We assessed the effects of aerobic and/or resistance training on thermoregulatory responses in older men and analyzed the results in relation to the changes in peak oxygen consumption rate (VO(2 peak)) and blood volume (BV). Twenty-three older men [age, 64 +/- 1 (SE) yr; VO(2 peak), 32.7 +/- 1.1 ml. kg(-1). min(-1)] were divided into three training regimens for 18 wk: control (C; n = 7), aerobic training (AT; n = 8), and resistance training (RT; n = 8). Subjects in C were allowed to perform walking of ~10,000 steps/day, 6-7 days/wk. Subjects in AT exercised on a cycle ergometer at 50-80% VO(2 peak) for 60 min/day, 3 days/wk, in addition to the walking. Subjects in RT performed a resistance exercise, including knee extension and flexion at 60-80% of one repetition maximum, two to three sets of eight repetitions per day, 3 days/wk, in addition to the walking. After 18 wk of training, VO(2 peak) increased by 5.2 +/- 3.4% in C (P > 0.07), 20.0 +/- 2.5% in AT (P < 0.0001), and 9.7 +/- 5.1% in RT (P < 0.003), but BV remained unchanged in all trials. In addition, the esophageal temperature (T(es)) thresholds for forearm skin vasodilation and sweating, determined during 30-min exercise of 60% VO(2 peak) at 30 degrees C, decreased in AT (P < 0.02) and RT (P < 0.02) but not in C (P > 0.2). In contrast, the slopes of forearm skin vascular conductance/T(es) and sweat rate/T(es) remained unchanged in all trials, but both increased in subjects with increased BV irrespective of trials with significant correlations between the changes in the slopes and BV (P < 0.005 and P < 0.0005, respectively). Thus aerobic and/or resistance training in older men increased VO(2 peak) and lowered T(es) thresholds for forearm skin vasodilation and sweating but did not increase BV. Furthermore, the sensitivity of the increase in skin vasodilation and sweating at a given increase in T(es) was more associated with BV than with VO(2 peak).

We examined whether oropharyngeal stimulation by drinking released the dehydration-induced suppression of cutaneous vasodilatation and decreased mean arterial pressure (MAP) in exercising subjects, and assessed the effects of hypovolaemia or hyperosmolality alone on these responses. Seven young males underwent four hydration conditions. These were two normal plasma volume (PV) trials: normal plasma osmolality (P osmol , control trial) and hyperosmolality (∆P osmol = +11 mosmol (kg H 2 O) −1 ); and two low PV trials: isosmolality (∆PV = −310 ml) and hyperosmolality (∆PV = −345 ml; ∆P osmol = +9 mosmol (kg H 2 O) −1 ), attained by combined treatment with furosemide (frusemide), hypertonic saline and/or 24 h water restriction. In each trial, the subjects exercised at 60% peak aerobic power for ∼50 min at 30• C atmospheric temperature and 50% relative humidity. When oesophageal temperature (T oes ) reached a plateau after ∼30 min of exercise, the subjects drank 200 ml water at 37.5• C within a minute. Before drinking, forearm vascular conductance (FVC), calculated as forearm blood flow divided by MAP, was lowered by 20-40% in hypovolaemia, hyperosmolality, or both, compared with that in the control trial, despite increased T oes . After drinking, FVC increased by ∼20% compared with that before drinking (P < 0.05) in both hyperosmotic trials, but it was greater in normovolaemia than in hypovolaemia (P < 0.05). However, no increases occurred in either isosmotic trial. MAP fell by 4-8 mmHg in both hyperosmotic trials (P < 0.05) after drinking, but more rapidly in normovolaemia than in hypovolaemia. PV and P osmol did not change during this period. Thus, oropharyngeal stimulation by drinking released the dehydration-induced suppression of cutaneous vasodilatation and reduced MAP during exercise, and this was accelerated when PV was restored.

This study was designed to test the hypothesis that myosin heavy (MHC) and light chain (MLC) plasticity resulting from hindlimb suspension (HS) is an age-dependent process. By using an electrophoretic technique, the distribution of MHC and MLC isoforms was quantitatively evaluated in the soleus muscles from 3- or 12-wk-old rats after 1-3 wk of HS treatment was maintained. In normal 12- and 15-wk-old rats, the soleus muscles contained a predominance of MHCI ( approximately 94%) with small amounts of MHCIIa, but not MHCIId or MHCIIb. The suspended muscles of adult rats were characterized by the appearance of MHCIIb and MHCIId, the latter reaching approximately 6% after 3 wk of HS treatment. In contrast to changes in MHC, HS did not induce a transition in the MLC pattern in the soleus muscles from adult rats. Compared with adult rats, in juveniles HS had a much more pronounced effect on the shift toward faster MHC and MLC isoform expression. The soleus muscles of 6-wk-old rats after 3 wk of HS were composed of 37.0% MHCI, 19.1% MHCIIa, 23.7% MHCIId, and 20.2% MHCIIb. Changes in MLC isoforms consisted of an increase in MLC1f and MLC2f concomitant with a decrease in MLC2s. These results indicate the existence of a differential effect of HS on MHC and MLC transitions that appears to be age dependent. They also suggest that the suspended soleus muscles from young rats may acquire the intrinsic contractile properties that are intermediate between those in the normal soleus and typical fast-twitch skeletal muscles.

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Myosin of human skeletal muscles was analyzed by means of several electrophoretic techniques. Myosin heavy chain (HC)-IIa-and HC-IIb-based isomyosins were identified by pyrophosphate-polyacrylamide gel electrophoresis (PP-PAGE). The electrophoretic mobilities of these fast-twitch muscle isomyosins differed in the order HC-IIa triplets < HC-IIb triplets. To determine the subunit composition of myosin molecules that function in intact muscle, two-dimensional electrophoresis in which the first and second dimensions were PP-PAGE and sodium dodecyl sulfate-PAGE, respectively, was also performed. Slow-twitch muscle isomyosin contained, in addition to slow-twitch light chain (LC) and HC-I isoforms, appreciable amounts of LC-2f, HC-IIa, and HC-IIb isoforms, and fast-twitch muscle isomyosin consisted of LC-2s and HC-I isoforms as well as fast-twitch LC and HC isoforms. Without consideration of HC- and slow-twitch alkali LC heterodimers, at least 31 possible isomyosins are derived from these findings on the subunit composition of isomyosins in human skeletal muscle.