VO2max refers to the maximum amount of oxygen that muscles can take in, absorb, and use during intense endurance exercise within a specific time frame. It is widely regarded as the gold standard for measuring cardiorespiratory fitness (Zheng et al., 2022).

Training is an effective means of preserving and enhancing VO₂max, albeit with variable outcomes influenced by both intensity and volume. Genetics largely determine VO₂max, with improvements typically ranging from 15% to 30%. Remarkably, elite athletes often achieve values exceeding 90 mL/kg/min. Research suggests that high volume training may foster future potential enhancements, while high-intensity training appears to elicit more rapid adaptations (Buchheit and Laursen, 2013). However, Attention must be given to the reversibility of VO₂max adaptability, signifying its return to pre-intervention values upon cessation or significant reduction of training stimuli (Zheng et al., 2022). Upon the cessation or reduction of training, a significant decline in VO₂max becomes apparent within just a few days of commencing detraining.

Coyle et al., reported a −7% decline of VO₂max in a group of runners and cyclists just 12 days later training interruption (Coyle et al., 1984). In a group of distance runners, 14 days of training cessation, caused −4.7% losses when compared with the training state (Houmard et al., 1992); similar results were observed after 15 days of total stop (−3.7%) (Chen et al., 2022). In contrast with previous studies, Cullinane et al. found no change in VO₂max after 10 days of training cessation (Cullinane et al., 1986): this result may be explained by the variability of daily physical activity, not specifically related to sports, performed by athletes during the period of detraining (Mujika and Padilla, 2001b). When inactivity is prolonged up to 3 weeks, there is a decrease of 4.18% (Martin et al., 1986). After 5 weeks there is a decrease of 10.1% (García-Pallarés et al., 2009), following 56 days a decrease of 13% (Coyle et al., 1984; Coyle et al., 1985) and after 2 months a decrement of 20% (Martin et al., 1986). No further significant decrements are found after 12 weeks (Coyle et al., 1985; Martin et al., 1986).

The decline in VO₂max observed between the 21st and 84th day of detraining seems attributed to a reduction in the maximum arterial-venous oxygen difference (Coyle et al., 1984). The drop in VO₂max following brief periods of detraining (less than 4 weeks) is primarily due to the decrease in total blood and plasma volume (Mujika and Padilla, 2001b). This reduction significantly impacts performance (Doherty et al., 2003).

When considering detraining as a partial reduction in training load (by both volume and intensity), VO₂max levels seems to be maintained after 4-week of low-volume and moderate-to-high intensity training (Madsen et al., 1993; McConell et al., 1993). In contrast, Garcia-Pallares reported a loss of–5.6% in VO₂max after 5 weeks of reduced training volume at moderate intensity in a group of elite kayakers (Martin et al., 1986).

Recent studies exploring the consequences of partial training reduction indicate that maintaining VO₂max levels is achievable by incorporating a single weekly high-intensity training (HIT) session alongside reduced low-intensity training (LIT) volume during an 8- week transition period. Conversely, using solely LIT during a partial cessation period, would not produce the same conservative effect (Rønnestad et al., 2014). Incorporating a weekly sprint session within a constrained LIT volume yields no significant alterations in VO₂max when compared to exclusively performing LIT over a shorter span of 3 transition training weeks (Almquist et al., 2020).

The decline of VO₂max is related to the reduction in blood volume and in plasma volume. According to Coyle et al., a period of complete detraining lasting between 2 and 4 weeks during orthostatic exercise (cycling on a stationary ergometer) resulted in a 9% reduction of blood volume, attributed to a 12% decline in plasma volume (Coyle et al., 1986). Houmard et al. presented a 5.1 %± 1.9% decrease in resting plasma volume following 14 days of inactivity (Houmard et al., 1992).

The decrease in blood volume significantly impacts cardiovascular regulation during exercise, likely influencing the low-pressure baroreceptors responsible for managing venous blood return to the heart. Consequently, there is a reduction in central venous pressure, triggering vasoconstriction in the splanchnic area, skin, and inactive muscles. This phenomenon potentially elucidates the observed increases in mean arterial pressure (Coyle et al., 1985).

Because of blood volume’s decline, there is an increase in maximal and submaximal heart rate following periods of training reduction or total cessation.

In short-term detraining, maximal heart rate (HRmax) increases by 2-9 beats per minute (Coyle et al., 1984; Cullinane et al., 1986; Houmard et al., 1992; Doherty et al., 2003; Chen et al., 2022) while submaximal heart rate is distinguished between orthostatic and supine exercise: in the first case, there is an increase of 2.6% after 21 days, of 10%–11% from day 56–84. In supine exercises there is an increase of 4.7%, 5.6%, 11.2% after 12, 56, 84 days respectively (Martin et al., 1986).

After 1 year of total detraining, resting heart rate increased by 13%, an average of 7 beats per minute higher than pre-detraining values (Pelliccia et al., 2002).

The rise in both maximal and submaximal heart rate during short-term detraining can be attributed to a decrease in stroke volume resulting from reduced ventricular filling, which is primarily caused by the decrease in plasma volume (Coyle et al., 1986). Additionally, the increase in peak heart rate can be viewed as a compensatory mechanism to maintain cardiac output despite the decrease in plasma volume (Cullinane et al., 1986).

However, there are some studies that found no change in this parameter after inactivity or reduced training periods of 10 days, 3, 4, and 6 weeks (Cullinane et al., 1986; Petretta et al., 1991; Maron et al., 1993).

Deconditioning after several years of intense training leads to a reduction, during orthostatic exercise, in stroke volume, calculated as the ratio of cardiac output to heart rate (Martin et al., 1986). On the other hand, during supine exercise no significant differences are found (Martin et al., 1986). The variance between orthostatic and supine positions could be attributed to pressure alterations resulting from position changes, consequently impacting venous return. Differently, a few days after training cessation, a reduction of stroke volume during orthostatic exercise can be registered: after 10 days −0.9% (Doherty et al., 2003), −4.1% after 2 weeks (Chen et al., 2022)and −14% after 56 days of inactivity (Coyle et al., 1984).

The reduction in stroke volume during upright exercise is linked to a decrease in the telediastolic dimension of the Left Ventricle (Martin et al., 1986) and does not appear to be due to a deterioration of myocardial contractility (Coyle et al., 1986; Martin et al., 1986).

As for cardiac output, it appears to remain unchanged after 5–10–15 days of detraining (Doherty et al., 2003): The maintenance of cardiac output in the absence of change appears to be influenced by the typical relationship between HR and SV, as observed during short-term detraining where an increase in HR coincides with a decrease in stroke volume. After 21 days, a decline of 8% is recorded, not falling beyond this decline as detraining days progressed (Coyle et al., 1984).

Following short-term training cessation, mean blood pressure increases by 7% during submaximal upright exercise (Coyle et al., 1986). Conversely, after long-term detraining, there is an 11% increase in blood pressure during orthostatic exercise and a 1% increase in supine positions (Martin et al., 1986). This rise indicates a concurrent increase in total peripheral resistance (TPR) by 7%–8% (Coyle et al., 1986; Petretta et al., 1991). Moreover, even after 12 weeks of detraining, TPR remains within the range of a 7.9%–9% increase (Martin et al., 1986).

Cerebrovascular system responds to insufficient training stimulus: in master athletes, after 10 days of inactivity, there is a decline in resting cerebral blood flow (rCBF) at 8 regions of the brain: inferior temporal gyrus, fusiform gyrus, inferior parietal lobule, cerebellar tonsil, lingual gyrus, precuneus, bilateral cerebellum and right and left hippocampus (Alfini et al., 2016). After short-term detraining, a decrease in cortical and hippocampal cerebral blood flow is observed, despite participants showing no changes in cognitive function in the study. However, these effects might significantly influence brain function in older individuals by altering arterial transit time or blood volume in the brain (Alfini et al., 2016).

A regular aerobic training regimen induces cardiac adaptations, including the augmentation of left ventricular size, mass, and thickness, which play a crucial role in health, longevity, and sports performance. However, cessation or reduction of daily physical activity leads to the loss of these trained heart adaptations (Petek et al., 2022).

After short-term inactivity (12 weeks of detraining), total peripheral resistance (TPR) increase by 7%–8% remaining in the range of 7.9%–9% increase (Coyle et al., 1986; Martin et al., 1986; Petretta et al., 1991).

Regarding changes in ventilatory function, a rapid decline due to the decrease in maximal expiratory ventilatory volume is evident, consequent to short-term training cessation (Houmard et al., 1992; Houmard et al., 1993). During submaximal intensity exercise, an increase in ventilatory volume and ventilatory equivalents is evidenced (DB and HS, 1972; Coyle et al., 1985). These increases indirectly suggest a rise in muscle and blood lactate levels as a consequence of detraining (Houmard et al., 1992). Similar results on maximal ventilatory volume are reported before and after 4 weeks partial training reduction (McConell et al., 1993).

The reversal of adaptations induced by the cessation or reduction of habitual physical activity leads to a decline in sports performance (Mujika and Padilla, 2000b; Houmard et al., 1992; Houmard et al., 1993), with no observed changes in running economy. Endurance is notably compromised after just 2 weeks of training cessation, evidenced by a 9% decrease in Time To Exhaustion (TTE), with no observed changes in running economy (Houmard et al., 1992). A group of runners showed that they were able to maintain muscle endurance despite 2 weeks of inactivity (Chen et al., 2022). Conversely, over a more extended period of partial training reduction, a cohort of triathlon athletes, proficient in running and cycling, experienced a decline in endurance capacity (specifically, Time To Exhaustion at 75% VO₂max), reducing it by 21% when engaging in only one weekly low-volume High-Intensity Interval Training (HIT) session (35 min at 95% HRmax) (Madsen et al., 1993).

Short-term detraining has shown an elevation in blood lactate concentration following submaximal exercise (García-Pallarés et al., 2009; Chen et al., 2022). This increase, coupled with altered Mg²⁺ transport from the extracellular to the intracellular compartment, potentially inhibits Ca²⁺ release from the sarcoplasmic reticulum (Głyk et al., 2022). Consequently, this inhibition could impair contractile capacity (García-Pallarés et al., 2009) and be a contributing factor to the reduction in TTE (García-Pallarés et al., 2009) (20).

Respiratory exchange ratio (RER) increases in short-term detraining during submaximal (Coyle et al., 1984; Madsen et al., 1993) and maximal exercises (Houmard et al., 1992). In seven endurance athletes, RER increases from 0.93 of the trained state to 1, after 84 days of detraining, during a submaximal exercise performed at the same absolute intensity (Coyle et al., 1985). These observed changes stem from an increased reliance on carbohydrates, compromising lipid metabolism (Mujika and Padilla, 2000b).

The primary alteration observed during detraining affects energy parameters in carbohydrate and lipid metabolism. Resting triglyceride concentration decreases with training, attributed to increased fatty acid turnover. Alongside this reduction, there’s an elevation in glycerol and apolipoprotein C3 (Apo-C3) levels. Higher concentrations of Apo-C3 are linked to hypertriglyceridemia and the release of VLDL and chylomicrons into the bloodstream (Petibois and Déléris, 2003).

Following short-term training cessation, there is a decrease in post-exercise glucose concentration (Petibois and Déléris, 2003) and an increase in resting glucose concentration. This rise may be attributed to a decreased rate of glucose disposal resulting from reduced insulin action (McCoy et al., 1994; Arciero et al., 1998; Petibois and Déléris, 2003).

While skeletal muscle exhibits heightened glycolytic utilization during detraining, the hepatic level experiences a decline in both glycogenolysis and glycogenosynthesis (Mikines et al., 1989; Petibois and Déléris, 2003). Inactivity leads to decreased triglyceride levels during exercise and in adipose tissue release, along with reductions in glycerol levels during both activity and rest (Coyle et al., 1985; Mikines et al., 1989; Petibois and Déléris, 2003). Apo-C3 levels tend to revert to pre-training cessation levels. Notably, no changes are observed in hemolytic parameters like haptoglobin and transferrin (Petibois and Déléris, 2003).

Long-term effects include increased resting triglyceride concentrations (Gill et al., 2003). During exercise, there’s heightened utilization of glycolysis, glycerol, and Apo-C3, accompanied by decreased neoglucogenesis and triglyceride utilization. Changes in haptoglobin and transferrin concentrations are observed, likely due to heightened erythrocyte dysfunction (Petibois and Déléris, 2003).

These results suggest the impairment of fatty acid availability, consequent to the reduction of adipose and muscle triglyceride release (Madsen et al., 1993; Petibois and Déléris, 2003).

A master cyclist, subjected to detraining consequent to a clavicular fracture, presented a 16.7% drop in lactate threshold (Nichols et al., 2000). After 12 weeks of inactivity, 14 swimmers showed a decline in speed at the lactate threshold (Głyk et al., 2022).

After 5 weeks of training cessation, 10 highly trained rowers exhibited a fourfold increase in blood lactate concentration compared to pre-detraining values. This change was observed during an incremental and exhaustive test on a rowing-ergometer, highlighting the impact of detraining on lactate levels in this cohort (Petibois and Déléris, 2003). Additionally, among a group consisting of 4 runners and 3 cyclists, a transition from 1.9 to 7.6 mmol/L in post-exercise blood lactate concentration was noted after 84 days of inactivity. This elevation occurred during a submaximal test with the same intensity, conducted on specific exercise equipment (treadmill for runners, cycle ergometer for cyclists) (Coyle et al., 1985). Such increases significantly contribute to compromised endurance performance.

In runners, cyclists and triathletes, 4 weeks of training reduction resulted in a decrease of muscle glycogen by 18% (Madsen et al., 1993). This seems to be caused by a lowering in glycogen synthesis and in the enzyme glycogen synthase’s activity (Kjaer et al., 1992; Mujika and Padilla, 2000b).

Body weight and body composition are not affected by short-term detraining (Coyle et al., 1984; Houmard et al., 1993; McCoy et al., 1994; Arciero et al., 1998). However, in the period longer than 4 weeks, body weight increases considerably (DB and HS, 1972; Głyk et al., 2022).

Analyzing cholesterol change induced by training cessation, a 0.9% decrease in high-density lipoprotein (HDL) type cholesterol after 6.5 days (Godfrey et al., 2005) was identified. During the same periods of detraining, Low Density Lipoprotein (LDL) cholesterol levels were increased up to 1.6% (Hardman et al., 1998) and 2.1% (Mikines et al., 1989). Very Low-Density Lipoprotein (VLDL) cholesterol manifested opposite results: no change (Hardman et al., 1998), compared with a 50% increase after 1 week of inactivity (Gill et al., 2003).

A few days after training cessation, the first signs of muscle atrophy occur with fiber denervation, with neuromuscular junction damage and with a reduction of muscle protein synthesis (Paoli and Musumeci, 2020). In this context, studies are scarce and inconsistent, yet some indicate the onset of muscle atrophy within a few days of inactivity (Houmard et al., 1992). As to the amount of oxidative fiber, results are limited and conflicting as well. In contrast to studies reporting no change in fiber composition (Houmard et al., 1992; McCoy et al., 1994), Coyle et al. showed an appreciable change in the percentage of type I and type II fibers: after 56 days from the initiation of detraining, a transition from type IIa to type IIx fibers occurred in runners and cyclists, with the latter increasing from 5% of the trained state to 19% (Coyle et al., 1985).

Regarding changes in capillary density resulting from inactivity, there is one study showing unchanged capillarization after 12–21-56–84 days (Coyle et al., 1984). Muscle capillary density maintenance appears to be a long-term adaptation resulting from prolonged training. Conversely, sedentary individuals who underwent 8 weeks of training exhibited a reduction in this parameter (Coyle et al., 1984). Other studies also indicate a regression after 2–3 weeks (Mujika and Padilla, 2001b), such as Houston et al. (1979) study reporting a 6% decrease after 15 days of inactivity.

The decrease in VO₂max is associated with the reduction in arterial-venous oxygen differences: this parameter appears to decrease when training cessation is prolonged for more than 3–8 weeks (Coyle et al., 1984). The reduction observed could be attributed to decreased mitochondria at the muscle level. However, other contributing factors such as reduced muscle blood flow or altered blood transit time in the capillaries cannot be excluded (Mujika and Padilla, 2001a). According to Coyle et al., initial decline in VO₂max is partially caused by the decrease in stroke volume, while the decrease in arterial-venous oxygen difference is responsible for the loss of VO₂max observed between the thirds and 12th week of detraining (Coyle et al., 1984).

As training cessation is prolonged, a decline in citrate synthase (CS) enzyme’s activity is identified in endurance trained subjects (Coyle et al., 1984; Houmard et al., 1992; Madsen et al., 1993; McCoy et al., 1994). This enzyme, involved in the process of cellular respiration, is responsible for both catalyzing the first reaction of the Krebs cycle, and for regulating the flow rate of the entire cycle. A 5% decrease in CS was observed following 6 days of inactivity (Coyle et al., 1984), a 28.6% CS decrease was seen after 10 days of inactivity (McCoy et al., 1994) while in the long-term detraining, after 56 days, the CS reduction was equal to 40% (Coyle et al., 1984). At the same time, reductions in the content of GLUT4 are reported. GLUT 4 is a glucose transporter primarily activated by insulin or muscle contraction. As a membrane protein present in adipocytes, myocytes, and cardiomyocytes, its main function involves facilitating the transfer of glucose from the interstitial fluid into the interior of the cell (Houmard et al., 1993). In highly trained athletes, GLUT4 protein content was reduced by 17% after 6 days of inactivity (Vukovich et al., 1996) and by 33% in the first 10 days (McCoy et al., 1994). In contrast to these results, Houmard et al. (1993) found that despite 14 days of detraining, the carrier content remained unchanged. The reduction in muscle oxidative capacity is further evident through the decrease in the activity of enzymes such as ß-hydroxyacyl-CoA dehydrogenase (Madsen et al., 1993) and succinate dehydrogenase (Houston et al., 1979; Coyle et al., 1984). The activity of the succinate dehydrogenase enzyme is estimated to have declined with a half-life of 12 days (Coyle et al., 1984).

Following 5 days of training cessation, a reduction in the activity of the enzyme glycogen synthase is seen, subsequently impacting the conversion of glucose into glycogen (Mikines et al., 1989; Madsen et al., 1993).

However, concerning the enzyme lactate ases have been observed (Houston et al., 1979; Coyle et al., 1985). In the context of glycolytic enzymes, specifically the activity of phosphorylase and phosphofructokinase enzymes, no changes have been noted.

A detraining period of 6.5 days has been shown to result in an increase in postprandial lipemia (Hardman et al., 1998).

The decrease in oxidative enzymes results in diminished ATP production at the mitochondrial level, occurring shortly after the cessation of training (Mujika and Padilla, 2001a). Specifically, the activity of citrate synthase decreased from 10.0 to 7.7 mol kg during the initial 3 weeks without training. Subsequently, this decline continued, reaching 6.0 mol kg over the following 8 weeks, and eventually stabilized (Coyle et al., 1985).

After 4 weeks of reduced training, there may be an impaired transport of magnesium from the extracellular to the intracellular compartment. This alteration could potentially inhibit calcium release from the sarcoplasmic reticulum, thereby compromising performance (Madsen et al., 1993).

Myoglobin concentration appears not to be affected by detraining status (Coyle et al., 1984).