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Medicine & Science in Sports & Exercise:

The acute versus the chronic response to exercise


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Preventive Cardiology, Division of Cardiology, Hartford Hospital, Hartford, CT; Department of Health and Kinesiology, Texas A&M University, College Station, TX; Division of Endocrinology, University of Pittsburgh Medical Center, Pittsburgh, PA; Exercise Physiology, City University of Dublin, Dublin, IRELAND; and School of Allied Health, University of Connecticut, Storrs, CT

Submitted for publication January 2001.

Accepted for publication March 2001.

Proceedings for this symposium held October 11–15, 2000, Ontario, Canada.

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THOMPSON, P. D., S. F. CROUSE, B. GOODPASTER, D. KELLEY, N. MOYNA, and L. PESCATELLO. The acute versus the chronic response to exercise. Med. Sci. Sports Exerc., Vol. 33, No. 6, Suppl., 2001, pp. S438–S445.

Purpose: There is strong and consistent evidence that a single exercise session can acutely reduce triglycerides and increase high-density lipoprotein (HDL) cholesterol (HDL-C), reduce blood pressure, and improve insulin sensitivity and glucose homeostasis. Such observations suggest that at least some of the effects on atherosclerotic cardiovascular disease (ASCVD) risk factors attributed to exercise training may be the result of recent exercise.

Results: These acute and chronic exercise effects cannot be considered in isolation. Exercise training increases the capacity for exercise, thereby permitting more vigorous and/or more prolonged individual exercise sessions and a more significant acute effect. The intensity, duration, and energy expenditure required to produce these acute exercise effects are not clearly defined. The acute effect of exercise on triglycerides and HDL-C appears to increase with overall energy expenditure possibly because the effect maybe mediated by reductions in intramuscular triglycerides. Prolonged exercise appears necessary for an acute effect of exercise on low-density lipoprotein (LDL) cholesterol (LDL-C) levels. The acute effect of exercise on blood pressure is a low threshold phenomenon and has been observed after energy expenditures requiring only 40% maximal capacity. The acute effect of exercise on glucose metabolism appears to require exercise near 70% maximal, but this issue has not been carefully examined.

Conclusions: Exercise has definite acute effects on blood lipids, blood pressure, and glucose homeostasis. Exercise also has acute effects on other factors related to atherosclerosis such as immunological function, vascular reactivity, and hemostasis. Considerable additional research is required to define the threshold of exercise required to produce these putatively beneficial effects.

Isolated exercise sessions elicit acute, transient cardiovascular, and metabolic responses. Frequent repetition of these isolated sessions produces more permanent adaptations, referred to as the exercise training response. Many of the potentially favorable changes in atherosclerotic cardiovascular disease (ASCVD) risk factors previously considered to require long-term exercise training are now known to have both an acute and chronic exercise component. These risk factors include blood lipids, blood pressure, and serum glucose, but many of the nonstructural changes that occur with exercise training are also affected by recent exertion. This overview will discuss the acute exercise effect and its influence on selected ASCVD risk factors.

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The acute exercise response and the chronic adaptations to exercise training cannot be viewed in isolation. Haskell (26) has proposed four patterns for an acute exercise effect (Fig. 1).

Figure 1
Figure 1
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a) Exercise may acutely reduce a risk factor, the effect dissipates rapidly and has no influence on the response to subsequent exertion.

b) The acute exercise effect may accrue in a cumulative yet diminishing manner so that subsequent sessions result in asymptotically smaller benefit.

c) Exercise training increases exercise capacity, which permits larger individual exercise sessions and a greater acute effect.

d) Low-level exercise may produce small reductions in risk that are not readily detectable in clinical studies but have benefit when applied to a large enough population.

These patterns are not exclusive, and each may contribute to the acute exercise response, depending on the subject and the risk factor. Indeed, many of the acute exercise changes in risk factors have been reported after prodigious amounts of exercise. Untrained individuals may be incapable of the exertion required to affect a risk factor emphasizing the interdependence of fitness and exercise training on the acute exercise response.

On the other hand, the absence or inconsistency of significant acute exercise effects in reports in untrained subjects doing moderate amounts of exercise does not mean that changes would not be detectable with sufficiently reliable measurement techniques and sufficient sample sizes. Many of the studies mentioned below used prolonged endurance exercise to determine whether any acute changes occurred. Subsequent studies have attempted to define the threshold of exercise required but used sample sizes of 10–20 people. The absence of changes in small study populations does not imply that such changes would not be detectable in larger samples. This review will attempt to identify the dose of exercise required for an acute exercise effect when available, but most studies reported below are really proof of concept reports. The minimal amount of exercise required to produce an important, acute exercise effect cannot be defined with certainty from the available literature.

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The conclusions presented in this review are generally based on Category A Evidence. The amount of information supporting an acute exercise effect on ASCVD risk factors is extensive and generally consistent. That said, it must also be appreciated that published reports probably overestimate an acute exercise effect because of the tendency for positive results to be submitted and accepted for publication. This is especially true in this field of research where the finding of an effect from a singular exercise session would be unexpected to many reviewers and therefore deemed worthy of publication.

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Endurance athletes have serum high-density lipoprotein (HDL) cholesterol (HDL-C) concentrations 10 to 20 mg·dL-1 or 40–50% higher than their sedentary counterparts (52,62,64,71). Triglyceride (TG) levels are 20% lower. Low-density lipoprotein (LDL) cholesterol (LDL-C) concentrations are often approximately 5–10% lower (52,62,64). The major HDL apoproteins (Apo) AI and AII are often 25% and 15% higher (62,64) whereas Apo B is generally 6–7% lower (64). Oral fat tolerance and the ability to clear intravenously administered triglycerides may be enhanced by 50%(52). The activity of enzymes involved with lipid metabolism is also altered with increases in lipoprotein lipase activity (LPLA) of approximately 13% and decreases in hepatic triglyceride lipase activity (HTGLA) as great as 27%(64). At least some of these differences are due to an acute effect of recent exercise. There are over 100 articles and abstracts that have examined the acute effect of exercise on lipids, as shown in Table 1. The results vary, but key factors affecting the results are the physical fitness of the subjects, the subjects’ preexercise lipid levels, and the intensity and duration of the exercise session. Also, because exercise produces an acute, delayed expansion of plasma volume after exercise, small changes in lipid concentrations can be overlooked if the results are not corrected for plasma volume. Nevertheless, the following conclusions can be made from a review of these studies.

Table 1
Table 1
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Exercise acutely reduces TGs.

This effect was first noted in 1964 when Holloszy et al. (27) described acute TG reductions in hypertriglyceridemic men, and Carlson and Mossfeldt (5) reported reductions in TGs in cross-country skiers after 8–9 h of exertion. The reduction in TGs is not immediate but occurs 18–24 h after exercise, consistent with the induction of metabolic changes, persists for up to 72 h (2,5,8–10,14,15,22,53,61,66), and is greatest in those with higher preexercise TG values (9). The effect appears to increase with energy expenditure and does not require a threshold of exertion (10) although untrained individuals may not expend sufficient calories to induce detectable changes in small studies. The most reproducible results have been obtained in fit subjects performing prolonged endurance events such as marathons.

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Exercise acutely increases HDL-C.

This increase has varied from 4 to 43% in various studies (2,5,8–10,14,15,22,53,61,66). The increase generally parallels the decrease in TGs in onset and disappearance, suggesting mediation by similar metabolic changes. The quality and quantity of exertion required to increase HDL-C acutely is not defined although changes in moderately fit (8,66) and well-trained (14) subjects have been reported after expenditures of 350–400 and 1000 kcal, respectively, in a single exercise session. Smaller changes may occur with less energy expenditure but require adjustments for the expansion in plasma volume (36). The increase in HDL-C in sedentary subjects appears to be due by increases in HDL3, whereas HDL2 increases in trained individuals (36). Acute changes in Apo AI and AII usually do not occur even with prolonged exertion, indicating that the acute changes in HDL-C are probably due to enhanced cholesterol delivery to the HDL particle (35,53).

Exercise acutely increases fat tolerance and LPLA (35,53). These changes have most frequently been demonstrated in fit subjects performing extreme exertion, but LPLA increases in untrained individuals exercising for as little as 1 h at 80% of maximal heart rate (36). These observations have lead to the hypothesis that exercise acutely depletes intramuscular triglycerides, which stimulates the synthesis or translocation of LPL, which hydrolyzes triglycerides from lower-density lipoproteins with transfer of the excess surface cholesterol to the HDL particle (61).

The acute effect of exercise on other enzymes involved in HDL metabolism is not established. Cholesterol ester transfer protein (CETP) transfers cholesterol from HDL to other lipoproteins. Reductions in CETP should increase HDL-C. CETP decreased in some (15), but not all, acute exercise studies (22). Lecithin cholesterol acyl transferase (LCAT) esterifies free cholesterol in the HDL particle, permitting its transport in the HDL core and an increase in cholesterol per HDL particle. LCAT has also increased acutely in some exercise studies (17) but has decreased in others (13).

Prolonged exercise generally produces small reductions in TC and LDL-C. The effect of exercise on TC is the summation of changes in the various lipoprotein subfractions so that changes in TC alone have little physiological significance. LDL-C generally decreases in trained men after prolonged exercise. This decrease is approximately 8%(53). LDL-C may also acutely decrease 5–8% in hypercholesterolemic men with exercise (8,9,22). Most of these studies estimated LDL-C using the Friedewald equation, and it is unclear whether changes in very LDL (VLDL) TG content affected the results. Furthermore, some of the reduction in LDL-C may be due to the expansion of plasma volume, which is itself a possibly beneficial acute exercise effect. Expanded plasma volume decreases blood viscosity and the concentrations of ASCVD risk factors, which may reduce their effect on the arterial wall. Exercise cessation in habitually active distance runners produced a 10% increase in LDL-C after only 2 d of inactivity that was not augmented by additional rest (63). This increase in LDL-C was accompanied by an acute decrease in plasma volume, suggesting that at least some of the lower LDL-C in endurance athletes is due to plasma volume expansion.

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Summary of the acute effect of exercise on serum lipids.

There is Category A evidence that endurance exercise acutely reduces triglycerides and increases HDL-C. It is likely that these changes are related to total energy expenditure, but there is insufficient evidence to define whether caloric expenditure, intensity of effort, or some combination is responsible. Exercise cessation studies confirm that the higher HDL levels in very active individuals are not due solely to an acute exercise effect. On the other hand, some of the changes in triglycerides and HDL-C that occur with brief exercise training may be largely if not entirely, an acute exercise effect. There is Category A evidence that prodigious amounts of exercise such as marathon running can acutely reduce LDL-C, but this reduction may be partly an indirect effect mediated by an acute expansion of plasma volume.

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The reduction in resting systolic (SBP) and diastolic (DBP) blood pressure immediately after a bout of aerobic exercise was noted by Kaul et al. (40) over 30 years ago and has subsequently been termed “postexercise hypotension” (PEH) (38). An accumulating body of scientific evidence indicates that PEH is an expected physiological response to moderate-intensity dynamic exercise. PEH has been observed in normotensive and hypertensive middle-aged and older people, with the largest absolute and relative blood pressure reductions seen in hypertensive subjects (23,38). Maximal decreases in SBP of 18–20 mm Hg and DBP of 7–9 mm Hg have been reported among those with Stage I hypertension. The emergence of ambulatory blood pressure monitoring has allowed assessment of the hypotensive influence of exercise beyond the laboratory. Subsequently, it has been found that PEH may persist for up to 16 h after exercise. This offers individuals with high normal to Stage I hypertension the benefit of having their blood pressure lowered into normotensive ranges for a major portion of the day (38,48,49,59).

The acute and chronic depressor effects of dynamic exercise are a low-threshold phenomenon with hypotensive responses noted at an exercise intensity of 40% of maximum oxygen consumption (23,38,48) and after just three sessions of aerobic activity in training studies (32,43,48). The depressor influence of exercise quickly subsides with blood pressure increasing to preexercise levels after 1–2 wk of detraining (38,43). The immediacy by which PEH occurs suggests that some if not all of the hypotensive benefits ascribed to endurance training programs may be an acute postexercise phenomenon related solely to recent exercise (56).

Ambulatory blood pressure monitoring has been used to assess the effect of exercise in 8 acute and 14 exercise-training studies. The subjects were primarily white men with an average age of 44 yr who were on no medications and were sedentary and overweight to obese. The mean intensity of the exercise intervention was 65% of maximum oxygen consumption, and the duration of the typical exercise session was 38 min. In the training studies, subjects trained an average of 3 d·wk-1 for 18 wk, and maximum oxygen consumption increased a mean of 10%. Ambulatory measurements suggest that exercise training produces greater blood pressure reductions than does acute exercise (Tables 1–3). Much of this apparent effect, however, may be related to the higher preexercise pressures in the exercise-training subjects. Merely based upon the law of initial values (70), the blood pressure reductions would be expected to be larger for subjects with higher initial pressures. Consequently, the relative contribution of PEH to the blood pressure reductions of exercise training remains undefined but may be substantial in studies where blood pressure was determined within 12 h of the last exercise session.

Table 3
Table 3
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Despite consensus that chronic exercise reduces blood pressure, multiple reports have failed to document such an effect probably because of methodological considerations (48) (Tables 1 and 2). These include insufficient sample sizes to detect the smaller decreases in blood pressure seen with ambulatory blood pressure monitoring, failure to include a control session of rest, failure to account for diurnal variation, and failure to consider the acute exercise effect of recent exercise.

Table 2
Table 2
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Summary of the acute effects of exercise on blood pressure.

There is Category A evidence that exercise produces a acute blood pressure reduction that may persist for 12–16 h. This effect possibly contributes to the reduction in blood pressure with exercise training but is unlikely to explain it completely because most measurements in training studies are performed more than 12 h after the last exercise.

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There is Category A evidence that even a single session of exercise can improve glucose control in Type 2 diabetics and ameliorate insulin resistance in other subjects. This acute improvement in insulin sensitivity is short-lived and lasts for only several days. Devlin and Horton (12) found that a single session of moderate exercise lowered hepatic glucose production for the following day in patients with Type 2 diabetes. Rogers et al. (50) noted that only one week of daily exercise at 70% of V̇O2max reduced insulin resistance in patients with Type 2 diabetes mellitus and improved glucose tolerance. A single exercise session increases the skeletal muscle’s insulin sensitivity and ability to resynthesize glycogen (47), probably by increasing the muscle’s number and activity of the GLUT 4 glucose transporters (28,29) and the content and activity of hexokinase (39).

We have summarized several studies that have examined the acute, dose-response effect of exercise on blood glucose control in Type 2 diabetes (Table 4) (37). In healthy nondiabetic individuals, blood glucose levels are well maintained, even during vigorous exercise. In patients with Type 2 diabetes mellitus, however, moderate-intensity exercise of approximately 45–60 min duration has been shown to lower plasma glucose by approximately 20–40 mg·dL-1 (1–2 mM) (18,34,42,44,54). The fall in blood glucose during exercise in these patients with Type 2 diabetes was remarkably similar, owing in part to the similar exercise protocols used and the level of glucose control before exercise. Only two of these studies observed no change in plasma glucose during exercise (6,31). None of the participants in these studies developed hypoglycemia; in fact, all remained with elevated plasma glucose despite the exercise-induced reductions of hyperglycemia. Although not specifically addressed in these studies, it is reasonable to anticipate potentially greater decreases in blood glucose when patients are using pharmacologic agents, such as sulfonylurea drugs or insulin. A clear dose-response effect of either exercise intensity or duration on blood glucose responses in Type 2 diabetes is difficult to ascertain from the reviewed studies.

Table 4
Table 4
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The acute effects of exercise on insulin sensitivity may relate to depletion of muscle glycogen (47) or triglycerides (46). There is regulation of muscle glycogen content so that depletion of muscle glycogen leads to enhanced glucose uptake and repletion of muscle glycogen. Kang et al. (34) compared the effect of exercise for 70 min at 50% or 50 min at 70% for 1 wk. Energy expenditures for the sessions were equivalent. After 1 wk of daily exercise, insulin sensitivity improved only when subjects exercised at 70% of V̇O2max, although changes in serum glucose levels were similar. The higher exercise intensity produced greater reductions in muscle glycogen and postexercise reductions in insulin were related to the amount of glycogen oxidized. This suggests that the short-term effects of exercise on insulin sensitivity are related to depletion of muscle glycogen and that vigorous exercise may be required to produce this acute exercise effect. Alternatively, insulin resistance is related to intramuscular triglyceride content and the acute effect of exercise on insulin resistance may be related to an exercise-induced reduction in muscle triglycerides. Pan and colleagues (46) found that among 38 nondiabetic male Pima Indians, muscle triglyceride content was inversely related to insulin sensitivity. Similarly, others have also shown an inverse relationship between muscle triglyceride content and insulin-stimulated glucose uptake (20,57). This observation suggests that vigorous exercise may not be required to produce the improvement in insulin sensitivity because free fatty acids are can be oxidized during low-level energy expenditure. Additional studies on the mechanism on how exercise affects glucose homeostasis are required before specific recommendations can be made on the intensity and duration of exercise required to acutely improve glucose control.

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Summary of the acute effects of exercise on glucose metabolism.

Exercise acutely reduces insulin resistance and improves glucose control, but the mechanisms and threshold required for this effect are not defined.

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There is Class A evidence that exercise has acute effects on blood lipids, blood pressure, and glucose homeostasis. Exercise also has acute effects on other factors related to atherosclerosis, such as immunological function, vascular reactivity, and hemostasis, which are beyond the scope of this overview. Additional research is required to define the threshold of exercise required to produce these putatively beneficial effects.

Address for correspondence: Paul D. Thompson, M.D., Cardiology, 7th Floor Jefferson, Hartford Hospital, 80 Seymour Street, Hartford, CT 06102; E-mail:

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© 2001 Lippincott Williams & Wilkins, Inc.


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