Previous studies have shown that the kinetics of heart rate (HR) recovery are delayed in older individuals after exercise. This study was designed to determine whether this observation held when the variables of physical fitness and work intensity were controlled. Twenty male subjects were categorized into four groups (n = 5) according to age and fitness level (peak O2 consumption ml. kg-1.min-1): young trained (YT) 24 +/- 2 yr, 63 +/- 3 ml.kg-1. min-1; old trained (OT) 51 +/- 2 yr, 57 +/- 3 ml.kg-1.min-1; young untrained (YU) 25 +/- 3 yr, 44 +/- 2 ml.kg-1.min-1; old untrained (OU) 57 +/- 4 yr, 36 +/- 4 ml.kg-1.min-1. Bicycle ergometry exercise was performed in incremental stages to a maximally tolerated level of exertion, and HR was monitored continuously postexercise. Regression analysis of the fast (15-120 s) and initial slow (120-240 s) phases of recovery showed no effect of age on HR recovery when comparing YT vs. OT and YU vs. OU. Trained subjects, irrespective of age, demonstrated a significantly faster HR recovery than untrained subjects which was particularly marked during fast-phase recovery (P less than 0.005). These results indicate that the slower HR recovery previously reported in older subjects may be due to a failure to control for variables that influence recovery HR.

The purpose of this study was to measure cardiovascular, respiratory, and metabolic responses to graded treadmill exercise in the horse. A five-stage treadmill test up to 90% of predicted maximal heart rate was administered to five sedentary horses. The highest measured level of exercise produced a sixfold increase in cardiac output and a 41% elevation of stroke volume over standing values. Left ventricular, arterial, and right atrial pressures as well as the maximal time derivative of left ventricular pressure were all elevated during exercise. Under the same two conditions hematocrit (Hct) increased from 33 +/- 2 to 47 +/- 1%, oxygen uptake (VO2) from 1.1 +/- 0.1 to 32.7 +/0 2.1 1.min-1, and respiratory exchange ratio (RQ) increased from 0.83 +/- 0.02 to 0.96 +/- 0.01. In addition, three of the horses were willing to trot at a sixth stage (14 km.h-1, 11.5% grade), which elicited a VO2 of 39.8 +/- 0.31.min-1 and an RQ of 0.98 +/- 0.01. In response to the sympathetic stimulation of exercise, the horse is able to elevate Hct, hemoglobin, and oxygen-carrying capacity by emptying the spleen, thus increasing total circulating red blood cells by as much as 50%. This enabled three of the five horses used in the present study to increase aerobic metabolism almost 40-fold above resting or twice that seen in humans. Therefore, in the horse "blood-boosting" is an efficient mechanism for increasing aerobic metabolism. This finding lends further support to the view that the oxygen transport system limits maximal aerobic capacity in humans.

We tested the hypothesis that alterations in arterioles in locomotor skeletal muscles in rats with myocardial infarction (MI), but before development of congestive heart failure (CHF), precede structural and functional changes commonly observed in limb muscle in association with CHF. Resting diameters of third- (A3) and fourth-order arterioles (A4) in extensor digitorum longus (EDL) muscle were significantly smaller in rats with nonfailing small and medium-sized MI compared with control animals. Dilation of A4 in response to 10−4 M adenosine was significantly attenuated in both groups ( P < 0.05), whereas dilation of A3 was unaltered. Microvessels from both groups of infarcted rats constricted to all doses of acetylcholine (10−9, 10−8, and 10−7 M) and showed a significantly exaggerated vasoconstrictor response to norepinephrine (10−9, 10−8, and 10−7 M) compared with microvessels in control rats ( P < 0.05). Peak isometric tension of combined tibialis anterior and EDL muscles and muscle fatigue (final/peak tension × 100), measured during 5-min isometric supramaximal twitch contractions at 4 Hz, were similar in control and MI rats (218 ± 7 vs. 213 ± 15 g/g muscle and 52 ± 1 vs. 51 ± 9%, respectively; n = 5 for both). There was also no difference with respect to the proportion of oxidative fibers or capillary-to-fiber ratios. Our results indicate that, in rats with left ventricular dysfunction but without failure, decreased diameter and perturbations in reactivity of small arterioles precede alterations in skeletal muscle performance often seen at a later date in association with CHF. These findings are consistent with the notion of aberrant endothelial and smooth muscle function and may contribute to the maintenance of blood pressure after MI but before CHF.

The effects of 5- and 10-wk treadmill exercise training on cardiorespiratory function were evaluated in the horse. Cardiac output (Q), heart rate (HR), and stroke volume (SV), as well as left ventricular (LVP), aortic (AoP), and mean right atrial (RAP) pressures and the peak first time derivative of LVP (LV dP/dtmax), were measured at rest and at five different levels of exercise up to 90% of initial predicted maximal HR (HRmax). Oxygen uptake (VO2) and respiratory exchange ratio (R) were also obtained under the same conditions. At rest, although HR was no different after training, LV dP/dtmax was lower at 10 wk (2,369 +/- 502 vs. 1,615 +/- 302 mmHg/s). At the different measured work loads during exercise, Q and VO2 remained unchanged with training, whereas there were consistent trends toward lower LVP, AoP, and LV dP/dtmax and significant reductions in HR and R (both P less than 0.05). In contrast, SV and mean RAP were elevated (P less than 0.05) during exercise after the 10-wk training program. Although the observed changes in cardiorespiratory function in response to a training program in the horse are generally similar to those reported for other species, our data also suggest a training-induced increase in venous pressures during exercise as measured by elevated mean RAP values.

The purpose of this study was to compare the effects of two different recovery modes from hind-limb suspension-induced hypodynamia on whole body and muscle (soleus) growth as well as soleus composition and size changes of different fiber types within this same muscle. Following 28 days of tail-suspension, rats were returned to their cages and sedentarily recovered (HS), or were exercised by running on a treadmill 5 days/wk, at progressively increasing workloads (HR) for one month. Sedentary and running control groups of animals (CS, CR) were also evaluated for comparative purposes. The exercise program, which was identical for CR and HR groups, had no effect on body wt., soleus wt., soleus muscle composition or fiber size in CR rats. Atrophied soleus muscle and reduced soleus wt./body wt. ratio (both 60% of control) had returned to control values by day 7 of recovery in both suspended groups despite the fact that whole body wt. gain was significantly reduced (p less than 0.05) in HR as compared to HS rats. Atrophied soleus Type I fiber mean cross-sectional area in both HR and HS groups demonstrated similar and significant (p less than 0.01) increases during recovery. Increases in Type IIa and IIc fiber area during this same period were significant only in the HR group. While the percentage area of muscle composed of Type I fibers increased in both hypodynamic groups during recovery, the reduction in area percentage of muscle made up of Type IIa fibers was again only significant in the HR group.(ABSTRACT TRUNCATED AT 250 WORDS)