in our previous study [A. Takamata, K. Nagashima, H. Nose, and T. Morimoto. Am. J. Physiol. 273 (Regulatory Integrative Comp. Physiol. 42): R197-R204, 1997], in which we determined the relationships during passive body heating following isotonic (0.9% NaCl) or hypertonic (2 or 3% NaCl) saline infusions in the same subjects. Posmol values at 5 min after the onset of exercise were 287.5 +/- 0.9 mosmol/kgH2O during light exercise and 293.0 +/- 1.2 mosmol/kgH2O during moderate exercise. Posmol just before passive body heating was 289.9 +/- 1.4 mosmol/kgH2O. The DeltaTes threshold for CVD was 0.09 +/- 0.05 degrees C during light exercise, 0.31 +/- 0. 09 degrees C during moderate exercise, and 0.10 +/- 0.05 degrees C during passive body heating. The relationship between the DeltaTes threshold for CVD and Posmol was shown to be on the same regression line both during exercise and during passive body heating with or without infusions [A. Takamata, K. Nagashima, H. Nose, and T. Morimoto. Am. J. Physiol. 273 (Regulatory Integrative Comp. Physiol. 42): R197-R204, 1997]. Our data suggest that the elevated body core temperature threshold for CVD during exercise could be the result of increased Posmol induced by exercise and is not due to reduced plasma volume or the intensity of the exercise itself.

Comparison of single- or multifrequency bioelectrical impedance analysis and spectroscopy for assessment of appendicular skeletal muscle in the elderly

Bioelectrical impedance analysis (BIA) is used to assess skeletal muscle mass, although its application in the elderly has not been fully established. Several BIA modalities are available: single-frequency BIA (SFBIA), multifrequency BIA (MFBIA), and bioelectrical impedance spectroscopy (BIS). The aim of this study was to examine the difference between SFBIA, MFBIA, and BIS for assessment of appendicular skeletal muscle strength in the elderly. A total of 405 elderly (74.2 ± 5.0 yr) individuals were recruited. Grip strength and isometric knee extension strength were measured. Segmental SFBIA, MFBIA, and BIS were measured for the arms and upper legs. Bioelectrical impedance indexes were calculated by squared segment length divided by impedance (L2/Z). Impedance at 5 and 50 kHz (Z5 and Z50) was used for SFBIA. Impedance of the intracellular component was calculated from MFBIA (Z250-5) and BIS (RICW). Correlation coefficients between knee extension strength and L2/Z5, L2/Z50, L2/RICW, and L2/Z250-5 of the upper legs were 0.661, 0.705, 0.790, and 0.808, respectively (P < 0.001). Correlation coefficients were significantly greater for MFBIA and BIS than SFBIA. Receiver operating characteristic curves showed that L2/Z250-5 and L2/RICW had significantly larger areas under the curve for the diagnosis of muscle weakness compared with L2/Z5 and L2/Z50. Very similar results were observed for grip strength. Our findings suggest that MFBIA and BIS are better methods than SFBIA for assessing skeletal muscle strength in the elderly.

Influence of exercise intensity and plasma volume on active cutaneous vasodilation in humans.

The influence of dynamic exercise on active cutaneous vasodilation was evaluated in eight male subjects. We measured the increase in internal body temperature (esophageal temperature, Tes) required to elicit active cutaneous vasodilation and the slope of the linear relationship between increases in forearm skin vascular conductance (delta FVC) and Tes during indirect heating (legs immersed in 44 degrees C water for 30 min), 30 min of light exercise (LEX; 75 +/- 5 W = 30% maximal oxygen uptake, VO2max), and 20 min of moderate exercise (MEX, 149 +/- 7 W = 60% VO2max). Studies were conducted in the supine position at 30 degrees C (RH < 30%) and mean skin temperature averaged 35.09 +/- 0.12 degrees C. During indirect heating and LEX, cutaneous vasodilation occurred after a similar increase in Tes, 0.03 +/- 0.02 degrees C and 0.11 +/- 0.02 degrees C, respectively. During MEX, Tes increased 0.42 +/- 0.06 degrees C before the onset of cutaneous vasodilation (P < 0.05, different from rest and LEX). The relationship between the increase in Tes threshold for vasodilation and exercise intensity was nonlinear, indicating that some minimal exercise intensity was required to elicit a delay in active cutaneous vasodilation. That minimal exercise intensity was greater than 30% VO2max (75 +/- 5 W). During MEX the increase in Tes threshold for vasodilation was inversely related to resting plasma volume (ml.kg-1) with a larger initial plasma volume associated with a smaller increase in Tes threshold for cutaneous vasodilation (r2 = 0.67, P = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Right atrial pressure and forearm blood flow during prolonged exercise in a hot environment.

Right atrial pressure (RAP) at rest is known to be reduced by an increase in skin blood flow (SkBF) in a hot environment. However, there is no clear evidence that this is so during exercise. To clarify the effect of the increase in SkBF on RAP during exercise, we measured forearm blood flow (FBF) (as an index of SkBF) and RAP continuously using a Swan-Ganz catheter in five male volunteers exercising on a cycle ergometer at 60% of peak aerobic power for 50 min in a hot environment (30°C, relative humidity 20%). Cardiac output increased from 5.5±0.21/min at rest to 17.9±1.21/min (mean±SE, P<0.01) in the first 10 min of exercise and then remained steady until the end of exercise. FBF did not change significantly during the first 5 min, but then increased from 2.7±0.5 ml/100 ml per min at rest to 10.8±1.7 ml/100 ml per min (P<0.001) by 25 min as pulmonary arterial blood temperature (Tb) rose from 37.0±0.1°C to 38.1±0.1°C (P<0.001). FBF then reached a plateau, despite a continuing increase in Tb. RAP increased significantly from 4.3±0.8 to 7.6±1.2 mm Hg (P<0.001) during the first 5 min of exercise and then gradually declined to 6.1±1.0 mm Hg by 25 min (P<0.001 vs. 5 min) and further to 5.7±1.0 mm Hg by 50 min, a value not significantly higher than at rest. This reduction in RAP during exercise was significantly correlated with the increase in FBF (r=−0.97, P<0.001) with a regression equation of RAP=−0.25×FBF+8.8. These results suggest that the decrease in RAP after 5 min exercise was caused by an increase in SkBF during exercise in a hot environment.

Phosphorus nuclear magnetic resonance of perfused salivary gland

Phosphorus nuclear magnetic resonance (31P-NMR) was used for the sequential measurement of phosphorus energy metabolites in perfused canine submandibular gland. Under resting conditions, ATP and creatine phosphate levels were 0.42 +/- 0.11 mM and 0.62 +/- 0.16 mM (mean +/- S.D., in nine glands). When perfusion of the gland was stopped, the tissue contents of ATP and creatine phosphate decreased, that of ADP increased and tissue pH decreased. Restarting perfusion led to recoveries of the tissue content of the phosphorus compounds and tissue pH to normal. Acetylcholine administration induced secretion of saliva, decreased the level of ATP, creatine phosphate and tissue pH, and increased the ADP level.

Relationship between aerobic power, blood volume, and thermoregulatory responses to exercise-heat stress

To clarify the relationship between aerobic power (VO2max), blood volume (BV), and thermoregulatory responses to exercise-heat stress, we analyzed the cross-sectional relationship between the resting BV, plasma volume (PV), erythrocyte volume (EV), VO2max, forearm blood flow (FBF), and sweating responses during exercise in a hot environment (31 degrees C, 50% relative humidity). Twelve college-aged male subjects with a mean maximal oxygen uptake of 48 (range 42-59) mL.kg-1.min-1, a mean PV of 54 (range 42-72) mL.kg-1, a mean EV of 31 (range 23-43) mL.kg-1, and a mean BV of 85 (range 67-115) mL.kg-1 (measured by the Evans Blue dye dilution method) performed three sessions of 20-min cycle exercise at two levels of intensity (40% and 60% VO2max). The BV, PV and EV correlated positively with peak FBF (r = 0.596-0.711, P < 0.05), the increase of FBF in response to a unit rise in esophageal temperature (Tes; peak delta FBF/peak delta Tes) (r = 0.592-0.656, P < 0.05) and with total sweat loss (TSL) (r = 0.599-0.634, P < 0.05) during the exercise. The VO2max correlated with TSL during exercise at 40% VO2max (r = 0.578, P < 0.05), but not with peak FBF and peak delta FBF/peak delta Tes. The VO2max per lean body mass also showed a significant positive correlation with BV (r = 0.769, P < 0.01), PV (r = 0.706, P < 0.05), and with EV (r = 0.841, P < 0.001). The peak delta FBF/peak delta Tes was correlated positively with peak FBF (r = 0.597-0.830, P < 0.05-0.01) and negatively with peak Tes (r = 0.641-0.769, P < 0.05-0.01) during the exercise at the two levels. However, the chest sweat rate (CSR), TSL, and the increase of CSR in response to a unit rise in Tes (peak delta CSR/peak delta Tes) showed no correlation with peak Tes during the exercise at the two levels. These findings suggest that 1) heat dissipation responses during exercise were related more to blood volume than aerobic power and 2) skin blood flow was related more to body temperature than sweating responses during exercise under mild heat stress.

Chapter 24 Thermoregulation and body fluid in hot environment

Publisher Summary This chapter explores the effect of thermoregulatory responses on body fluid and circulation. Modifications of thermoregulatory control induced by dehydration are discussed concerning the influence of hyperosmolality and hypovolemia. The chapter also deals with the effect of hyperosmolality and hypovolemia on hypothalamic thermoregulatory mechanisms and the competition between body temperature cardiovascular and body fluid homeostasis. The physiological responses to a heat load in homeothermic animals include cutaneous vasodilation to transfer heat from the body core to the body surface by circulation and evaporative heat loss from the body surface. Heat stress causes dehydration due to sweating, leading to hyperosmolality of body fluid and hypovolemia. Dehydration impairs thermoregulation, reducing both sweating and cutaneous vasodilation, while dehydration-induced hyperosmolality causes a shift of body fluid from intracellular fluid to extracellular fluid and stimulates drinking behavior, which counteracts the decrease in blood volume. The redistribution of blood flow for thermoregulation causes a lowering of central venous pressure, which serves as an input signal for drinking behavior and circulatory regulation, including the increases in total peripheral resistance and vascular compliance.

Effect of aerobic capacity on sweat rate and fluid intake during outdoor exercise in the heat

AbstractWe measured the aerobic capacity, sweat rate and fluid intake of trained athletes during outdoor exercise and examined the relationship between aerobic capacity and thermoregulatory responses at high ambient temperatures. The maximal aerobic capacity (