I’ve now done some more reading (including reading the 2012 paper more carefully).
What is surprising about the 2012 result (at least to me) is not that TEE (adjusted for FFM) is similar in different populations. That is consistent with other results, e.g. Westererp & Speakman (2008), which finds that TEE (which they call DEE) (a) has not changed significantly over time in Europe since the 1980s, (b) is not significantly different between populations in Europe/North America and those in the third world and (c) is not significantly different between modern humans and wild animals of the same size.
What makes the 2012 result surprising is that the PALs are different. For TEE to remain constant with varying PAL would require a strict negative relationship between PAL and RMR, so that increases in AEE were exactly compensated for by decreases in RMR. This seems intuitively unlikely. In fact, Pontzer et al (2016) finds that RMR is not correlated with physical activity.[1] I read the 2016 paper as showing some shift in Pontzer’s view generally, as he there advocates for a “constrained total energy expenditure model”, while allowing that TEE can and does vary within those contraints.
The surprising difference in PALs between the groups in the 2012 paper may plausibly be a result of a limitation in the experimental method, namely that the PALs for the Hadza subjects have been calculated using estimated rather than measured BMRs. Rather oddly, the experimenters did measure the Hadza subjects’ RMRs, but then threw the measurements out (giving some cogent reasons for doing so). The Hadza BMRs were estimated by “enter[ing] each subject’s body mass and height into age-specific prediction equations developed in a large sample (n = 10,552) from a geographically broad set of populations that includes populations in sub-Saharan Africa,” but formulaic estimates of BMR notoriously differ widely from measured BMRs, and a broad sample will necessarily not reflect any factors particular of the Hadza.
What is true is that PAL behaves in some unintuitive ways. See, for example, Westererp (2013). This tells us that 72-78% of the variance in PAL is genetic. PAL decreases with age after 50 (and increases with age in children), but it does not vary significantly with body weight (save for subjects with BMI>35) or with body composition (after controlling for age). Exercise increases PAL in young adults eating ad libitum (who increase dietary intake to compensate) but does not increase PAL either in older adults or in young adults subject to an energy-restricted diet. It appears that the second two groups compensate for the increase in intentional activty by decreasing non-intentional activity, so as to keep AEE roughly constant. PAL decreases under starvation (i.e. significant underfeeding of normal weight subjects), but does not seem to be significantly affected by underfeeding in overweight and obese subjects.[2] Similarly, there is no significant effect of overfeeding on PAL, when the overfeeding is lower than twice maintenance. PALs in Western countries have increased slightly since 1990 (during which time obesity levels have increased markedly) and as previously noted are in line with those found in wild mammals, so the common perception that we are particularly inactive is mistaken.
Looking the evidence as a whole, I do not believe it supports the claim that exercising more causes your body to expend less energy on maintenance and repair, although it does usually cause your body to compensate by either (a) eating more food or (b) reducing non-intentional activity.
Although see Westererp (2016). This cites different studies showing that underfeeding obese individuals leads to a small reduction in both AEE and RMR (which he calls REE). These would tend to cancel each other out, to keep PAL constant. But the reduction in AEE is not sustained after energy intake is raised to match TEE, whereas the reduction in RMR is, which should lead to an increase in PAL. These numbers are all small though.
I’ve now done some more reading (including reading the 2012 paper more carefully).
What is surprising about the 2012 result (at least to me) is not that TEE (adjusted for FFM) is similar in different populations. That is consistent with other results, e.g. Westererp & Speakman (2008), which finds that TEE (which they call DEE) (a) has not changed significantly over time in Europe since the 1980s, (b) is not significantly different between populations in Europe/North America and those in the third world and (c) is not significantly different between modern humans and wild animals of the same size.
What makes the 2012 result surprising is that the PALs are different. For TEE to remain constant with varying PAL would require a strict negative relationship between PAL and RMR, so that increases in AEE were exactly compensated for by decreases in RMR. This seems intuitively unlikely. In fact, Pontzer et al (2016) finds that RMR is not correlated with physical activity.[1] I read the 2016 paper as showing some shift in Pontzer’s view generally, as he there advocates for a “constrained total energy expenditure model”, while allowing that TEE can and does vary within those contraints.
The surprising difference in PALs between the groups in the 2012 paper may plausibly be a result of a limitation in the experimental method, namely that the PALs for the Hadza subjects have been calculated using estimated rather than measured BMRs. Rather oddly, the experimenters did measure the Hadza subjects’ RMRs, but then threw the measurements out (giving some cogent reasons for doing so). The Hadza BMRs were estimated by “enter[ing] each subject’s body mass and height into age-specific prediction equations developed in a large sample (n = 10,552) from a geographically broad set of populations that includes populations in sub-Saharan Africa,” but formulaic estimates of BMR notoriously differ widely from measured BMRs, and a broad sample will necessarily not reflect any factors particular of the Hadza.
What is true is that PAL behaves in some unintuitive ways. See, for example, Westererp (2013). This tells us that 72-78% of the variance in PAL is genetic. PAL decreases with age after 50 (and increases with age in children), but it does not vary significantly with body weight (save for subjects with BMI>35) or with body composition (after controlling for age). Exercise increases PAL in young adults eating ad libitum (who increase dietary intake to compensate) but does not increase PAL either in older adults or in young adults subject to an energy-restricted diet. It appears that the second two groups compensate for the increase in intentional activty by decreasing non-intentional activity, so as to keep AEE roughly constant. PAL decreases under starvation (i.e. significant underfeeding of normal weight subjects), but does not seem to be significantly affected by underfeeding in overweight and obese subjects.[2] Similarly, there is no significant effect of overfeeding on PAL, when the overfeeding is lower than twice maintenance. PALs in Western countries have increased slightly since 1990 (during which time obesity levels have increased markedly) and as previously noted are in line with those found in wild mammals, so the common perception that we are particularly inactive is mistaken.
Looking the evidence as a whole, I do not believe it supports the claim that exercising more causes your body to expend less energy on maintenance and repair, although it does usually cause your body to compensate by either (a) eating more food or (b) reducing non-intentional activity.
Although the authors make no attempt to distinguish between aerobic and resistance exercise.
Although see Westererp (2016). This cites different studies showing that underfeeding obese individuals leads to a small reduction in both AEE and RMR (which he calls REE). These would tend to cancel each other out, to keep PAL constant. But the reduction in AEE is not sustained after energy intake is raised to match TEE, whereas the reduction in RMR is, which should lead to an increase in PAL. These numbers are all small though.